PURPOSE:: The greater accuracy of apical dissection and reconstruction in our first 100 patients undergoing transperitoneal laparoscopic radical prostatectomy (TLRP) was not matched by a proportionate increase in the rate of return to normal continence compared with our prior open prostatectomy experience. We postulated that greater bladder dysfunction due to the almost total bladder dissection mandated by TLRP might be responsible and this might be rectified by the adoption of laparoscopic radical prostatectomy using an extraperitoneal approach (ELRP).MATERIALS AND METHODS:: A total of 100 patients undergoing TLRP were compared with 100 undergoing ELRP. The groups were subdivided into halves to investigate the influence of any learning curve effect. All patients had clinical stage T3aN0M0 or less prostate cancer and they were operated on by a single surgeon.RESULTS:: Mean operative time (238.9 vs 190.6 minutes), blood loss (310.5 vs 201.5 ml), postoperative hospitalization (3.8 vs 2.6 nights) and catheterization duration (11.3 vs 10.1 days) were significantly greater in the TLRP group. After the first 50 cases were excluded in each group statistical significance persisted only for operative time (218.3 vs 184.2 minutes) and hospitalization (3.5 vs 2.5 nights). The pad-free rate was significantly lower 3 months following ELRP (80% vs 56%, p = 0.02). The overall 12-month pad-free rate for TLRP and ELRP was 90% and 96%, respectively. The overall 12-month erection rate for TLRP and ELRP was 61% and 82%, respectively.CONCLUSIONS:: ELRP is superior to TLRP with respect to operative time, hospitalization and early continence.

BJU InternationalVolume 92, Issue 5 p. 510-515 Renal transplantation into the abnormal lower urinary tract M.E. Sullivan, M.E. Sullivan Department of Urology, Churchill Hospital, Oxford, &Search for more papers by this authorJ.M. Reynard, J.M. Reynard Department of Urology, Churchill Hospital, Oxford, & The National Spinal Injuries Centre, Stoke Mandeville Hospital, Aylesbury, Bucks, UKSearch for more papers by this authorD.W. Cranston, D.W. Cranston Department of Urology, Churchill Hospital, Oxford, &Search for more papers by this author M.E. Sullivan, M.E. Sullivan Department of Urology, Churchill Hospital, Oxford, &Search for more papers by this authorJ.M. Reynard, J.M. Reynard Department of Urology, Churchill Hospital, Oxford, & The National Spinal Injuries Centre, Stoke Mandeville Hospital, Aylesbury, Bucks, UKSearch for more papers by this authorD.W. Cranston, D.W. Cranston Department of Urology, Churchill Hospital, Oxford, &Search for more papers by this author First published: 21 August 2003 https://doi.org/10.1046/j.1464-410X.2003.04377.xCitations: 17 M.E. Sullivan, Churchill Hospital, Old Road, Oxford OX3 7LJ, UK. e-mail: •• Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL REFERENCES 1 Kelly WD, Merkel FK, Markland C. Ileal urinary diversion in conjunction with renal homotransplantations. Lancet 1966; 1: 222– 6 2 Tunner WS, Whitsell JC, Rubin AL et al. Renal transplantation in children with corrected abnormalities of the lower urinary tract. J Urol 1971; 106: 133– 9 3 Hatch DA. Kidney transplantation in patients with an abnormal lower urinary tract. Urol Clin North Am 1994; 21: 311– 20 4 Nguyen DH, Reinberg Y, Gonzalez R, Fryd D, Najarian JS. Outcome of renal transplantation after urinary diversion and enterocystoplasty: a retrospective controlled study. J Urol 1990; 144: 1349– 51 5 Rudge CJ. Transplantation and the abnormal bladder. In PJ Morris ed. Kidney Transplantation. 5th edn. Philadelphia: WB Saunders, 2001: 173– 83 6 Errando C, Batista JE, Caparros J, Vicente J, Arano P. Urodynamic evaluation and management prior to renal transplantation. Eur Urol 2000; 38: 415– 8 7 Kogan SJ, Levitt SB. Bladder evaluation in paediatric patients before undiversion in previously diverted urinary tracts. J Urol 1976; 118: 443– 6 8 Cerilli J, Anderson GW, Evans WE, Smith JP. Renal transplantation in patients with urinary tract abnormalities. Surgery 1976; 79: 248– 52 9 Tanagho E. Congenitally obstructed bladders: fate after prolonged defunctionalisation. J Urol 1974; 111: 102– 9 10 Firlit CF. Use of defunctionalised bladders in paediatric renal transplantation. J Urol 1976; 116: 634– 7 11 MacGregor P, Novick AC, Cunningham R et al. Renal transplantation in end-stage renal disease patients with existing urinary diversion. J Urol 1986; 135: 686– 8 12 Serrano DP, Flechner SM, Modlin CS, Wyner LM, Novick AC. Transplantation into the long-term defunctionalised bladder. J Urol 1996; 156: 885– 8 13 McGuire EJ, Woodside JR, Borden RA et al. Prognostic value of urodynamic testing in myelodysplastic patients. J Urol 1981; 126: 205– 9 14 Churchill BM, Sheldon CA, McLorie GA et al. Factors influencing patient and graft survival in 300 cadaveric paediatric renal transplants. J Urol 1988; 140: 1129– 33 15 Houle AM, Gilmour RF, Churchill BM, Gaumond M, Bissonnette B. What volume can a child normally store in the bladder at a safe pressure? J Urol 1993; 149: 561– 4 16 Gill IS, Hayes JM, Hodge EE, Novick AC. Clean intermittent catheterisation and urinary diversion in the management of renal transplant recipients with lower urinary tract dysfunction. J Urol 1992; 148: 1397– 400 17 Confer DJ, Banowsky LH. The urological evaluation and management of renal transplant donors and recipients. J Urol 1980; 124: 305– 10 18 Reinberg Y, Bumgardner GL, Aliabadi H. Urological aspects of renal transplantation. J Urol 1990; 143: 1087– 92 19 Najarian JS, Matas AJ. The present and future of kidney transplantation. Trans Proc 1991; 23: 2075– 82 20 US Renal Data System. USRDS 1989 renal data report. Bethesda, MD: National Institute of Diabetes and Digestive and Kidney Diseases, 1989 21 Glazier DB, Whang MIS, Geffner SR et al. Evaluation of voiding cystourethrography prior to renal transplantation. Transplantation 1996; 62: 1762– 5 22 Marshall FF, Smolev JK, Spees EK et al. The urological evaluation and management of patients with congenital lower urinary tract anomalies prior to renal transplantation. J Urol 1982; 127: 1078– 81 23 Thomalla JV, Mitchell ME, Leapman RS. Renal transplantation in a patient with an artificial urinary sphincter device. J Urol 1988; 139: 573– 4 24 Gelet A, Sanseverino R, Salas M et al. The AS800 urinary sphincter in renal transplantation. Br J Urol 1990; 66: 549– 50 25 Griffin PJ, Stephenson TP, Brough S, Salaman JR. Transplanting patients with abnormal lower urinary tracts. Transpl Int 1994; 7: 288– 91 26 Zaragoza MR, Ritchey ML, Bloom DA, McGuire EJ. Enterocystoplasty in renal transplantation candidates. Urodynamic evaluations and outcome. J Urol 1993; 150: 1463– 6 27 McInerny PD, Picramenos D, Koffman CG, Mundy AR. Is cystoplasty a safe alternative to urinary diversion in patients requiring renal transplantation? Eur Urol 1995; 27: 117– 20 28 Gruessner RW, Tzardis PJ, Matas AJ et al. Ileal and colon conduits in renal transplantation. Clin Transplant 1990; 4: 125– 8 29 Mitchell ME, Burns MW. Urinary undiversion and augmentation cystoplasty. In PP Kelalis, LR King, AB Belman eds. Clinical Paediatric Urology, 3rd edn. Philadelphia: WB Saunders, 1992: 904– 9 30 Malone MJ, Khauli RB, Lowell J. Use of small and large bowel in renal transplantation. Urol Clin North Am 1997; 24: 837– 43 31 Cairns HS, Leaker B, Woodhouse CRJ, Rudge CJ, Neild GH. Renal transplantation into abnormal lower urinary tract. Lancet 1991; 338: 1376– 9 32 Coosemans W, Baert L, Kuypers D et al. Renal transplantation onto abnormal urinary tract: Ileal conduit urinary diversion. Trans Proc 2001; 33: 2493– 4 33 Streem SB. Endourological management of urological complications following renal transplantation. Semin Urol 1994; 12: 123– 33 34 Cecka JM. The UNOS renal transplant registry. Clin Transpl 2001: 1– 18 35 McDonald MW, Zincke H, Engen DE, Sterioff S. Adaptation of existing cutaneous ureterostomy for urinary drainage after renal transplantation. J Urol 1985; 133: 1026– 8 36 Purohit RS, Bretan PN. Successful long-term outcome using existing native cutaneous ureterostomy for renal transplant drainage. J Urol 2000; 163: 446– 9 37 Prieto M, Sierra M, De Francisco ALM et al. Long-term outcome in renal transplantation with terminal cutaneous ureterostomy. Br J Urol 1993; 72: 844– 7 38 Mansson W, Willen R. Mucosal morphology and histochemistry of continent cecal reservoir for urine. J Urol 1988; 139: 1199– 201 39 Colombo T, Ziguener R, Zitta S, Petritsch PH, Hubmer G. Orthotopic neobladder in a woman after kidney transplantation. J Urol 1997; 158: 2236– 7 Citing Literature Volume92, Issue5September 2003Pages 510-515 ReferencesRelatedInformation

BJU InternationalVolume 87, Issue 9 p. 838-845 Vascular risk factors and erectile dysfunction M.E. Sullivan, M.E. Sullivan Department of Urology, Northampton General Hospital, Northampton, UKSearch for more papers by this authorS.R. Keoghane, S.R. Keoghane Department of Urology, Northampton General Hospital, Northampton, UKSearch for more papers by this authorM.A.W. Miller, M.A.W. Miller Department of Urology, Northampton General Hospital, Northampton, UKSearch for more papers by this author M.E. Sullivan, M.E. Sullivan Department of Urology, Northampton General Hospital, Northampton, UKSearch for more papers by this authorS.R. Keoghane, S.R. Keoghane Department of Urology, Northampton General Hospital, Northampton, UKSearch for more papers by this authorM.A.W. Miller, M.A.W. Miller Department of Urology, Northampton General Hospital, Northampton, UKSearch for more papers by this author First published: 12 January 2002 https://doi.org/10.1046/j.1464-410x.2001.02211.xCitations: 157 M.E. Sullivan, Department of Urology, Northampton General Hospital, Cliftonville, Northampton NN1 5BD, UK. Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat References 1 Kinsey AC, Pomeroy W, Martin CE. Age and sexual outlet. In AC Kinsey, W Pomeroy, CE Martin eds. Sexual Behaviour in the Human Man. Philadelphia: WB Saunders, 1948: 218–62 2 McCulloch DK, Campbell IW, Wu FC, Prescott RJ, Clarke BF. The prevalence of diabetic impotence. Diabetalogia 1980; 18: 279–83 3 Virag R, Bouilly P, Frydman D. Is impotence an arterial disorder? A study of arterial risk factors in 440 impotent men. Lancet 1985; 1: 181–4 4 Shabsigh R, Fishman IJ, Schum C et al. Cigarette smoking and other vascular risk factors in vasculogenic impotence. Urology 1991; 38: 227–32 5 Wei M, Macera CA, Davis DR, Hornung CA, Nankin HR, Blair SN. Total cholesterol and high density lipoprotein cholesterol as important predictors of erectile dysfunction. Am J Epidem 1994; 140: 930–7 6 Feldman HA, Goldstein I, Hatzichristou DG, Krane RJ, McKinlay JB. Impotence and its medical and psychosocial correlates: results of the Massachusetts Male Aging study. J Urol 1994; 151: 54–61 7 Johannes CB, Araujo AB, Feldman HA, Derby CA, Kleinman KP, McKinley JB. Incidence of erectile dysfunction in men 40–69 years old: longitudinal results from the Massachusetts Male Aging Study. J Urol 2000; 163: 460–3 8 Kaiser FE, Viosca SP, Morley JE, Mooradian AD, Davis SS, Korenman SG. Impotence and aging: clinical and hormonal factors. J Am Geriat Soc 1988; 36: 511–9 9 Greenstein A, Chen J, Miller H, Matzkin H, Villa Y, Braf Z. Does severity of ischaemic coronary disease correlate with erectile function. Int J Impotence Res 1997; 9: 123–6 10 Krane R, Goldstein I, Saenz de Tejada I. Impotence. N Eng J Med 1989; 321: 1648–59 11 Michal V. Arterial disease as a cause of impotence. Clin Endocrinol Metab 1982; 11: 725–48 12 Azadzoi KM & Saenz de Tejada I. Erectile dysfunction due to atherosclerotic vascular disease: the development of an animal model. J Urol 1992; 147: 1675–81 13 Levine FJ, Greenfield AJ, Goldstein I. Arteriographically determined occlusive disease within the hypogastric-cavernous bed in impotent patients following blunt perineal and pelvic trauma. J Urol 1990; 144: 1147–11 14 Rosen MP, Greenfield AJ, Walker TJ et al. Arteriogenic impotence: findings in 195 impotent men examined with selective internal pudendal angiography. Radiology 1990; 174: 1043–50 15 Azadzoi KM, Siroky MB, Goldstein I. Study of aetiologic relationship of arterial atherosclerosis to corporal veno-occlusive dysfunction in the rabbit. J Urol 1996; 155: 1795–800 16 Garban H, Vernet D, Freedman A, Rajfer J, Gonzalez-Cadavid NF. Effect of aging on nitric oxide-mediated penile erection in the rat. Am J Physiol 1995; 268: H467–75 17 Haas CA, Seftel AD, Razmjouei K, Ganz MB, Hampel N, Ferguson K. Erectile dysfunction in aging: upregulation of endothelial nitric oxide synthase. Urology 1998; 51: 516–22 18 Champion HC, Bivalacqua TJ, Hyman AL, Ignarro LJ, Hellstrom WJ, Kadowitz PJ. Gene transfer of endothelial nitric oxide synthase to the penis augments erectile responses in the aged rat. Proc Nat Acad Sci USA 1999; 96: 11648–52 19 Christ GJ, Maayani S, Valcic M, Melman A. Pharmacological studies of human erectile tissue: characteristics of spontaneous contractions and alterations in alpha-adrenoceptor responsiveness with age and disease in isolated tissues. Br J Pharmacol 1990; 101: 375–81 20 Mannino DM, Kievens RM, Flanders WD. Cigarette smoking: an independent risk factor for impotence? Am J Epidemiol 1994; 140: 1003–8 21 Hirshkowitz M, Karakan I, Howell JW, Arcasoy MO, Williams RL. Nocturnal penile tumescence in cigarette smokers with erectile dysfunction. Urology 1992; 39: 101–7 22 Pittilo RM. Cigarette smoking and endothelial injury: a review. In JN Dana ed. Tobacco Smoking and Atherosclerosis. New York: Plenum Press, 1990: :61–78 23 Ishii DN. Implication of insulin-like growth factors in the pathogenesis of diabetic neuropathy. Brain Res Rev 1995; 20: 47–67 24 Jacobs MC, Lenders JW, Kapma JA, Smits P, Thien T. Effect of chronic smoking on endothelium-dependent vascular relaxation in humans. Clin Sci 1993; 85: 51–5 25 Raichlen JS, Healy B, Achuff SC, Pearson TA. Importance of risk factors in the angiographic progression of coronary artery disease. Am J Cardiol 1986; 57: 66–70 26 Mersdorf A, Goldsmith PC, Diederichs W et al. Ultrastructural changes in impotent penile tissue: a comparison of 65 patients. J Urol 1991; 145: 749–58 27 Xie Y, Garban H, Ng C, Rajfer J, Gonzalez-Cadavid NF. Effect of long-term passive smoking on erectile function and penile nitric oxide synthase in the rat. J Urol 1997; 157: 1121–6 28 Jeremy JY, Mikhailidis DP, Thompson CS, Dandona P. The effect of cigarette smoke and diabetes mellitus on muscarinic stimulation of prostacyclin synthesis by the rat penis. Diab Res 1986; 3: 467–9 29 Levine LA & Gerber GS. Acute vasospasm of penile arteries in response to cigarette smoking. Urology 1990; 36: 99–100 30 Juenemann KP, Lue TF, Luo JA, Benowitz NL, Aboseid M, Tanagho EA. The effect of cigarette smoking on penile erection. J Urol 1987; 138: 438–41 31 Ellenberg M. Impotence in diabetes. The neurologic factor. Ann Int Med 1971; 75: 213–9 32 Tattersall R. Sexual problems of diabetic men. Br Med J 1982; 285: 911–2 33 Ruzbarsky V & Michal V. Morphologic changes in the arterial bed of the penis with aging: relationship to the pathogenesis of impotence. Invest Urol 1977; 15: 194–9 34 Abelson D. Diagnostic value of the penile pulse and blood pressure: a doppler study of impotence in diabetics. J Urol 1975; 113: 636–9 35 Faerman I, Glocer L, Fox D, Jadzinsky MN, Rapaport M. Impotence and diabetes: histological studies of the autonomic nervous fibres of the corpora cavernosa in impotent diabetic males. Diabetes 1974; 23: 971–6 36 Fani K, Lundin AP, Beyer MM, Jimenez FA, Friedman EA. Pathology of the penis in long-term diabetic rats. Diabetologia 1983; 25: 424–8 37 Gu J, Polak JM, Lazarides M et al. Decrease of vasoactive intestinal polypeptide (VIP) in the penises from impotent men. Lancet 1984; 2: 315–8 38 Lincoln J, Crowe R, Blacklay PF, Pryor JP, Lumley JS, Burnstock G. Changes in VIPergic, cholinergic and adrenergic innervation of human penile tissue in diabetic and non-diabetic impotent males. J Urol 1987; 137: 1053–9 39 Melman A, Bressler RS, Henry DP, Macadoo VK. Ultrastructure of human penile erectile tissues in patients with abnormal norepinephrine content. Invest Urol 1981; 19: 46–8 40 Saenz de Tejada I, Goldstein I, Azadzoi KM, Krane RJ, Cohen RA. Impaired neurogenic and endothelium-mediated relaxation of penile smooth muscle from diabetic men with impotence. N Eng J Med 1989; 320: 1025–30 41 Azadzoi KM & Saenz de Tejada I. Diabetes mellitus impairs neurogenic and endothelium-mediated relaxation of rabbit corpus cavernosum smooth muscle. J Urol 1992; 148: 1587–91 42 Pickard RS, Powell PH, Zar MA. Nitric oxide and cyclic GMP formation following relaxant nerve stimulation in isolated human corpus cavernosum. Br J Urol 1995; 75: 516–22 43 Sullivan ME, Bell CRW, Dashwood MR et al. Autoradiographic localisation of nitric oxide synthase binding sites in normal and diabetic rat corpus cavernosum. Eur Urol 1996; 30: 506–11 44 Kiff RJ, Gardiner SM, Compton AM, Bennet T. The effects of endothelin-1 and N-nitro-l-arginine methyl ester on regional haemodynamics in conscious rats with streptozotocin induced diabetes mellitus. Br J Pharmacol 1991; 103: 1321–6 45 Sullivan ME, Thompson CS, Mikhailidis DP, Morgan RJ, Angelini DG, Jeremy JY. Differential alterations of prostacyclin, cyclic AMP and cyclic GMP formation in the corpus cavernosum of the diabetic rabbit. Br J Urol 1998; 82: 578–84 46 Pieper GM & Dondlinger LA. Plasma and vascular tissue arginine are decreased in diabetes: acute arginine supplementation restores endothelium-dependent relaxation by augmenting cGMP production. J Pharmacol Exp Ther 1997; 283: 684–91 47 Zorgniotti AW & Lizza EF. Effect of large doses of the nitric oxide precursor, l-arginine, on erectile dysfunction. Int J Impotence Res 1994; 6: 33 48 Moody JA, Vernet D, Laidlaw S, Rajfer J, Gonzalez-Cadavid N. Effect of long-term oral administration of l-arginine on the rat erectile response. J Urol 1997; 158: 942–7 49 Bucala R, Tracey KJ, Cerami A. Advanced glycosylation products quench nitric oxide and mediate defective endothelium-dependent vasodilatation in experimental diabetes. J Clin Invest 1991; 87: 432–8 50 Hoffmann D, Seftel AD, Hampel N, Resnick MI. Advanced glycation end-products quench cavernosal nitric oxide. J Urol 1995; 153: 441A 51 Azadzoi KM, Goldstein I, Krane RJ, Saenz de Tejada I. Characterisation of the fibroelastic properties of human corpus cavernosum. Int J Impotence Res 1990; 2 (Suppl. 2): 81 52 Seftel AD, Vaziri ND, Ni Z et al. Advanced glycation end products in human penis: elevation in diabetic tissue, site of deposition, and possible effects through iNOS or eNOS. Urology 1997; 50: 1016–26DOI: 10.1016/s0090-4295(97)00512-8 53 Garban H, Marquez D, Magee T et al. Cloning of rat and human inducible penile nitric oxide synthase: application for gene therapy for erectile dysfunction. Biol Reprod 1997; 56: 954–63 54 Shirai M, Maki A, Takanama M et al. Content and distribution of vasoactive intestinal polypeptide (VIP) in cavernous tissue of human penis. Urology 1990; 35: 360–3 55 Crowe R, Lincoln J, Blacklay PF, Pryor JP, Lumley JS, Burnstock G. Vasoactive intestinal polypeptide-like immunoreactive nerves in diabetic penis. A comparison between streptozotocin-treated rats and man. Diabetes 1983; 32: 1075–7 56 Maher E, Bachoo M, Elabbady AA et al. Vasoactive intestinal polypeptide and impotence in experimental diabetes mellitus. Br J Urol 1996; 77: 271–8 57 Blanco R, Saenz de Tejada I, Goldstein I, Krane RJ, Wotiz HH, Cohen RA. Dysfunctional penile cholinergic nerves in diabetic impotent men. J Urol 1999; 144: 278–80 58 Kim SC, Ahn SY, Park SH, Lee MY, Uhm DY. A comparison of the relaxation responses of isolated cavernosal smooth muscles by endothelium-independent and endothelium-dependent vasodilators in diabetic men with impotence. J Korean Med Sci 1995; 10: 1–6 59 Kirkeby HJ, Forman A, Sorensen S, Andersson KE. Alpha-adrenoceptor function in isolated penile circumflex veins from potent and impotent men. J Urol 1989; 142: 1369–71 60 Takahashi K, Ghatei MA, Lam H-C, O'Halloran DJ, Bloom SR. Elevated plasma endothelin in patients with diabetes mellitus. Diabetalogia 1990; 33: 306–10 61 Francavilla S, Properzi G, Bellini C, Marino G, Ferri C, Santucci A. Endothelin-1 in diabetic and non-diabetic men with erectile dysfunction. J Urol 1997; 158: 1770–4 62 Bell CRW, Sullivan ME, Dashwood MR, Muddle JR, Morgan RJ. The density and distribution of endothelin 1 and endothelin receptor subtypes in normal and diabetic rat corpus cavernosum. Br J Urol 1995; 76: 203–7 63 Sullivan ME, Dashwood MR, Thompson CS, Muddle JR, Mikhailidis DP, Morgan RJ. Alterations in endothelin B receptor sites in cavernosal tissue of diabetic rabbits: potential relevance to the pathogenesis of diabetic erectile dysfunction. J Urol 1997; 158: 1966–72 64 Zhao W & Christ GJ. Endothelin-1 as a putative modulator of erectile dysfunction. II. calcium mobilisation in cultured human corporal smooth muscle cells. J Urol 1995; 154: 1571–9 65 Christ GJ, Lerner SE, Kim DC, Melman A. Endothelin-1 as a putative modulator of erectile dysfunction: I. characteristics of contraction of isolated corporal tissue strips. J Urol 1995; 153: 1998–2003 66 Sullivan ME, Shukla N, Thompson CS, Dashwood MR, Mikhailidis DP, Morgan RJ. Endothelin receptor antagonists inhibit diabetic rabbit cavernosal smooth muscle cell proliferation. Br J Urol 1997; 79 (Suppl. 4): 55 67 Giraldi A, Serels S, Autieri M, Melman A, Christ GJ. Endothelin-1 as a putative modulator of gene expression and cellular physiology in cultured human corporal smooth muscle cells. J Urol 1998; 160: 1856–62 68 Aboseif S, Riemer RK, Stackl W. Quantification of PGE1 receptors in cavernous tissue of men, monkeys and dogs. Urol Int 1993; 50: 48–52 69 Miller MAW, Morgan RJ, Thompson CS, Mikhailidis DP, Jeremy JY. Adenylate and guanylate cyclase activity in the penis and aorta of the diabetic rat: an in vitro study. Br J Urol 1994; 74: 106–11 70 Miller MW, Morgan RJ, Thompson CS, Mikhailidis DP, Jeremy JY. Hydrolysis of cyclic guanosine monophosphate and cyclic adenosine monophosphate in the penis and aorta of diabetic rats. Br J Urol 1996; 78: 252–6 71 Khan N, Miller MW, Thompson CS, Mikhailidis DP, Morgan RJ, Jeremy JY. 5′nucleotidase activity in the aorta and penis of the diabetic rat. J Molec Cardiol 1994; CCLII: 26 72 Jeremy JY, Thompson CS, Mikhailidis DP, Dandona P. Experimental diabetes mellitus inhibits prostacyclin synthesis by the rat penis; pathological implications. Diabetologia 1985; 28: 365–8 73 Burchardt M, Burchardt T, Baer L et al. Hypertension is associated with severe erectile dysfunction. J Urol 2000; 164: 1188–91 74 Oaks WW & Moyer JH. Sex and hypertension. Med Asp Hum Sex 1972; 6: 128–37 75 Jaffe A, Chen Y, Kisch ES, Fischel B, Alon M, Stern N. Erectile dysfunction in hypertensive subjects. Assessment of potential deteminants. Hypertension 1996; 28: 859–62 76 Heaton JPW & Varrin SJ. Effects of castration and exogenous testosterone supplementation in an animal model of penile erection. J Urol 1994; 151: 797–800 77 Toblli JE, Stella I, Ferder L, Zeller F, Mazza ON. Morphological changes in cavernous tissue in spontaneously hypertensive rats. Am J Hypertension 2000; 13: 686–92 78 Tanner FC, Noll G, Boulanger CM, Luscher TF. Oxidised low density lipoproteins inhibit relaxations of porcine coronary arteries. Circulation 1991; 83: 2012–20 79 Rosenfeld ME. Oxidised LDL affects multiple atherogenic cellular responses. Circulation 1991; 83: 2137–40 80 Kugiyama K, Kerns SA, Morrisett JD, Roberts R, Henry PD. Impairment of endothelium-dependent arterial relaxation by lysolecithin in modified low-density lipoproteins. Nature 1990; 344: 160–2 81 Leung WH, Lau CP, Wong CK. Beneficial effect of cholesterol-lowering therapy on coronary endothelium-dependent relaxation in hypercholesterolaemic patients. Lancet 1993; 341: 1496–500 82 Azadzoi KM & Saenz de Tejada I. Hypercholesterolaemia impairs endothelium-dependent relaxation of rabbit corpus cavernosum smooth muscle. J Urol 1991; 146: 238–40 83 Kim JH, Klyachkin ML, Svendsen E, Davies MG, Hagen PO, Carson CC. Experimental hypercholesterolaemia in rabbits induces cavernosal atherosclerosis with endothelial and smooth muscle cell dysfunction. J Urol 1994; 151: 198–205 84 Arendt RM, Wilbert-Lampen U, Heucke L. Increased plasma endothelin in patients with hyperlipoproteinaemia and stable or unstable angina. Circ Res 1990; 83 (Suppl. 3): 244–8 85 Sullivan ME, Dashwood MR, Thompson CS, Mikhailidis DP, Morgan RJ. Decreased endothelin B receptor binding sites on corpus cavernosa of hypercholesterolaemic rabbits. Br J Urol 1998; 81: 128–34 86 Masaki T, Vane JR, Vanhoutte PMV. International Union of Pharmacology Nomenclature of endothelin receptors. Pharmacol Rev 1994; 46: 137–42 87 MAAS investigators. Effect of simvastatin on coronary atheroma: the Multicentre Anti-Atheroma Study (MAAS). Lancet 1994; 344: 633–8 88 Scandinavian Simvastatin Survival Study Group. Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study. Lancet 1994; 344: 1383–9 89 Ernst E & Resch KL. Fibrinogen as a cardiovascular risk factor: a meta-analysis and review of the literature. Ann Int Med 1993; 118: 956–63 90 Koenig W & Ernst E. The possible role of blood haemorheology in atherothrombogenesis. Atherosclerosis 1992; 94: 93–107 91 Miller MAW, Sullivan ME, Winder AF, Mikhailidis DP, Morgan RJ. Fibrinogen and hyperlipidaemia: Risk factors for impotence? Int J Impotence Res 1994; 6 (Suppl. 1): P51 92 Sullivan M, Miller M, Bell R et al. The effects of cigarette smoking on vascular risk factors in patients with erectile dysfunction. Eur Urol 1996; 30 (Suppl. 2): 250(A933) Citing Literature Volume87, Issue9June 2001Pages 838-845 ReferencesRelatedInformation

BACKGROUND:Erectile dysfunction is associated with cardiovascular risk factors (e.g. hypertension, smoking, dyslipidemia and diabetes) and is more common in patients with cardiovascular disease. We therefore assessed the prevalence of two predictors of vascular events, fibrinogen and lipoprotein-a, in patients with and without erectile dysfunction.METHODS:Men with erectile dysfunction (48 non-smokers, 48 smokers), aged 45-70 years, were compared with controls (21 non-smokers, 21 smokers) with normal erectile function and no known pathology.RESULTS:Serum total cholesterol was significantly higher in non-smokers with erectile dysfunction compared to both control non-smokers and erectile dysfunction smokers. Men with erectile dysfunction who smoked had a significantly higher plasma fibrinogen level than control smokers. Similarly, men with erectile dysfunction, who did not smoke had higher levels of plasma fibrinogen compared to both smokers and non-smokers without erectile dysfunction. No significant difference in serum lipoprotein-a values was found.CONCLUSIONS:These findings support the concept that cardiovascular risk factors are predictors of erectile dysfunction and that this may be another manifestation of vascular disease.

Recent studies suggest that the body produces two gaseous messengers, nitric oxide (NO) and carbon monoxide (CO), both of which activate soluble guanylyl cyclase and thus modulate the activity of smooth muscle cells. In the present study, the effects of NO and CO on the smooth muscle of the lower urinary tract were compared. In addition, the modulation of tissue NO- and CO-induced relaxation by hydrogen peroxide was examined. NO, produced endogenously by electrical field stimulation (EFS) or applied exogenously as a solution, induced a concentration-dependent relaxation of rabbit cavernosal and urethral smooth muscle strips, but not of bladder tissues. The cavernosal tissue was found to be three times more sensitive to the actions of NO than the urethra. CO also induced relaxation of both tissue types, but with no apparent difference in sensitivity between the tissues. However, CO was much less potent than NO with respect to smooth muscle relaxation. The mechanism of action of the two mediators was cyclic guanosine monophosphate (cGMP)-dependent, as evidenced by enhanced formation of cGMP and inhibition of relaxation by the guanylyl cyclase inhibitor, oxadiazoloquinoxaline-1-one (ODQ.) The data suggests that NO is the dominant messenger in these tissues, but does not exclude a role for CO. In the presence of hydrogen peroxide, the relaxation responses induced by both NO and CO were significantly increased, regardless of tissue type. The mechanism for this effect is unclear, but evidence points to a requirement for the activation of guanylyl cyclase and enhanced formation of cGMP, since potentiation by the peroxide was blocked by a specific guanylyl cyclase inhibitor. We suggest that H(2)O(2) may play a positive role in the amplification or NO and CO-mediated responses.

Objective To evaluate the natural history of a group of patients who underwent contact laser prostatectomy or transurethral resection of the prostate (TURP). Patients and methods Patients were followed up at 5 years after enrolling in a prospective double‐blind randomized controlled trial of TURP vs contact laser prostatectomy. Results Of the initial trial patients, 11.5% had died (seven in the laser and 10 in the TURP arm) and eight (5.4%) were too incapacitated by coexistent medical disease to respond to the questionnaires. Thirty‐eight patients were not available for follow‐up, despite numerous invitations. Thirteen of the laser patients (18%) and 11 of the TURP patients (14.5%) had undergone re‐operation. Two patients from each arm had received α‐blockers for worsening symptoms. Conclusions Five years after prostatic surgery, a significant number of patients were dead or disabled by coexistent medical disease. The re‐operation rate after TURP and contact laser prostatectomy were similar.

ObjectiveTo evaluate the effect of contact laser prostate surgery in the treatment of benign prostatic hyperplasia. Patients and methodsA prospective double‐blind ran‐domized controlled trial of transurethral resection of the prostate (TURP) and contact laser prostatectomy was conducted, with an economic evaluation of both procedures. The primary outcome measure was the change in the American Urologic Association symptom score, with secondary outcome measures being the peak urinary flow rate, treatment‐related complications, re‐operation rate and health service costs. ResultsThe perioperative blood loss and transfusion requirements were statistically significantly lower for laser prostatectomy than for TURP. There was no clinically significant difference between TURP and contact laser prostatectomy in the mean change in symptom scores and flow rates. There were distinct perioperative advantages in favour of the contact laser treatment, but some disadvantages in terms of re‐catheterization and re‐operation rates. ConclusionsContact laser prostatectomy is a valid treatment for benign prostatic hypertrophy. The performance of contact laser prostatectomy as day‐case surgery would have cost advantages to the National Health Service.

Objectives To determine the effect of diabetes mellitus on the density and distribution of endothelin A (ETA) and endothelin B (ETB) receptor subtypes in the rabbit urinary bladder, and to assess the in vitro functionalproperties of endothelin-1 (ET-1) receptors in bladder smooth muscle strips from diabetic and healthy rabbits,Materials and methods Diabetes mellitus was induced in six male New Zealand White rabbits with alloxan and their urinary bladders excised 6 months after the induction of diabetes, On serial detrusor and bladder neck sections, low- and high-resolution autoradiography was performed using radioligands for ET-1, ETA and ETB receptors; these sections were then analysed densitometrically. The results were compared with those from six age-matched healthy control rabbits, Functional responses were investigated using isometric tension studies.Results ETA and ETB receptor binding sites were localized to both the urothelium and smooth muscle of the detrusor and bladder neck. There were significantly more ETB receptor binding sites in the diabetic detrusor and bladder neck sections than in controls. ET-1 smooth muscle contractile responses were ETA receptor-mediated. The smooth muscle contractile responses to ET-1 were unaltered in the detrusor, but significantly impaired in the bladder neck of diabetic animals compared with controls.Conclusion Alteration in the expression of ETB receptors and in vitro contractile smooth muscle responses to ET-1 in the diabetic rabbit urinary bladder neck may play a role in the pathophysiology of diabetic cystopathy.

Endothelium-derived vasoactive mediators (endothelin-1 with its vasoconstrictive and mitogenic properties and nitric oxide with its vasodilatory and antiproliferative properties) play an important role in the regulation of vascular smooth muscle tone and cellular proliferation. Several recent studies have now demonstrated the presence of these vasoactive agents in the urinary tract where they are thought to play a prominent role in urinary tract physiology and disease. This article reviews the synthesis, localisation and actions of endothelin and nitric oxide in the lower urinary tract and examines the possible role of these mediators in disease.

PURPOSE:To investigate the effect of diabetes mellitus (DM) on the density and distribution of nitric oxide synthase (NOS) and the smooth muscle responses to non-adrenergic, non-cholinergic (NANC) nerve stimulation and exogenous nitric oxide (NO) in the rabbit lower urinary tract. MATERIALS AND METHODS:Transverse sections of detrusor, bladder neck and urethra, from control and six months alloxan-induced DM New Zealand White rabbits were incubated with a radioligand for NOS ([3H]-L-N(G)-nitroarginine). Densitometric analysis was performed on the autoradiographs. NADPH diaphorase histochemistry was also used as a marker for NOS activity. Responses to NANC nerve stimulation (5 to 20 Hz) and to NO (10(-6) to 3x10(-4) M.) on smooth muscle strips from detrusor, bladder neck and urethra were measured in organ baths. RESULTS:NOS binding sites were significantly (p<0.03) more dense in the bladder neck than in the detrusor in both DM and control groups. In DM bladder neck, NOS binding sites were significantly (p<0.04) increased compared with the controls. NADPH diaphorase activity appeared markedly increased in the detrusor, bladder neck and urethra of DM animals compared with controls. The mean IC50 for exogenous NO in control versus DM were not statistically different in the bladder neck (1.03x10(-4) M versus 9.8x10(-5) M) and urethra (8.1x10(-5) M versus 8.8x10(-5) M), but the relaxations to 5x10(-6) M of NO were significantly impaired (p<0.04) in the DM urethral smooth muscle. NANC nerve-mediated relaxations were significantly impaired (p<0.001) in the DM urethral smooth muscle. CONCLUSIONS:Alterations of both the NOS binding sites and functional responses to NANC nerve stimulation suggest that NO may have a pathophysiological role in the urinary bladder dysfunction associated with DM.

Both animal and human penile tissue synthesize prostaglandins (PGs). Furthermore, intracavernous injection of certain PGs elicits erection in men with erectile dysfunction (ED). It is also well established that PGs are involved in the pathophysiology of atherosclerosis and diabetes mellitus (DM). Since atherosclerosis and DM are major risk factors for ED, it has been suggested that the disruption of PG synthesis in penile tissues and related vasculature may play a role in the pathogenesis of ED. In this review, we discuss the role of PGs in normal penile erection as well as on the pathophysiology and treatment.

OBJECTIVE:To investigate the density and distribution of endothelin-1 (ET-1) and endothelin receptor subtypes in cavernosal tissue of healthy New Zealand White (NZW) rabbits (controls) and to assess any changes in a genetic model of hypercholesterolaemia (the Watanabe rabbit).MATERIALS AND METHODS:Penises were excised from six hypercholesterolaemic (HC) rabbits 6 months after birth. Low- and high-resolution autoradiography was performed on cavernosal sections using radioligands for ET-1, endothelin A (ETA) and endothelin B (ETB) receptors, and the autoradiographs analysed densitometrically. The results were compared with those from six age-matched control rabbits. Immunohistochemical localization of ET-1-like immunoreactivity was also performed on adjacent cavernosal sections.RESULTS:ET-1, ETA and ETB receptor binding sites were primarily localized to the smooth muscle cells of the corpus cavernosum and the endothelium lining the cavernosal spaces. There was a significant decrease in ETB receptor binding sites in cavernosal tissue from HC rabbits when compared to age-matched healthy controls.CONCLUSIONS:The findings suggest that ET-1 may have a role in the pathophysiology of erectile dysfunction in HC. These effects may partly be due to enhanced vasoconstrictor actions and smooth muscle cell proliferation, consequent on a reduction in endothelial ETB receptors.

An association between diminution in the quality of male sexual function and ischemic coronary disease has been suggested. Patients with ischemic heart disease who underwent coronary angiography participated in this study which aimed to document the impact of the extent of coronary disease upon sexual function in 40 patients (mean age 56.6 y). The 11-questions accepted questionnaire addressing sexual drive, erectile function, and ejaculation was used. Information regarding, age, medications, hypertension, diabetes, relevant risk factors, medical history, and the number of occluded coronary vessels was retrieved from the patients' records. A statistically significant correlation was demonstrated between erectile function and the number of coronary vessels involved. Patients with one-vessel disease had more (P < 0.04) and firmer erections (P < 0.001) with fewer difficulties in achieving an erection (P < 0.007) than men with two- or three-vessel disease. Age, diabetes, and hypertension also had a negative effect on the quality of the erection (P < 0.05) in all patients.

Purpose: Diabetes Mellitus (DM) is a major risk factor for erectile dysfunction in both patients and animal models, The pathogenesis of this dysfunction has not been fully elucidated. However, alterations in the synthesis of a number of vasoactive compounds, such as nitric oxide (NO) and prostacyclin (PGI(2)), have been reported in various diabetic tissues. The interaction between NO, PGI(2) and endothelin-1 (ET-1), a powerful vasoconstrictor and smooth muscle cell mitogen, is thought to be important in maintaining vascular tone and the erectile process. We investigated the density and distribution of ET-1 and endothelin receptor subtypes in cavernosal tissue and assessed any changes brought about by DM in a rabbit model.Materials and Methods: DM was induced in New Zealand White rabbits using alloxan. Penises were excised from the diabetic rabbits three months (n = 6) and six months in = 6) after the induction of DM. Low and high resolution autoradiography was performed using radioligands for ET-1, endothelin A (ETA) and endothelin B (ETB) receptors and were analyzed densitometrically. The results were compared with those from six age-matched healthy control rabbits for each group. Immunohistochemical localization of ET-1 immunoreactivity was also performed, together with ultrastructural evaluation of the corpus cavernosum.Results: ET-1, ETA and ETB receptor binding sites were primarily localized to the smooth muscle cells of the corpus cavernosum and the endothelium lining the cavernosal spaces. A significant increase in ETB receptor binding sites was found only in cavernosal tissue six months after induction of DM, when compared with age-matched healthy controls. These receptor changes were accompanied by ultrastructural changes in the corpus cavernosum indicative of an early, atherosclerosis-like process.Conclusions: The autoradiographic and immunohistochemical findings in this study suggest that ET-1 may have a role in the pathophysiology of diabetic ED. This peptide may be released in an autocrine fashion causing cavernosal smooth muscle cell (CSMC) contraction and/or proliferation.

OBJECTIVES:To investigate density and distribution of nitric oxide synthase (NOS) binding sites in rat cavernosal tissue, and to assess any changes brought about by the onset of diabetes mellitus. METHODS:Hyperglycaemic non-ketonuric diabetes mellitus was induced in 5 rats using streptozotocin. The penises were excised from these rats 2 months after the administration of streptozotocin and stored at -70 degrees C. Longitudinal serial sections (6 microns) were cut in a cryostat and thaw mounted onto gelantinized microscope slides. Low- and high-resolution autoradiography was performed using a radioligand for NOS. Densitometric analysis was performed on the autoradiographs and the results compared with those obtained from 5 age-matched no-diabetic rats. RESULTS:NOS binding was primarily localized to the endothelium lining the cavernosal lacunar spaces. Significantly increased binding of NOS was seen in the diabetic cavernosal tissue 2 months after induction of diabetes mellitus. CONCLUSIONS:NOS binding is present on the endothelium of the rat corpus cavernosum and is increased in diabetic rats 2 months after streptozotocin administration. This increase in NOS binding may be part of the endothelial dysfunction which is reported in the corpus cavernosum of diabetic patients or rats.

British Journal of UrologyVolume 77, Issue 2 p. 329-329 Diabetes mellitus increases nitric oxide synthase in penises but not in major pelvic ganglia of rats M.E. Sullivan, M.E. Sullivan Department of Urology The Royal Free Hospital and School of Medicine, Pond Street London NW3 2QG UKSearch for more papers by this authorC.R.W. Bell, C.R.W. Bell Department of Urology The Royal Free Hospital and School of Medicine, Pond Street London NW3 2QG UKSearch for more papers by this authorM.A.W. Miller, M.A.W. Miller Department of Urology The Royal Free Hospital and School of Medicine, Pond Street London NW3 2QG UKSearch for more papers by this authorC.S. Thompson, C.S. Thompson Department of Chemical Pathology The Royal Free Hospital and School of Medicine, Pond Street London NW3 2QG UKSearch for more papers by this authorM.R. Dashwood, M.R. Dashwood Department of Physiology The Royal Free Hospital and School of Medicine, Pond Street London NW3 2QG UKSearch for more papers by this authorJ.Y. Jeremy, J.Y. Jeremy Department of Chemical Pathology The Royal Free Hospital and School of Medicine, Pond Street London NW3 2QG UKSearch for more papers by this authorD.P. Mikhailidis, D.P. Mikhailidis Department of Chemical Pathology The Royal Free Hospital and School of Medicine, Pond Street London NW3 2QG UKSearch for more papers by this authorR.J. Morgan, R.J. Morgan Department of Urology The Royal Free Hospital and School of Medicine, Pond Street London NW3 2QG UKSearch for more papers by this author M.E. Sullivan, M.E. Sullivan Department of Urology The Royal Free Hospital and School of Medicine, Pond Street London NW3 2QG UKSearch for more papers by this authorC.R.W. Bell, C.R.W. Bell Department of Urology The Royal Free Hospital and School of Medicine, Pond Street London NW3 2QG UKSearch for more papers by this authorM.A.W. Miller, M.A.W. Miller Department of Urology The Royal Free Hospital and School of Medicine, Pond Street London NW3 2QG UKSearch for more papers by this authorC.S. Thompson, C.S. Thompson Department of Chemical Pathology The Royal Free Hospital and School of Medicine, Pond Street London NW3 2QG UKSearch for more papers by this authorM.R. Dashwood, M.R. Dashwood Department of Physiology The Royal Free Hospital and School of Medicine, Pond Street London NW3 2QG UKSearch for more papers by this authorJ.Y. Jeremy, J.Y. Jeremy Department of Chemical Pathology The Royal Free Hospital and School of Medicine, Pond Street London NW3 2QG UKSearch for more papers by this authorD.P. Mikhailidis, D.P. Mikhailidis Department of Chemical Pathology The Royal Free Hospital and School of Medicine, Pond Street London NW3 2QG UKSearch for more papers by this authorR.J. Morgan, R.J. Morgan Department of Urology The Royal Free Hospital and School of Medicine, Pond Street London NW3 2QG UKSearch for more papers by this author First published: February 1996 https://doi.org/10.1111/j.1464-410X.1996.tb00546.xCitations: 1AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL No abstract is available for this article.Citing Literature Volume77, Issue2February 1996Pages 329-329 RelatedInformation

OBJECTIVE:To assess the changes in overall coagulation status and define the degree of systemic fibrinolysis occurring in patients undergoing transurethral prostatectomy (TURP).PATIENTS AND METHODS:Thirty patients undergoing TURP, 23 for benign prostatic hyperplasia and seven for prostatic carcinoma, were studied prospectively. Serial venous blood samples were taken using the two-syringe technique. Samples were taken before, during and at intervals up to 72 h and 10-14 days after surgery. Thrombelastography (TEG) was performed on native whole blood samples. Peri-operative blood loss was assessed, until the catheter was removed, by photometric estimation of the haemoglobin content of the irrigant fluid and the measurement of clot volume.RESULTS:There was no evidence of fibrinolysis (TEG Percentage Clot Lysis Ly60 > 15%) in any patient over the whole peri-operative period. There was a significant change in the mean TEG variables towards hypercoagulation from 3 h until 10-14 days postoperatively, compared with the pre-operative values (P < 0.05). There was a significant correlation between blood loss and clot volume.CONCLUSION:These results question the role of systemic fibrinolysis in primary and secondary haemorrhage following TURP and thus the rationale of using antifibrinolytics in these patients. The persistent hypercoagulable state post-operatively indicates a possible role of hypercoagulability in clot retention.