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Biomedical subjects

M L Marcus

Publications and source records attributed to M L Marcus.

At least 145 records · Page 8Linked to original sources
PubMed1982

Effects of chronic hypertension and left ventricular hypertrophy on the incidence of sudden cardiac death after coronary artery occlusion in conscious dogs.

When acute myocardial infarction occurs in patients with hypertension and left ventricular hypertrophy (LVH), the incidence of sudden cardiac death increases markedly. Possible explanations include increased size of the occluded vascular bed secondary to more extensive atherosclerotic coronary vascular disease in the presence of hypertension, decreased coronary reserve secondary to LVH, and intrinsic electrophysiologic abnormalities in hypertrophied cardiac muscle. To explore these possibilities, we produced acute circumflex coronary occlusion during the resting, conscious state in 32 control dogs and in 28 dogs with hypertensive LVH. Before coronary occlusion, mean arterial pressure was 96 +/- 0.1 mm Hg in control dogs and 125 +/- 5 mm Hg in dogs with hypertensive LVH (p less than 0.01). The control left ventricular/body weight ratio was 4.5 +/- 0.1 g/kg, compared with 6.1 +/- 0.1 g/kg in hypertensive LVH (p less than 0.01). Cumulative mortality at 6, 24 and 48 hours was 9%, 13% and 16% in control dogs and 32%, 43% and 54%, respectively, in dogs with hypertensive LVH (all p less than 0.01 vs control). The perfusion fields of the occluded vessel defined by postmortem coronary angiography were similar in the two groups (31 +/- 2% of left ventricular mass for control vs 29 +/- 2% for hypertensive LVH). Thus, the increased incidence of sudden cardiac death after coronary artery occlusion in hypertensive LVH dogs cannot be explained by increased size of the occluded vascular bed and is probably related to the decreased coronary reserve or intrinsic electrophysiologic abnormalities that characterize pressure-induced hypertrophied cardiac muscle.

Animals↗
PubMed1982

Normal exercise capacity in patients with severe left ventricular dysfunction: compensatory mechanisms.

About one-third of patients who have severe left ventricular dysfunction can achieve normal levels of exercise. To elucidate the mechanisms that permit this to occur, we studied six patients with severe left ventricular dysfunction (average left ventricular ejection fraction 17 +/- 2.5% [mean +/- SEM]) who achieved nearly normal levels of exercise tolerance (greater than 11 minutes of treadmill exercise, Sheffield protocol). All patients had normal pulmonary function at rest and during exercise. Hemodynamics were measured at rest and during supine and upright exercise. The major mechanisms of the preserved exercise capacity in these patients were chronotropic competence, ability to tolerate elevated wedge pressures (33 +/- 3 mm Hg) without dyspnea, ventricular dilation, and increased levels of plasma norepinephrine at rest and during exercise. Also, whereas peripheral vascular resistance was unchanged during supine exercise, it decreased by 50% during similar levels of upright exercise. As a consequence, increases in cardiac output from rest to exercise were greater during upright than supine exercise (100% vs 50%, respectively) (p less than 0.05), and pulmonary wedge pressures were lower during upright than supine exercise (21 +/- 5 mm Hg vs 33 +/- 3 mm Hg). Thus, multiple mechanisms permit some patients with severe left ventricular dysfunction to achieve normal levels of exercise. These studies emphasize that left ventricular function must be assessed by direct means rather than inferring function of the left ventricle from the results of an exercise tolerance test.

Aged↗
PubMed1982

Phasic coronary blood flow velocity in intramural and epicardial coronary arteries.

Knowledge concerning phasic coronary blood flow is based primarily on measurements obtained from epicardial coronary arteries, which, in part, function as capacitors. If present, epicardial capacitance effects could obscure the dynamic nature of phasic intramyocardial perfusion. To analyze this effect of epicardial capacitance, we simultaneously measured coronary blood flow velocity in an epicardial artery (left anterior descending) and an intramural artery (septal) in open-chest, anesthetized dogs. During control conditions, the percentage of total coronary blood flow velocity occurring during diastole per cardiac cycle was significantly greater (P less than 0.05) in the septal artery (92%) than in the left anterior descending artery (75%). Furthermore, blood flow velocity during mid-systole in the septal artery was retrograde (-7.2%), whereas blood flow velocity at this time was antegrade in the left anterior descending artery (+3.5%). Blood flow velocity measurements from small epicardial arteries just before they penetrated into the myocardium revealed a phasic pattern similar to that of the septal artery. This suggests that the phasic blood velocity pattern in penetrating coronary arteries, in general, is different than that in large epicardial arteries. During vasodilation following nitroglycerin, dipyridamole, or a 20-second occlusion of the left main coronary artery, the retrograde component of mid-systolic blood velocity persisted in the septal artery, despite large increases (300-400%) in the mid-systolic antegrade component of blood flow velocity in the left anterior descending artery. These qualitative and quantitative differences in phasic blood flow velocity between intramural and large epicardial arteries are best reconciled by postulating the existence of a significant coronary capacitor.

Animals↗
PubMed1982

Effects of duration and severity of arterial hypertension and cardiac hypertrophy on coronary vasodilator reserve.

Cardiac hypertrophy is associated with a decrease in coronary reserve. However, factors which may modulate the interaction between myocardial growth and vascular proliferation, such as duration and severity of hypertrophy, have not been evaluated. We measured myocardial perfusion with microspheres in conscious, chronically instrumented. Wistar-Kyoto (WKY) and spontaneously hypertensive (SHR) rats at 3, 7, and 15 months of age; and in SHR stroke-prone (SHR-SP) rats at 13-14 months of age. Myocardial perfusion was measured with microspheres in awake rats at rest and during maximal coronary dilation produced by dipyridamole infusion (2.0 mg/kg per min, iv). Arterial pressure was significantly elevated (P less than or equal to 0.05) in all hypertensive groups (vs. age-matched WKY), both at rest and during dipyridamole infusion. Left ventricular mass in the SHR rats was increased significantly (P less than or equal to 0.05) by 14%, 28%, and 29% at 3, 7, and 15 months, respectively. Left ventricular mass in the SHR-SP group was increased by 50% (P less than or equal to 0.05) compared to the 15-month-old WKY. Left ventricular minimal coronary vascular resistance (per gram) was significantly greater (P less than or equal to 0.05) in SHR at 7 months, and in the SHR-SP group (66% and 60%, respectively). Right ventricular minimal coronary vascular resistance was significantly greater (P less than or equal to 0.05) in SHR at 7 and 15 months (50%), and in the SHR-SP group (122%), compared to 15-month-old WKY. The results indicate the following: (1) the increase in minimal coronary vascular resistance between SHR and WKY rats was greatest when left ventricular hypertrophy peaked (7 months) and was no longer present after left ventricular hypertrophy had stabilized. (2) In 14-month-old SHR-SP rats, with more severe left ventricular hypertrophy and hypertension, minimal coronary vascular resistance was considerably higher than in SHR of approximately the same age. (3) Long-term arterial hypertension was associated with a higher right ventricular minimal coronary vascular resistance. Resistance appeared to change in proportion to the severity of hypertension, and the changes were independent of the presence of right ventricular hypertrophy.

Animals↗
PubMed1982

The effects of atrial fibrillation on atrial pressure-volume and flow relationships.

To study whether atrial fibrillation might produce local changes in the atrium which could facilitate the tendency of this arrhythmia to become chronic and self-perpetuating, we compared the effect of atrial fibrillation, atrial pacing, and acute volume loading on the perfusion and oxygen consumption of the atrium in anesthetized dogs. Measurement of atrial perfusion with microspheres indicates that during atrial fibrillation, atrial blood flow increases 2- to 3-fold. Right atrial pacing is a significantly less potent metabolic stimulus for atrial vasodilation. Using Doppler velocity recordings of sinus node artery blood flow velocity, a marked increase in velocity is observed within 5 seconds after the initiation of atrial fibrillation. During atrial fibrillation, the sinus node artery reactive hyperemia response is markedly attenuated. Atrial fibrillation acutely decreases atrial distensibility; atrial pressure increased 81 +/- 19% with only a small increase (9.7 +/- 3%) in atrial diameter measured by echocardiography. During sinus rhythm, volume expansion to equivalent levels of atrial pressure as seen during atrial fibrillation increased atrial diameter 21 +/- 5% P less than 0.05. Atrial oxygen consumption determined by the microspectrophotometric method markedly increases during atrial fibrillation, compared to control conditions (12.3 +/- 2.8 vs. 3.9 +/- 0.6 ml O2/min per 100 g, respectively) P less than 0.05. Atrial O2 extraction was 5.5 +/- 0.4 ml O2/ml blood in the control state, and did not change with interventions. There was a linear relationship between left atrial O2 consumption and blood flow in all experimental conditions. Atrial fibrillation therefore alters atrial hemodynamics and metabolism by increasing atrial blood flow and oxygen consumption and decreasing atrial distensibility. Since atrial perfusion during atrial fibrillation is high and atrial flow reserve is limited, it is possible that additional atrial metabolic requirements might lead to atrial ischemia, fibrosis, and, thereby, perpetuation of the arrhythmia.

Animals↗
PubMed1982

Determination of coronary reserve in patients with supravalvular aortic stenosis.

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.

Adolescent↗
PubMed1981

Effects of volume expansion and vasodilators in acute pericardial tamponade.

Pharmacologic therapy may be useful as emergency treatment for acute pericardial tamponade while preparing for pericardiocentesis. We studied the effects of volume expansion and vasodilators in acute pericardial tamponade in spontaneously breathing mongrel dogs. Hemodynamic parameters and blood flow (15-micrometer microspheres) to brain, heart, kidney, colon, stomach, liver, and temporalis muscle were measured. Arterial pressure and cardiac output rose, and blood flow to all major organs, except stomach, increased after volume expansion (n = 17) by infusion of 20 ml/kg of dextran after tamponade. With nitroprusside (8-75 microgram/min) after volume expansion (n = 5), ventricular filling pressures were reduced to control levels, whereas the favorable effects of volume expansion on cardiac output, blood pressure, and kidney and heart blood flow were maintained. Hydralazine alone or hydralazine plus volume expansion was not as effective as the combination of nitroprusside and volume expansion. Thus, volume expansion alone or the combination of volume expansion and nitroprusside infusion should be beneficial as emergency therapy while preparing for pericardiocentesis in patients with acute pericardial tamponade.

Acute Disease↗
PubMed1981

Effect of adenosine and dipyridamole on cerebral blood flow.

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.

Adenosine↗
PubMed1981

Role of vasa vasorum in nourishment of the aortic wall.

Vasa vasorum are present in the middle and outer layers of media in the thoracic aorta of dogs and humans. To examine the role of vasa vasorum in nourishment of the aorta, we ligated four contiguous pairs of intercostal arteries in anesthetized dogs. These arteries are the source of vasa to the descending aorta but not the aortic arch. Blood flow through vasa vasorum was measured with microspheres. Acute intercostal ligation did not reduce conductance in the aortic arch but reduced conductance in the middle third of the descending aorta from 7 +/- 1 to 3 +/- 0.7 (SE) ml.min-1.100 g-1.mmHg-1 (P less than 0.05). After intercostal ligation, infusion of adenosine (5 mumol.kg-1.min-1 iv) increased conductance in the aortic arch 3- to 4-fold but did not increase conductance in the descending aorta. Six to ten days after intercostal ligation, conductance in the middle third of the descending aorta remained low. Vasodilator capacity was partially restored in outer layers of the descending aorta, probably by collateral vessels or formation of new vessels. Morphological changes ranged from broad bands of necrosis to patchy areas of cell loss, primarily in middle layers of descending aorta. We conclude that vasa vasorum are critical in nourishment of aortic media.

Adenosine↗
PubMed1981

Continuous measurement of cerebral blood flow in anesthetized cats and dogs.

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.

Anesthesia↗
PubMed1981

Baroreflex control of heart interval in conscious renal hypertensive dogs.

The purpose of this study is to determine if baroreflex control of heart interval is abnormal in conscious dogs with renal hypertension. Changes in heart interval in response to transient nitroglycerin-induced decreases in arterial pressure and transient phenylephrine-induced increases in arterial pressure were determined in nine normotensive [mean arterial pressure 92 +/- 4 (SE) mmHg] and nine renal hypertensive conscious dogs (mean arterial pressure 139 +/- 10 mmHg). Data were acquired before and after beta-adrenergic blockade with 2 mg/kg iv propranolol and before and after parasympathetic blockade with 0.5 mg/kg iv atropine. Control heart rates for the normotensive and hypertensive dogs were not different (91 +/- 4 and 93 +/- 7 beats/min, respectively). Before autonomic blockade, the responses of normotensive and hypertensive dogs to nitroglycerin were not different. However, prolongation of the heart interval in response to phenylephrine in hypertensive dogs was significantly less than in normotensive dogs. In both groups, atropine nearly abolished the decrease in heart interval in response to nitroglycerin and the increase in heart interval in response to phenylephrine, although there were small but significant residual responses. Propranolol was without significant effect on heart interval responses to nitroglycerin and phenylephrine. We conclude that the baroreflex control of heart interval during transient decreases in arterial pressure is preserved in hypertensive dogs and is mediated mainly by decreases in parasympathetic outflow to the heart. In contrast, baroreflex control of heart interval during transient increases in arterial pressure is impaired in hypertension and is mediated mainly by activation of parasympathetic cholinergic mechanisms.

Animals↗
PubMed1981

Effects of short- and long-term left ventricular hypertrophy on coronary circulation.

Although most studies suggest that coronary vasodilator responses are impaired in dogs with cardiac hypertrophy, the factors that contribute to this impairment have not been elucidated. To determine if the duration of hypertrophy was an important determinant, we studied coronary vasodilator responses in awake dogs with two-kidney renal hypertension of 6 wk (n = 11) and 6 mo (n = 8) duration. The dogs with hypertension (6 wk and 6 mo) and left ventricular hypertrophy (LVH) had about a 25% (P less than 0.05) increase in LV mass and mean arterial pressure. During maximal coronary vasodilation induced with 4.7 microM . kg-1 . min-1 iv adenosine, maximal flow was significantly decreased in both groups of hypertensive dogs, and minimal coronary vascular resistance was increased by about 50% (P less than 0.05). Minimal coronary vascular resistance was similar in dogs with 6 wk and 6 mo of hypertension and LVH. These experiments suggest that 1) mild LVH (25% increase in LV mass) can significantly decrease coronary dilator reserve and 2) within the time frame examined (6 wk to 6 mo), the duration of hypertension and LVH does not increase the coronary vascular abnormalities associated with cardiac enlargement.

Animals↗
PubMed1981

A method for continuously assessing coronary blood flow velocity in the rat.

We have developed a directional pulsed-Doppler system to make blood flow velocity measurements in the coronary arteries of the rat. The probe consists of a 1-mm2 crystal mounted in a 6-mm suction cup, which can be attached by vacuum to the vessel without requiring dissection. Recordings of phasic coronary blood flow velocity (CBV) in the rat indicate that 82 +/- 2% (mean +/- SE) of the area under the CBV recording occurs in diastole. CBV increased during an infusion of dipyridamole and changed in parallel with alterations in left-ventricular pressure. To validate the technique we correlated changes in CBV wih changes in microsphere-measured left-ventricular perfusion (range, 20--780 ml/min x 100 g). These two methods of estimating coronary flow correlated closely (r = 0.93). Measurements of phasic CBV in the rat with this Doppler system should permit a detailed characterization of the coronary circulation in many models of disease that have been developed in the rat.

Animals↗
PubMed1981

Effect of direct-current countershocks on regional myocardial contractility and perfusion. Experimental studies.

Very high energy electrical countershocks can cause morphologic damage to the myocardium. In this study we searched for functional correlates of these shock-induced morphologic changes. We used ultrasonic sonomicrometers to measure myocardial contractility and radiolabeled microspheres to assess perfusion. Acute and chronic experiments were conducted in 45 dogs, assessing the effect of both direct (epicardial) and transthoracic shocks on beating and fibrillating hearts. High-energy or rapidly repeated epicardial shocks caused subepicardial contraction abnormalities. This indicates that electrical current delivered to the myocardium in sufficiently high amounts and concentration can cause functional damage. Thus, in open-chest defibrillation during cardiac surgery, low energies (10-20 J) should be used initially and higher energies resorted to only if lower-energy shocks fail. However, single and multiple transthoracic shocks up to 460 J delivered energy caused no detectable contraction abnormalities. Myocardial perfusion did not fall after shocks. Thus, high-energy transthoracic shocks may have no deleterious effects on the contraction and perfusion of normal myocardium.

Animals↗