A procedure for automatic sorting of three-dimensional (3-D) shapes is proposed. The procedure is applied to sort into normal and abnormal categories, human left ventricles (LV) using in vivo data from 19 subjects (ten normal and nine abnormal LV's) studied by ultrafast tomography (Cine-CT). The procedure starts by utilizing a vector in a helical coordinate system to describe the spatial geometry of each individual LV cavity. This individual vector is then anatomically aligned and normalized to eliminate effects due to size, yielding a dimensionless vector, denoted as "geometrical cardiogram" (GCG). The GCG characterizes the instantaneous 3-D geometrical information of the individual LV. For the group of healthy subjects, the Karhunen-Loeve Transform (KLT) is then applied to compress the geometric information contained in their individuals' GCG vectors, at end diastole (ED) and end systole (ES), and yield a unique set of basis vectors. The "normal shape domain" is next defined as a truncated set of the KLT basis vectors from which a normal GCG can be reconstructed with a mean squared error (MSE) smaller than a defined threshold. The calculated MSE of any individual GCG reconstructed in this domain is then used as a criterion for sorting the 3-D shapes. Hearts which yield MSE greater than the threshold are considered abnormal. When applied to the study group of 19 subjects a significant difference (p less than 0.0001) between the MSE values obtained for the normal LV's, and those obtained for the abnormal LV's was detected, thus leading to a successful sorting of all the studied LV's. Finally, the KLT is applied to yield a compact representation of the 3-D geometry of any LV (normal or abnormal).

We examined effects of hypercholesterolemia and atherosclerosis on vasoconstrictor responses to norepinephrine and serotonin. Responses were compared in normal, atherosclerotic, and hypercholesterolemic but non-atherosclerotic cynomolgus monkeys. The hindlimb was perfused at constant flow so that changes in perfusion pressure indicated changes in vascular resistance. We measured the pressure gradient from the iliac to the dorsal pedal artery so that responses of the large artery segment could be determined. Serotonin decreased total hindlimb resistance in normal and hypercholesterolemic monkeys, but increased total resistance in atherosclerotic monkeys. There was a greater than 10-fold increase in constrictor responses of large arteries to serotonin in atherosclerotic monkeys, compared with normal and hypercholesterolemic monkeys. In contrast, we found that vasoconstrictor responses to norepinephrine are normal in atherosclerotic monkeys and increased in hypercholesterolemic monkeys prior to development of atherosclerosis. Hypercholesterolemia augmented responses of small vessels to norepinephrine. We conclude that, during early stages of hypercholesterolemia in cynomolgus monkeys, vasoconstrictor responses to norepinephrine are increased in small vessels. At a later stage, as atherosclerosis develops, responses to norepinephrine return to normal, but vasoconstrictor effects of large arteries to serotonin are greatly potentiated.

Utilizing radioactive microspheres, blood flow to the femoral head of immature dogs was measured. Blood flow was measured with the leg in the control position, maximal abduction, submaximal abduction, and the human position of hip immobilization. Maximal abduction (to 90 degrees) significantly decreased flow to the capital femoral epiphysis. Submaximal abduction and the human position did not reduce blood flow. Measurement of flow in the control position immediately after forced abduction demonstrated marked reactive hyperemia. These data indicate that ischemia occurs during 90 degrees forced abduction of the hip. This finding supports the use of lesser degrees of abduction for hip immobilization in the treatment of congenital dislocation of the hip. The vascular anatomy of the head of the femur in puppies and children suggests that these data can be extrapolated to man.

Coronary reserve in patients with supravalvular aortic stenosis may be limited by coronary artery ostial obstruction or left ventricular hypertrophy. To assess the relative effect of these two factors on coronary reserve, seven patients with supravalvular aortic stenosis were studied intraoperatively before and after repair. Six patients who underwent elective cardiac surgery for conditions that did not involve the left ventricle or the left anterior ascending coronary artery served as controls (control group 1). Four patients were studied before and after cardiopulmonary bypass to determine if cardiopulmonary bypass altered coronary reserve in normal vessels perfusing normal ventricle (control group 2). Using a pulsed Doppler probe to determine coronary velocity, coronary reactive hyperemia was induced in the left anterior descending coronary artery (patients with supravalvular aortic stenosis and group 1 controls) or right ventricular branches of the right coronary artery (group 2 controls) during maximal coronary dilation produced by a 20-second coronary occlusion. All patients with supravalvular aortic stenosis underwent patch aortoplasty to relieve left coronary artery ostial obstruction and outflow tract obstruction; three patients also underwent aortic valvotomy and one patient also underwent valve replacement. Coronary reactive hyperemia was calculated as the ratio of peak to resting velocity. This ratio was 5.0 +/- 0.6 (mean +/- SEM) preoperatively and 3.6 +/- 0.3 postoperatively in control group 2. Thus, coronary reserve was only modestly reduced after cardiopulmonary bypass. Before repair, the ratio of peak to resting velocity was markedly reduced in patients with supravalvular aortic stenosis compared with control group 1 (1.8 +/- 0.3 vs 4.9 +/- 0.5, p less than 0.05) and did not change after repair (1.7 +/- 0.2), even though the aortic gradient was reduced (80 +/- 14 vs 38 +/- 6 mm Hg, p less than 0.05) and real or potential coronary ostial obstruction was eliminated by the operation. Because coronary reserve did not improve after surgery in patients with supravalvular aortic stenosis, we conclude that left ventricular hypertrophy is probably the primary determinant of decreased coronary reserve in these patients.

The aortic wall is nourished by diffusion from the aortic lumen and from vasa vasorum in the adventitia and outer layers of media. Intimal proliferation in atherosclerosis might be expected to reduce the effectiveness of diffusion from the lumen and increase dependence on nourishment by vasa. This study was performed to determine whether there is increased perfusion of the aortic wall by vasa vasorum in atherosclerosis. We used microspheres to measure flow through vasa in normal and atherosclerotic cynomolgus monkeys. Blood flow to inner layers of the thoracic and abdominal aorta was less than 1 ml/min X 100 g in normal monkeys, and there was a minimal increase in atherosclerotic monkeys. Flow to the outer layers of the thoracic and abdominal aorta was 1.3 +/- 0.9 and 2.2 +/- 0.8 ml/min per 100 g in normal monkeys. Flow to outer layers of the thoracic and abdominal aorta was increased in atherosclerotic monkeys to 17 +/- 8.9 and 31 +/- 12 ml/min per 100 g (P less than 0.05 vs. normal). Thus there is increased perfusion of the atherosclerotic aorta, particularly in the outer layers. During maximal vasodilation induced by infusion of adenosine, flow through vasa was 3- to 8-fold greater in atherosclerotic than in normal monkeys. This finding suggests that proliferation of new vessels, rather than dilation of existing vessels, accounts for the increase in blood flow through vasa. We speculate that hyperemia of the aortic wall in atherosclerosis may be in part a compensatory response to increased oxygen requirements and possibly to ischemia produced by intimal proliferation and a resulting increase in diffusion distance.

The purpose of these experiments was to determine whether infusions of adenosine and of dipyridamole, which raise levels of endogenous adenosine, increase cerebral blood flow (CBF). In anesthetized dogs and cats, intracarotid infusions of adenosine increased blood flow to cranial muscle but did not alter CBF (measured with microspheres). Anatomical limitations may prevent satisfactory examination of cerebral vascular responsiveness during intracarotid infusion of vasodilator drugs in these species. In anesthetized rabbits, infusion of adenosine 10 microM/min in the carotid artery produced a 2-fold increase in CBF. Infusion of dipyridamole 20 microM/min increased CBF 2.7-fold. Dipyridamole produced a small decrease in cerebral oxygen consumption, which indicates that the vasodilator effect of the drug is not an indirect effect secondary to increased metabolism. These data indicate that exogenous and endogenous adenosine increase CBF in rabbits.

We have developed a method for virtually continuous measurement of changes in cerebral blood flow (CBF) in cats and dogs. CBF was computed by multiplying cross-sectional area (CSA) and mean blood velocity in a pial artery. CSA was determined by measuring pial artery diameter with an electronic micrometer every 2-4 s through a cranial window. Velocity was measured continuously with a pulsed Doppler crystal positioned under a pial artery. CBF was determined in 12 anesthetized cats during 1) control, 2) hypocapnia, 3) hypercapnia, and 4) hypercapnia plus hypertension. Microspheres were injected under steady-state conditions to compare the two methods. During control, the diameter of the cerebral arteries observed was 388 +/- 28 (SE) micrometers, and CBF measured with microspheres was 40 +/- 4 ml.min-1.100 g-1. CBF decreased 18 +/- 2% during hypocapnia and increased 152 +/- 36% during hypercapnia. During steady-state conditions, the correlation coefficient between changes in CBF (CSA X velocity and microspheres) was 0.94, and the slope of the regression line was 1.02. In similar studies on seven anesthetized dogs, the correlation coefficient between CSA X velocity and microspheres was 0.98, and the slope of the regression line was 0.94. We conclude that the product of CSA and blood velocity of a pial artery provides accurate on-line measurement of changes in CBF.

These experiments were performed to determine whether the neurotransmitters acetylcholine (ACh) and vasoactive intestinal peptide (VIP) increase cerebral blood flow (CBF). In anesthetized dogs, infusion of very large doses of ACh (500 microgram/min) into the carotid artery increased CBF (measured with microspheres) 50%. Anatomical limitations prevented adequate testing of cerebrovascular responses in dogs. In anesthetized rabbits, infusion of ACh (10 microgram/min) into the carotid artery produced a twofold increase in CBF. Vessels in gray matter were more responsive than vessels in white matter. ACh did not alter cerebral oxygen consumption, which indicates that the dilator effect of the drug is not an indirect effect mediated through an increase in metabolism. The vasodilator response to ACh was attenuated by atropine (1 mg iv). Intracarotid infusion of VIP in rabbits increased blood flow to cerebral gray matter: infusion of VIP (10 microgram/min) incresed flow 33%. We conclude that 1) cerebral vasodilator responses to ACh and VIP are larger than previously recognized and 2) responses to these drugs occur primarily in cerebral gray matter. Because the neurotransmitters increase CBF significantly, these studies should encourage further studies concerning effects of cholinergic and peptidergic nerves on cerebral vessels.

Chronic hypertension increases the risk of myocardial infarction and the morbidity and mortality associated with it. Although accelerated atherosclerosis is partially responsible, other abnormalities in the coronary circulation associated with hypertension, such as decreased coronary vascular capacity and capillary density, could also contribute. To evaluate the effects of these nonatherosclerotic abnormalities, we produced sudden coronary occlusion in nine chronically hypertensive dogs. The mean aortic pressure and left ventricular mass were about 50% greater in hypertensive dogs than in the nine controls. Before occlusion and 5 min and 49 h after occlusion, myocardial blood flow was measured with tracer microspheres. Also, the extent of infarction in selected myocardial segments was quantified histologically. We found that coronary occlusion reduced flows to a similar extent, and that, over a 48-h period, collateral flow increased to a similar extent in the two groups. In addition, the amount of necrosis associated with a given degree of ischemia was similar in the two groups. Although the extent of the left ventricle that became ischemic was greater in the hypertensive dogs (28 +/- 2 vs. 18 +/- 4%; P < 0.05), chronic hypertension and left ventricular hypertrophy did not limit the recruitment of collateral supply or increase the amount of necrosis associated with a given degree of ischemia.

HomeCirculation ResearchVol. 50, No. 4Responsiveness to cardiac sympathetic nerve stimulation during maximal coronary dilation produced by adenosine. Free AccessAbstractPDF/EPUBAboutView PDFSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessAbstractPDF/EPUBResponsiveness to cardiac sympathetic nerve stimulation during maximal coronary dilation produced by adenosine. U J Johannsen, A L Mark and M L Marcus U J JohannsenU J Johannsen Search for more papers by this author , A L MarkA L Mark Search for more papers by this author and M L MarcusM L Marcus Search for more papers by this author Originally published1 Apr 1982https://doi.org/10.1161/01.RES.50.4.510Circulation Research. 1982;50:510–517 Previous Back to top Next FiguresReferencesRelatedDetailsCited By Camici P, Rimoldi O and Crea F (2018) Coronary Microvascular Dysfunction Chronic Coronary Artery Disease, 10.1016/B978-0-323-42880-4.00005-4, (55-68), . Shome J, Perera D, Plein S and Chiribiri A (2017) Current perspectives in coronary microvascular dysfunction, Microcirculation, 10.1111/micc.12340, 24:1, (e12340), Online publication date: 1-Jan-2017. Heusch G and Kleinbongard P (2016) Ivabradine: Cardioprotection By and Beyond Heart Rate Reduction, Drugs, 10.1007/s40265-016-0567-2, 76:7, (733-740), Online publication date: 1-May-2016. 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April 1, 1982Vol 50, Issue 4 Advertisement Article InformationMetrics Copyright © 1982 by American Heart Associationhttps://doi.org/10.1161/01.RES.50.4.510 Originally publishedApril 1, 1982 PDF download Advertisement