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Biomedical subjects

M L Marcus

Publications and source records attributed to M L Marcus.

At least 181 records · Page 10Linked to original sources
PubMed1980

Measurements of coronary reactive hyperemia with a Doppler probe. Intraoperative guide to hemodynamically significant lesions.

The physiological significance of coronary obstructions of intermediate severity are difficult to assess from the angiogram alone. The hemodynamic significance of clinical coronary stenoses can be readily assessed, however, with a miniaturized Doppler probe developed at The University of Iowa Hospitals and Clinics to measure phasic coronary velocity. No dissection of the coronary vessel is required. The probe is held in place over the coronary vessel with a small suction cup. Reactive hyperemia responses obtained following a 20 second occlusion clearly demonstrate the hemodynamic significance of a coronary stenosis. We have employed this approach in 64 patients with coronary artery disease. In 12 (19%) in whom the degree of stenosis of the vessel was equivocal (diameter narrowing 25% to 70%), the use of the Doppler probe and a 20 second reactive hyperemia curve allowed accurate and immediate assessment of the need for a bypass. Five of these equivocal lesions did not produce any alterations in coronary reserve and, accordingly, the vessels were not bypassed. In seven of them, the reactive hyperemia response was markedly depressed and as a result the vessel in question was bypassed. Thus measurements of coronary reactive hyperemia in vessels with obstruction of intermediate severity can influence the operative plan by assessing the physiological significance of the obstruction.

Adult↗
PubMed1979

Effects of cardiac hypertrophy secondary to hypertension on the coronary circulation.

For many years clinicians have suspected that hypertrophied ventricles have an inadequate coronary circulation. Recent studies have confirmed early observations that flow per gram in hypertrophied ventricles is normal at rest. However, coronary vascular resistance is greatly increased when hypertension is the cause of left ventricular hypertrophy. Studies that have employed labeled microspheres to assess regional myocardial perfusion have shown that the transmural distribution of myocardial perfusion is often abnormal in dogs with left ventricular hypertrophy. In addition, studies of cardiac hypertrophy in many animal models have shown that maximal coronary vasodilatation is limited substantially. Furthermore, when hypertrophied hearts are subjected to a physiologic stress that induces coronary vasodilatation, endocardial underperfusion occurs frequently. Thus, studies in animals suggest that cardiac hypertrophy adversely affects the coronary circulation. The availability of new techniques for estimating phasic and transmural coronary blood flow in man should make it possible to extend these studies to patients with cardiac hypertrophy.

Adenosine↗
PubMed1979

Effects of sympathetic nerves on cerebral blood flow in awake dogs.

Although cerebral blood vessels are densely innervated by sympathetic nerve fibers, the functional significance of the nerves is controversial. Because previous studies have been primarily performed in anesthetized animals, it is possible that failure to observe prominent neural control of the cerebral circulation was secondary to anesthetic-induced depression of the sympathetic nervous system. Therefore, we studied sympathetic control of the cerebral circulation in 11 awake chronically instrumented dogs. Total and regional cerebral blood flow was measured with 15-micrometer microspheres at control blood pressure and during three levels of progressive hemorrhagic hypotension. Sympathetic nerves had only a small effect (11% decrease; P less than 0.05) on flow to the cerebrum during moderate hypotension (mean arterial pressure 49 +/- 2 mmHg). Also, during severe hypotension, there was a bilateral redistribution of brain blood flow that tended to preserve flow to the medulla. Although these studies suggest that sympathetic nerves have a definite constrictor effect on cerebral vessels, the data support the concept that the functional importance of sympathetic nerves to cerebral vessels is limited.

Animals↗
PubMed1979

Effect of sympathetic nerves on cerebral vessels during seizures.

The purpose of this study was to determine the effect of activation of sympathetic pathways during seizures on cerebral blood flow and integrity of the blood-brain barrier. We measured cerebral blood flow with microspheres and disruption of the blood-brain barrier with labeled albumin in cats. One cerebral hemisphere was denervated by cutting the superior cervical sympathetic trunk on one side. During bicuculline-induced seizures, superior cervical sympathetic nerve activity increased about threefold. Blood flow to the innervated hemibrain was significantly lower than flow to denervated hemibrain. However, in relation to the total increase in flow, this effect of nerves was minor. Blood-brain barrier permeability increased about sixfold during seizures, but there was no difference between the innervated and denervated sides of the brain. We conclude that sympathetic nerves attenuate the increase in cerebral blood flow during seizures, despite the increase in metabolism, but this effect is small. Activation of sympathetic nerves does not reduce disruption of the blood-brain barrier during seizures.

Animals↗
PubMed1979

Neurohumoral regulation of blood flow to bones and marrow.

We used labeled microspheres to measure bone and marrow blood flow under control conditions and during several interventions. In dogs, blood flow to compact cortical bone (femoral diaphysis) was 2 +/- 0.1 ml.min-1. 100 g-1, and in hematopoietic marrow (femur), flow was 24 +/- 5 ml.min-1. 100 g-1. Hematopoietic cancellous bones (sternum, ilium) received substantial blood flow. We estimate that as much as 11% of cardiac output is directed to the skeleton. Bone and marrow vessels were responsive to several stimuli. During exercise, vascular resistance in bone increased two- to fourfold, in contrast to profound vasodilation in adjacent skeletal muscle. Hemmorrhage also increased bone vascular resistance. Bone and marrow vessels responded to humoral stimuli: norepinephrine increased vascular resistance and adenosine decreased resistance. Bone vessels also responded to neural stimuli: stimulation of carotid baroreceptors decreased vascular resistance, and activation of sympathetic pathways by baroreceptor deafferentation in cats increased vascular resistance. These studies indicate that bone and marrow vessels respond actively to physiological stresses and to several humoral and neurogenic stimuli

Animals↗
PubMed1979

Role of vasa vasorum in nourishment of the aorta.

The media of arteries is virtually avascular. Thus, oxygen and nutrients must reach the cells of the media by diffusion from the lumen of the vessel and from adventitial vessels. The thickness of the thoracic aorta of man and dog exceeds the effective diffusion distance of oxygen, but nutrition is supplemented by vasa vasorum which enter into the outer layers of the media. Occlusion of vasa vasorum in dogs produces medial necrosis, which indicates that these vessels are essential for the nourishment of the aorta. Recently the microsphere method has been used to provide the first measurements of blood flow through vasa vasorum. There is substantial flow to the outer layers of media of the thoracic aorta in dogs, with virtually no blood flow in the inner layers. The vessels are very responsive to physiological stimuli: they dilate during infusion of adenosine and constrict during stimulation of sympathetic nerves. During acute increases in arterial pressure, blood flow to the media decreases probably from distortion of vasa vasorum. Vasa vasorum may play role in disease states. Insufficient blood flow through vasa vasorum may contribute to medial necrosis of the aorta and to aortic atherosclerosis. A role of vasa vasorum in aortic changes in hypertension and other vascular diseases merits further study.

Animals↗
PubMed1979

Effect of acute ischemia, nitroglycerin and nitroprusside on regional myocardial thickening, stress and perfusion. Experimental echocardiographic studies.

The purposes of this study were to demonstrate that echocardiography can be used to demonstrate the systolic wall thinning of acutely ischemic myocardium, and to compare the effects of nitroglycerin and nitroprusside on systolic thinning, wall stress and perfusion of ischemic myocardium. In 37 dogs, the ratio of end-systolic-to-end-diastolic posterior wall thickness fell from 1.30 +/- 0.02 to 0.88 +/- 0.01 ((p less than 0.001) after circumflex coronary occlusion; perfusion of the area supplied by the occluded artery fell from 98.2 +/- 7.5 ml/100 g/min to 36.5 +/- 2.9 ml/100 g/min (p less than 0.001). Nitroglycerin and nitroprusside were given to lower mean arterial pressure by 7% and 15%. Despite the reduction in coronary perfusion pressure, transmural perfusion, endocardial/epicardial perfusion ratio and systolic thinning remained constant. Both drugs reduced the ischemic "wall stress index" (ventricular pressure x ventricular diameter/wall thickness) by almost 50%. Thus, both nitroglycerin and nitroprusside were equally beneficial in this model of acute myocardial ischemia.

Animals↗
PubMed1979

Effects of neural stimuli on blood flow through vasa vasorum in dogs.

The purpose of this study was to determine whether neural stimuli alter blood flow through vasa vasorum in the thoracic aorta. We measured flow with microspheres in anesthetized dogs and observed responses to sympathetic stimulation and baroreceptor stimulation. During these interventions, changes in arterial pressure were prevented with propranolol or an arterial reservoir, to minimize indirect effects on vasa vasorum mediated through changes in aortic wall tension. Electrical stimulation of the stellate ganglion at 10 Hz reduced blood flow to vasa vasorum in the thoracic aorta from 11 +/- 1.6 (mean +/- SE to 6.8 +/- 1.1 ml/min per 100 g (p less than 0.05). Aortic diameter, measured with a sonomicrometer technique, did not change during sympathetic stimulation. Thus, the reduction in blood flow through vasa vasorum during sympathetic stimulation appears to be a direct effect, and not the result of constriction of the aorta and compression of vasa. To determine effects of physiological alterations in neurogenic vasoconstrictor activity, we examined responses to stimulation of carotid baroreceptors. When pressure in isolated, perfused carotid sinus baroreceptors was raised from 81 +/- 3 to 198 +/- 2 mm Hg, blood flow to vasa vasorum of the thoracic aorta increased from 3.7 +/- 0.6 to 10 +/- 2.2 ml/min per 100 g (P less than 0.05). We conclude that vasa vasorum are responsive to neural stimuli, since they constrict during sympathetic stimulation and dilate in response to baroreceptor stimulation.

Animals↗
PubMed1978

Comparison of interventricular septal motion studied by ventriculography and echocardiography in patients with atrial septal defect.

Abnormal systolic interventricular septal motion is an echocardiographic manifestation of right ventricular volume overload. In order to determine the anatomical basis for this echocardiographic finding, septal motion recorded by left lateral or left anterior oblique ventriculograms was compared with echocardiography ventricular septal motion. Thirteen patients with secundum atrial septal defects and 7 control patients with trivial or no heart disease were included in the study. We found that on ventriculograms the systolic motion of the interventricular septum was similar in both atrial septal defect and control patients. That is, the cephalic third of the septum moved anteriorly in systole in 9 of the 13 patients with atrial septal defect and in 3 of the 7 controls. The caudal two-thirds of the septum moved posteriorly in all patients. These results are compatible with the theory that argues that the echocardiographic abnormalities of septal motion in patients with atrial septal defect result from an end-diastolic septal flattening or bowing of the septum into the cavity of the left ventricle.

Adolescent↗
PubMed1978

Effects of sympathetic nerves on cerebral vessels in dog, cat, and monkey.

Cerebral vascular responses to sympathetic stimulation and denervation were examined in three species during acute severe hypertension as well as normal conditions. Cerebral blood flow (CBF) was measured with microspheres after the superior cervical sympathetic trunk was cut and during electrical stimulation of the superior cervical sympathetic ganglion. Sympathetic denervation did not increase CBF in anesthetized cats or monkeys. Under normal conditions, sympathetic stimulation decreased CBF significantly in monkeys (-26 +/- 3%) (mean +/- SE) but not in cats. During acute severe hypertension, decreases in CBF due to sympathetic stimulation were greatly augmented in cats (-29 +/- 7%, compared to -3 +/- 3%), only modestly augmented in dogs (-9 +/- 3%, compared to -1 +/- 2%), and not augmented in monkeys (-17 +/- 3%, compared to -23 +/- 4%). Disruption of the blood-brain barrier during hypertension was reduced by sympathetic stimulation. We conclude that 1) sympathetic tone to cerebral vessels is minimal because denervation does not increase CBF; 2) sympathetic stimulation decreases CBF under normal conditions in monkeys and during severe hypertension in cats, dogs, and monkeys, and it reduces disruption of the blood-brain barrier; and 3) there is an important species difference in responses to sympathetic stimulation under normal conditions and during acute hypertension.

Animals↗
PubMed1978

Regulation of blood flow to the aortic media in dogs.

Morphologic observations suggest that the inner layers of the thoracic aorta in man and dog are avascular and the outer layers have vasa vasorum. It appears that vasa vasorum are essential in the thoracic aorta because their interruption produces medial necrosis. These experiments provide the first measurements of blood flow through aortic vasa vasorum and examine physiologic regulation of that flow. During control conditions the outer two-thirds of the media of the thoracic aorta received 10 ml/min per 100 g blood flow through vasa vasorum. Flow to the inner third of the aorta was 1 ml/min per 100 g. Flow to both the inner and outer media of the abdominal aorta was less than 1 ml/min per 100 g. Adenosine increased blood flow to vasa vasorum in the outer media of the thoracic aorta from 7 to 18 ml/min per 100 g, but did not increase flow to the inner layers of the aorta. Hemorrhagic hypotension decreased flow in the outer media of the thoracic aorta from 14 to 2 ml/min per 100 g. Acute hypertension failed to increase blood flow through vasa vasorum, as conductance decreased significantly. These studies indicate that vasa vasorum provide a considerable amount of blood flow to the outer layers of the thoracic aorta. The vessels are responsive to physiologic stimuli because they dilate during infusion of adenosine and constrict during both hemorrhagic hypotension and acute hypertension. We speculate that the failure of blood flow to the aortic wall to increase during acute hypertension might, if it were sustained, contribute to aortic medial necrosis.

Adenosine↗