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Biomedical subjects

M L Marcus

Publications and source records attributed to M L Marcus.

227 records · Page 13Linked to original sources
PubMedDate not supplied

The effects of ventricular hypertrophy on the coronary circulation.

Recent animal studies suggest that cardiac hypertrophy compromises the coronary circulation. Although flow per gram of ventricle in most animal models of hypertrophy is normal, coronary vasodilator responses to pharmacological or physiological stimuli are mildly impaired. Studies of regional perfusion indicate that the limitation of coronary vasodilator capacity in hypertrophied ventricles primarily affects the endocardium. In contrast to studies in animals, measurements of coronary reactive hyperemia in man suggest that coronary dilator responses are profoundly depressed in patients with severe left ventricular hypertrophy secondary to aortic stenosis. These studies in man demonstrate that alterations in the coronary circulation secondary to cardiac hypertrophy are of sufficient magnitude to contribute to the development of angina and heart failure (secondary to endocardial fibrosis) in patients with aortic stenosis.

Animals↗
PubMedDate not supplied

Regional three-dimensional geometry of the normal human left ventricle using cine computed tomography.

The aim of this study is to provide accurate three-dimensional measurements of left ventricular geometrical indices in relation to regional myocardial function. The analysis of the three-dimensional regional geometry and function of left ventricles of ten normal human volunteers is based on three-dimensional reconstructions of the left ventricle from cine computed tomography images, at end diastole and end systole, demonstrating normal left ventricular spatial, geometrical, and functional variability. Regional wall thickness, curvature and surface normals, as well as wall thickening and endocardial wall motion, are calculated and mapped for the entire left ventricle. The circumferential asymmetry of the left ventricle is reflected by the smaller circumferential and meridional curvatures at the septum. Thickening is highest at the anterior and lateral walls. Longitudinally, circumferential curvature increases toward the apex, whereas both wall thickness and wall thickening at end systole are largest at the midventricular level, decreasing toward the apex and base. This study describes the circumferential and apex-to-base variations in regional left ventricular geometric parameters of the normal human left ventricle, using three-dimensional imaging and analysis.

Adult↗
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Evaluation of regional myocardial function in ischemic heart disease by echocardiography.

Echocardiography can display motion abnormalities of acutely or chronically ischemic myocardium. In experimental studies, this permits the evaluation of the effect on regional dyskinesis of potentially therapeutic interventions. In clinical studies, the demonstration of segmental dyskinesis has been primarily useful for diagnostic purposes. As more experience is gained with the newer two-dimensional cross-sectional ultrasound techniques, it appears likely that these will afford a major advance in the diagnosis of ischemic heart disease by permitting the routine noninvasive demonstration of segmental ventricular dyskinesis and assessment of regional myocardial function.

Animals↗
PubMedDate not supplied

Small vessel phenomena in the coronary microcirculation: phasic intramyocardial perfusion and coronary microvascular dynamics.

To place the characteristics of the coronary microcirculation in perspective to another muscular organ system, we have compared various parameters from exchange vessels in the heart and red skeletal muscle. The major differences between cardiac and skeletal muscle microcirculations relate to the larger density of capillaries in the heart. This increased density is responsible primarily for a greater capillary filtration coefficient-permeability-surface area product to various solutes, surface area, and decreased intercapillary distances. These features most likely represent an adaptation of the microcirculation of the heart to the very high, continual metabolic demands. Interestingly, capillary permeabilities and reflection coefficients of different solutes are in the same range (although the heart tends to have higher capillary permeabilities). Thus, the adaptation of the coronary circulation to facilitate exchange of nutrients and solutes is mediated via an increase in the numbers of exchange vessels, rather than modifications of the membrane characteristics of these exchange vessels. Within the last decade, there has been much information assimilated on the regulation of the coronary microcirculation. Most of the knowledge has been the result of many indirect approaches to studying the coronary microcirculation (indicator-dilution techniques, nuclide-labeled microspheres, plasma-lymph concentration of solutes). There are relatively few direct observations on regulation of the coronary microcirculation. This is primarily due to difficulties in techniques. Exploration of the phasic nature of intramyocardial perfusion is handicapped by the location of these intramuscular vessels. Visualization of the coronary microcirculation is hampered by movements of the heart, and such measurements are restricted to the superficial layers of the myocardium. It is worth emphasizing that direct observations of red cell velocities in epicardial capillaries, measurements of microvascular caliber, and the pressure profiles in the coronary microcirculation are restricted to the superficial, epicardial layer. It is not unreasonable to speculate that microvascular events and regulation occurring in the subepicardium may be quite different than that in the subendocardium. There are several salient points in this review that are worth emphasizing.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMedDate not supplied

Structural and hemodynamic response of peripheral arteries of macaque monkeys to atherogenic diet.

The arteries of monkeys given atherogenic diets develop marked intimal thickening and medial thinning, but luminal size apparently changes minimally. The hemodynamic significance of the atherosclerotic changes is therefore uncertain. To evaluate vascular function in atherosclerotic arteries, we studied the hind-limb vessels of adult male rhesus and cynomolgus monkeys to assess the structural and hemodynamic responses to an atherogenic diet given for about 1.5 years or for much longer periods (6.5 years for rhesus and 4.3 years for cynomolgus monkeys). The intimal cross-sectional area greatly increased after the atherogenic diet, but there was no significant luminal narrowing after either the 1.5-year diet or the longer diet periods. The media of atherosclerotic arteries showed focal atrophy and focal thinning after pressure fixation, but the total medial mass was not decreased even after the long diet periods. Hemodynamic studies indicated mild functional impairment in the atherosclerotic vessels; resting resistance increased and vasodilator responses decreased, but adrenergic responses were preserved. Thus, the marked changes that occur in the arterial wall in experimental primate atherosclerosis include adaptations to lesion formation that permit a long prestenotic phase of atherosclerosis in which vascular dysfunction is minimal.

Animals↗
PubMedDate not supplied

Total and regional cerebral blood flow during stimulation of carotid baroreceptors.

The concept that reflex control of cerebral vessels is unimportant has been challenged by recent studies which suggest that carotid baroreceptors have an important role in regulation of cerebral blood flow (CBF). In this study we have tested the hypothesis that arterial baroreceptors contribute to regulation of total or regional CBF. CBF was measured in anesthetized dogs with 15 mu microspheres. Stimulation of carotid baroreceptors, by raising carotid sinus pressure, did not alter or redistribute cerebral flow. Responses to baroreceptor stimulation were intact, as manifested by vasodilation in skeletal muscle. CBF decreased during systemic hypocapnia and increased during hypercapnia, which indicates that failure of cerebral flow to change during baroreceptor stimulation was not due to unresponsiveness of cerebral vessels. During hypercapnia, baroreceptor stimulation also failed to alter CBF. In other studies CBF was measured during increases in systemic arterial pressure, before and after denervation of arterial baroreceptors. Increases in arterial pressure did not increase CBF either before or after denervation of baroreceptors. We conclude that baroreceptor stimulation does not alter total or regional CBF and that baroreceptors do not regulate cerebral flow during systemic hypertension.

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