Background: Our Nurse Without Borders program started in January, 2006 to see all heart failure patients in the hospital for education, verifying CHF core measures, screening for depression and sleep apnea. We have used the Cardiocom scale for telehealth management of frequent CHF readmissions for the past 10 years. A nurse phones patients at home within 30 days of discharge. Our hospital has the lowest CHF readmission 21.2% for the state vs 24.9% for the nation. We utilize a multidisciplinary outpatient heart failure clinic however we still needed to improve. Using H2H (Hospital to Home) initiative started by American College of Cardiology, we want to be even more aggressive in decreasing our CHF readmissions.

Environmental ProgressVolume 9, Issue 3 p. A10-A11 Pollution Prevention/Waste Minimization Waste minimization in a leading ethical pharmaceutical company E. S. Venkataramani, E. S. Venkataramani Merck & Co., Inc., P.O. Box 2000, Rahway, NJ 07065-0900Search for more papers by this authorS. Bacher, S. Bacher Merck & Co., Inc., P.O. Box 2000, Rahway, NJ 07065-0900Search for more papers by this authorW. Olsen, W. Olsen Merck & Co., Inc., P.O. Box 2000, Rahway, NJ 07065-0900Search for more papers by this author E. S. Venkataramani, E. S. Venkataramani Merck & Co., Inc., P.O. Box 2000, Rahway, NJ 07065-0900Search for more papers by this authorS. Bacher, S. Bacher Merck & Co., Inc., P.O. Box 2000, Rahway, NJ 07065-0900Search for more papers by this authorW. Olsen, W. Olsen Merck & Co., Inc., P.O. Box 2000, Rahway, NJ 07065-0900Search for more papers by this author First published: August 1990 https://doi.org/10.1002/ep.670090311Citations: 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 Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article.Citing Literature Volume9, Issue3August 1990Pages A10-A11 RelatedInformation

Vasodilators were characterized on the basis of their first-dose effect on systolic and diastolic blood pressure, heart rate, on the product of heart rate and systolic blood pressure and on plasma renin activity (PRA) in conscious normotensive dogs. The compounds were given orally to the animals and the effects were studied over a period of 4 h. The arterial vasodilators (propyldazine, dihydralazine and labetalol) caused a marked reduction of systolic and diastolic blood pressure with excessive stimulation of the sympathetic nervous system, leading to an increase in myocardial oxygen demand. The blood pressure effect of urapidil and prazosin resembled more the pattern seen with typical venous dilators (molsidomine and nitrates) and was not accompanied by significant increases in heart rate and in PRA. Hence, the magnitude of diastolic blood pressure reduction seems to be an essential determinant of reflex counterregulation. The results prove that some few parameters can give information about the overall pattern of hemodynamic effects of vasodilators.

The effects of a continuous iv infusion (osmotic minipumps) of angiotensin II (80 ng . kg-1 . min-1) and isoprenaline (10 ng . kg-1 . min-1) lasting 28 days were studied in six normotensive, conscious dogs. The parameters measured were systolic and diastolic blood pressure, heart rate, levels of angiotensin II, renin activity, aldosterone and antidiuretic hormone in plasma, baroreceptor reflex sensitivity and body weight. The treatment resulted in an approximately sevenfold increase in plasma angiotensin II level from 62.9 +/- 24.5 pg . ml-1 to 455.3 +/- 95.6 pg . ml-1. Systolic and diastolic blood pressure, measured for the first time 2 days after implanting the minipumps, were markedly increased throughout the infusion period (pretreatment value: 123.8 +/- 5.3/68.3 +/- 3.8 mmHg; after 2 days: 159.8 +/- 12.0/100.5 +/- 9.8 mmHg; after 28 days: 159.8 +/- 7.1/98.3 +/- 6.4 mmHg, whereas the heart rate remained unchanged due to the combined effects of angiotensin II and the concomitantly given isoprenaline. A high correlation was found between angiotensin II level in plasma and mean arterial blood pressure (r = 0.846; p less than 0.001). Furthermore, plasma renin activity was markedly suppressed by the treatment, and aldosterone levels rose. Plasma antidiuretic hormone levels were found to be unchanged at the chosen sampling time. A decrease in baroreceptor reflex sensitivity accompanied the development of the hypertensive state. There was also a loss of body weight during the infusion of angiotensin II and isoprenaline. The data provide evidence for the usefulness of the presented experimental protocol as an alternative model of arterial hypertension in chronically instrumented, conscious dogs.

An investigation is presented of the effects of the acylcarnitine-transferase blocking agent sodium 2[5-(4-chlorophenyl)-pentyl]-oxirane-2-carboxylate (POCA; 20 mg/kg i.v.) on cardiodynamics and myocardial metabolism in normoxic, anesthetized dogs. POCA induced an initial increase in pulmonary vascular resistance; pulmonary vascular pressure was increased up to 4 h. All other hemodynamic parameters were unchanged. POCA induced a continuous rise in arterial free fatty acid (FFA) level and a marked initial increase in arterial lactate level. Arterial glucose level decreased. Myocardial FFA uptake was almost completely inhibited by POCA; myocardial lactate uptake increased markedly and myocardial glucose uptake remained unchanged. These changes were accompanied by an increase in respiratory quotient from 0.72 to 1.0 and a decrease in myocardial oxygen consumption by 15-20%. In conscious dogs, POCA (20 mg/kg i.v.) induced similar changes in arterial substrate levels. The increase in arterial FFA level was accompanied by an increase in arterial glucagon. Ketone body levels decreased initially but increased simultaneously with glucagon levels. These findings confirm the efficacy of POCA in inhibiting FFA oxidation and, consequently, in decreasing myocardial oxygen consumption. However, possible deleterious effects of the increase in arterial FFA levels on the ischemic myocardium require further experimental evaluation.

The magnitude and the persistence of blood pressure reduction by dihydralazine and urapidil were investigated following treatment over a period of 4 days. The experiments were performed on six normotensive dogs, trained to submit to puncture of the femoral artery and to stand quietly in a special frame. The first-dose effects of orally administered dihydralazine (1.42, 7.1 mg X kg-1) and urapidil (2.0, 10.0 mg X kg-1) on heart rate, arterial blood pressure and plasma renin activity (PRA) were compared with the effects of the substances after 4 days of treatment. Both compounds caused a dose-dependent decrease in blood pressure but in contrast to urapidil the effect of dihydralazine was accompanied by large increases in heart rate and PRA. Dose-dependent tolerance to dihydralazine but not to urapidil was observed after treatment over only 4 days. However, basal blood pressure was significantly lowered after 4 days of treatment with urapidil at the high dosage and no further reduction was achieved on the fifth day. The importance of persistent counterregulation in the development of tolerance to the antihypertensive effect of dihydralazine is discussed.

The magnitude and the persistence of blood pressure reduction by propyldazine (PDZ) was investigated following treatment over a period of 4 days. The experiments were performed on 6 normotensive dogs trained to submit to puncture of the femoral artery and to stand quietly in a special frame over the experimental period of 7 to 8 hours.

The effects of prazosin (0.1, 0.5 and 2.5 mg/kg, orally) on blood pressure, heart rate and PRA were investigated after acute and chronic administration in conscious, normotensive dogs. The acute administration of prazosin caused a reduction in both systolic and diastolic blood pressure and an increase in heart rate and PRA. After chronic administration, twice daily for four days, tolerance developed, which was not due to persistent counterregulation. On comparison with urapidil, another α-adrenoceptor antagonist, the hypotensive and counterregulatory response to acute administration were similar with both substances; the development of tolerance to prazosin after chronic administration contrasted with the results with urapidil.

The responses of plasma renin activity (PRA) and plasma catecholamine levels to molsidomine, administered both intravenously and orally, were investigated in conscious trained dogs.

Radioactively labeled microspheres were used to investigate the effect of 2′,3′-di-O-nitro-5′-(N-ehtylcarboxamido)-adenosine (10 μg/kg orally), a long-acting adenosine analog, on blood flow through various organs over an experimental period of three hours in conscious dogs. There was a significant increase in myocardial, cerebral, intestinal, and renal cortical blood flow, whereas the flow through skeletal muscle, liver, pancreas, and renal medulla was unaffected. The endocardial/epicardial flow ratio, which was more than one under control conditions, decreased significantly. Arterial blood pressure and heart rate remained virtually unchanged. Since the adenosine analog is rapidly and completely denitratedin vivo, the denitration product 5′-(N-ethylcarboxamide)-adenosine, a highly potent adenosine receptor agonist, must be considered as the vasoactive metabolite.

The relevance of the steric configuration to the effects of two non-selective beta-adrenoceptor antagonists without intrinsic sympathomimetic activity (+)- and (--)-bupranolol (10 and 50 micrograms/kg i.v.) and (4)- and (--)-propranolol (100 and 500 micrograms/kg i.v.) on the i.v. glucose tolerance test (IVGTT) were investigated in conscious, normoglycemic dogs. The effects of the beta-adrenoceptor antagonists on plasma glucose, and insulin levels and insulin-glucagon ratio following IVGTT were evaluated by calculating the respective areas under the curve (AUC). The AUC values for plasma glucose were significantly increased by the (--)-configuration of both beta-adrenoceptor increased by the (--)-configuration of both beta-adrenoceptor antagonists. In the (+)-configuration only propranolol (500 micrograms/kg i.v.) increased the AUC value for plasma glucose significantly. The AUC values for plasma insulin and also for the plasma insulin-glucagon ratio were significantly increased by (--)-propranolol (500 micrograms/kg i.v.) and by (--)-bupranolol (10 and 50 micrograms/kg i.v.). Thus the impairment of glucose tolerance, due to suppression of the plasma insulin level, depends mainly on the beta-adrenoceptor antagonistic activity of the (--)-configuration.

The effect of beta-adrenoceptor antagonists on the intravenous glucose tolerance test was investigated in conscious dogs. dl-Celiprolol (cardioselective with ISA = intrinsic sympathomimetic activity) 200 and 1000 microgram/kg i.v., dl-metoprolol (cardio-selective without ISA) 200 and 1000 microgram/kg i.v., dl-pindolol (non-selective with ISA) 5 and 25 microgram i.v. and l-bupranolol (non-selective without ISA) 10 and 50 microgram/kg i.v. were used in the study. The influence of beta-adrenoceptor antagonists on the plasma glucose and immunoreactive insulin following intravenous glucose tolerance test were evaluated by calculating the respective areas under the plasma curve. The present investigation clearly demonstrates the marked difference between the various beta-adrenoceptor antagonists on heart rate and, especially on metabolic parameters. dl-Metoprolol, a beta-adrenoceptor antagonist with cardioselectivity and without ISA can be assumed not to alter plasma insulin level and glucose assimilation. l-Bupranolol, a non-selective beta-adrenoceptor antagonist without ISA reduces plasma insulin level and probably enhances peripheral glucose uptake, resulting in an "unchanged" glucose tolerance. dl-Celiprolol or dl-pindolol, beta-adrenoceptor antagonists with ISA, but cardioselective or non-selective enhance both, basal insulin level and insulin level after glucose stimulation but must be assumed to decrease peripheral glucose uptake since here too glucose tolerance was unchanged.

The effect of β-adrenoceptor antagonists on the intravenous glucose tolerance test was investigated in conscious dogs. dl-Celiprolol (cardioselective with ISA=intrinsic sympathomimetic activity) 200 and 1000 μg/kg i.v., dl-metoprolol (cardio-selective without ISA) 200 and 1000 μg/kg i.v., dl-pindolol (non-selective with ISA) 5 and 25 μg i.v. and l-bupranolol (non-selective without ISA) 10 and 50 μg/kg i.v. were used in the study. The influence of β-adrenoceptor antagonists on the plasma glucose and immunoreactive insulin following the intravenous glucose tolerance test were evaluated by calculating the respective areas under the plasma curve.

The effect of adenosine-5′-N-ethylcarboxamide, (NECA), a long-lasting adenosine derivative with pronounced vasoactivity was investigated on glucagon and insulin release from the in situ isolated blood perfused pancreas in the anesthetized dog: NECA (10−9 to 10−5 mol/l) led to a dose-dependent glucagon release. Insulin release was inhibited by NECA at low concentrations, but significantly increased at higher concentrations of the adenosine analogue. Similar effects were observed with infusion of adenosine at 10−7 and 10−6 mol/l. Aminophylline (10−4 mol/l) produced a 10-fold attenuation of the actions of NECA.

The adenosine analogue 765-21 (10 micrograms/kg intravenously), substituted at the 5'-position, caused a sustained increase in plasma glucose and a decrease in plasma free fatty acid concentrations in conscious dogs. Concomitantly, plasma glucagon levels rose threefold. Changes in plasma insulin concentration were relatively small and of no statistical significance. A simultaneous fall in arterial blood pressure was also observed. Aminophylline, an adenosine antagonist, inhibited the haemodynamic as well as the metabolic responses evoked by the adenosine analogue. - In collagenase-isolated rat islets of Langerhans 765-21 inhibited glucose-induced insulin release in a dose-dependent manner (concentration range 10(-8) to 10(-5) M). In contrast to the data obtained on conscious dogs, 765-21 did not promote glucagon release from the pancreatic islets. Since stimulation of glucagon secretion was also not observed on decreasing the glucagon concentration in the incubation medium, the collagenase technique of isolation may be responsible for the insensitivity of the islets to glucagon-releasing stimuli. - The results are indicative of a specific inhibition of glucose-induced insulin release by 765-21. The data obtained in vivo additionally suggest a glucagon-releasing activity of the adenosine analogue investigated.