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Biomedical subjects

M L Marcus

Publications and source records attributed to M L Marcus.

At least 73 records · Page 4Linked to original sources
PubMed1988

Pulmonary inflation reflex: its lack of physiological significance in coronary circulation of humans.

In awake dogs, voluntary deep inspiration results in a marked, reflex-mediated increase in coronary blood flow. To study this reflex in humans, we subselectively measured coronary blood flow velocity (CBFV) with a 3-F coronary Doppler catheter in 12 subjects with angiographically normal coronary arteries. In each subject, intracoronary papaverine increased CBFV to 4.8 +/- 0.2 X resting CBFV and reduced coronary resistance to 0.20 +/- 0.01 X resting coronary resistance, demonstrating normal vasodilator reserve in the vessel under study. Valsalva maneuver reduced CBFV to 0.67 +/- 0.09 X resting CBFV and increased coronary resistance to 1.37 +/- 0.20 X resting coronary resistance (P less than 0.05 vs. control). Maximum voluntary inspiration, however, did not significantly change CBFV (peak response 1.03 +/- 0.05 X resting CBFV) or coronary resistance (0.96 +/- 0.04 X resting). To determine whether augmentation of resting alpha-adrenergic tone would potentiate the reflex, eight patients performed a sustained 33% maximal handgrip for 2 min. Maximal deep inspiration during handgrip failed to result in any significant change in CBFV or coronary resistance. These studies demonstrate that the canine pulmonary inflation reflex has little or no physiological significance in the coronary circulation of conscious humans. Additionally, these data suggest that the magnitude of reflex control of the coronary circulation may vary considerably between dogs and humans.

Adult↗
PubMed1988

Videodensitometric analysis of human coronary stenoses: validation in vivo by intraoperative high-frequency epicardial echocardiography.

Videodensitometry is a nongeometric method of coronary angiographic analysis that can be used to provide an index of coronary luminal area. However, there are few direct studies in vivo of the relationship of videodensitometric data to independent measures of luminal area in humans. Although videodensitometry is theoretically independent of angiographic projection and luminal shape, validation of these assumptions in vivo is also limited. We therefore used intraoperative high-frequency epicardial echocardiography, a technique that can directly determine human coronary luminal area and shape in vivo, to further validate videodensitometry. A total of 36 arterial segments in the left anterior descending and right coronary arteries were studied by videodensitometry and high-frequency echocardiography. Videodensitometry was performed on angiograms in which the arterial segment of interest was not markedly foreshortened and was uniformly filled with contrast. In 22 discrete lesions (13 with circular lumens and nine with oval or complex lumens), videodensitometric and echocardiographic measures of luminal area correlated well (r = .86). In 33 coronary arterial segments, the effect of angiographic projection on videodensitometry was determined by comparison of the results of videodensitometry performed on left anterior oblique vs right anterior oblique angiograms of the segments. Here too, the correlation was good (r = .94, y = 1.04x + 0.002). The good correlation of left anterior oblique with right anterior oblique videodensitometric results held true for lesions with circular and oval or complex lumens. This study further validates the ability of videodensitometry to provide an index of coronary luminal area and confirms in vivo previous assumptions that the results of videodensitometric analysis are independent of angiographic projection and luminal shape.

Adult↗
PubMed1988

The effect of coronary angioplasty on coronary flow reserve.

To determine the effects of coronary angioplasty on coronary flow reserve (CFR), we studied 32 patients before and immediately after single-vessel coronary angioplasty and 31 patients evaluated late after angioplasty (7.5 +/- 1.2 months, mean +/- SEM). The geometry (percent area stenosis and minimal cross-sectional area) of each lesion was determined by quantitative coronary angiography (Brown/Dodge method) and the integrated optical density was measured by videodensitometry. CFR was measured with a No. 3F coronary Doppler catheter placed immediately proximal to the lesion and a maximally vasodilating dose of intracoronary papaverine. The translesional pressure gradient was obtained in all lesions before and immediately after angioplasty and in 18 of 31 vessels late after angioplasty. CFR immediately after angioplasty returned to normal levels (greater than 3.5 peak/resting velocity ratio) in 14 of 31 patients and was improved, although not normalized, in the remaining 17 patients. CFR immediately after dilation was not significantly correlated with any of the angiographic variables of arterial stenosis nor the resting pressure gradient. Moreover, the pressure gradient and absolute distal coronary pressure at peak hyperemia were not significantly different in vessels with normal and those with abnormal flow reserve immediately after dilation, suggesting that the residual stenosis did not significantly limit hyperemia. Late after angioplasty, however, a significant relationship emerged between CFR and all four indexes of residual arterial stenosis (percent area stenosis r = .70, p less than .01; minimum arterial cross-sectional area r = .70, p less than .01; integrated optical density r = .60, p less than .01; and translesional pressure gradient r = .77, p less than .01). Furthermore, in the absence of restenosis, CFR eventually normalized in all patients. These findings demonstrate that in one-half of patients there is a transient reduction in coronary flow reserve immediately after angioplasty. In the absence of restenosis, coronary flow reserve later normalizes. Consequently, measurements of coronary flow reserve immediately after angioplasty may not reflect the eventual success of the procedure in removing physiologic obstruction to coronary blood flow.

Angiography↗
PubMed1988

The effect of hypertension and left ventricular hypertrophy on the lower range of coronary autoregulation.

These studies were performed to test the hypothesis that left ventricular hypertrophy arising as a complication of chronic hypertension is associated with impaired coronary autoregulation. Twelve dogs with hypertension and left ventricular hypertrophy (one-kidney, one-clip model) and 11 normal dogs were instrumented and subsequently studied while conscious. Circumflex pressure, measured with an intracoronary catheter, was adjusted to 100, 75, and 40 mm Hg with a hydraulic occluder that was placed proximally. At each circumflex pressure, myocardial perfusion was measured with radioactive microspheres. Reduction of circumflex pressure over this range did not significantly alter heart rate, left atrial pressure, or arterial pressure. In normal dogs, reduction of circumflex pressure did not alter total myocardial perfusion or the transmural distribution of perfusion. In contrast, in dogs with hypertension and left ventricular hypertrophy, circumflex subendocardial perfusion decreased 46% when pressure was decreased from 100 to 40 mm Hg (p less than .05 compared with normal). Autoregulation was quantified for each third of myocardium with the use of autoregulatory gain values (1 = perfect autoregulation; 0 = the absence of autoregulation). For pressure changes of 100 to 75 mmHg, values for autoregulatory gain were near unity for all layers of myocardium in both groups of animals. When pressure was decreased from 75 to 40 mm Hg, values for autoregulatory gain among the normal and hypertensive groups were, respectively: for subepicardium 1 +/- 0.2 (mean +/- SE) vs 0.9 +/- 0.2 (p = NS), for the midwall 0.8 +/- 0.2 vs 0.5 +/- 0.2 (p = NS), and for the subendocardium 0.8 +/- 0.1 vs 0.1 +/- 0.2 (p less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Acceleration of the wavefront of myocardial necrosis by chronic hypertension and left ventricular hypertrophy in dogs.

Previous studies have shown that hypertension and left ventricular hypertrophy (HT-LVH) increase completed infarct size. Myocardial infarction progresses in a wavefront of myocardial necrosis from the subendocardium to the subepicardium. We tested two hypotheses: First, HT-LVH accelerates the wavefront of myocardial necrosis when compared with normotensive animals; and second, lowering of arterial pressure by infusing nitroprusside 1 hour after coronary artery occlusion exerts a salutary effect on infarct size. To test these hypotheses, systemic hypertension (mean aortic pressure = 141 +/- 3 mm Hg) and left ventricular hypertrophy (18% increase in left ventricular mass) were induced in dogs using a single-kidney, single-clip model. Seventeen adult mongrel dogs were used as controls. We measured mean aortic pressure, heart rate, left atrial pressure, and myocardial perfusion (microspheres) in several groups of normal and HT-LVH awake dogs. In two groups (normal and HT-LVH), 1 hour of circumflex coronary artery occlusion was followed by 4 hours of reperfusion. In two additional groups (normal and HT-LVH), 3 hours of circumflex coronary artery occlusion was followed by 90 minutes of reperfusion. In another group with HT-LVH, nitroprusside was infused to reduce mean arterial pressure to 100 mm Hg beginning 1 hour after occlusion and was continued for the duration of reperfusion period (HT-LVH + N). Infarct size was assessed using triphenyltetrazolium chloride stain and risk area was determined using postmortem barium angiography. Fifteen of 17 (88%) control animals survived coronary artery occlusion, whereas only 17 of 42 (40%) dogs with HT-LVH survived coronary occlusion (p less than 0.05). Infarct-to-risk ratios in the various layers of the left ventricular wall were determined for survivors in all groups. After 1 hour of coronary occlusion more than twice as much mid-wall and epicardium was infarcted in the HT-LVH group compared with the control group. After 3 hours of coronary occlusion significantly more endocardium, mid-wall, and epicardium was infarcted in the dogs with HT-LVH. In the nitroprusside-treated HT-LVH dogs, the infarct sizes were similar to control animals. From these data we conclude: 1) the rate of infarction is accelerated in animals with HT-LVH; 2) nitroprusside infused 1 hour after coronary artery occlusion and continued throughout the reperfusion period exerts beneficial effect on infarct size when compared with control animals; and 3) acute coronary artery occlusion in animals with HT-LVH is associated with significantly greater mortality when compared with control animals.

Animals↗
PubMed1987

Delineation of the extent of coronary atherosclerosis by high-frequency epicardial echocardiography.

Postmortem studies suggest that coronary angiography does not always accurately delineate the extent of coronary-artery disease. We examined this problem in living human hearts by performing high-frequency epicardial echocardiography at the time of cardiac surgery. The ratio of the diameter of the lumen of the coronary artery to the thickness of its wall was used to quantify the severity of coronary lesions. In 11 patients with no angiographic evidence of coronary disease anywhere in the coronary tree, the mean (+/- SEM) ratio was 5.9 +/- 0.3. In 21 patients with angiographic disease at the site evaluated by echocardiography, the mean ratio was lower (2.3 +/- 0.2, P less than 0.05), reflecting encroachment into the arterial lumen by atherosclerotic plaque. In 15 patients with arterial segments that were angiographically normal but with arterial stenoses elsewhere in the coronary tree, the mean ratio was 4.1 +/- 0.3, with marked overlap with the values in the patients who had angiographic disease at the site of the echocardiographic evaluation. These results demonstrate, in living human hearts, that diffuse coronary atherosclerosis is often present when coronary angiography reveals only discrete stenoses. This finding suggests that coronary angiography may underestimate the severity and extent of coronary disease.

Adult↗
PubMed1987

Use of ultrafast computed tomography to quantitate regional myocardial perfusion: a preliminary report.

The purpose of this study was to assess the potential for rapid acquisition computed axial tomography (Imatron C-100) to quantify regional myocardial perfusion. Myocardial and left ventricular cavity contrast clearance curves were constructed after injecting nonionic contrast (1 ml/kg over 2 to 3 seconds) into the inferior vena cava of six anesthetized, closed chest dogs (n = 14). Independent myocardial perfusion measurements were obtained by coincident injection of radiolabeled microspheres into the left atrium during control, intermediate and maximal myocardial vasodilation with adenosine (0.5 to 1.0 mg/kg per min, intravenously, respectively). At each flow state, 40 serial short-axis scans of the left ventricle were taken near end-diastole at the midpapillary muscle level. Contrast clearance curves were generated and analyzed from the left ventricular cavity and posterior papillary muscle regions after excluding contrast recirculation and minimizing partial volume effects. The area under the curve (gamma variate function) was determined for a region of interest placed within the left ventricular cavity. Characteristics of contrast clearance data from the posterior papillary muscle region that were evaluated included the peak myocardial opacification, area under the contrast clearance curve and a contrast clearance time defined by the full width/half maximal extent of the clearance curve. Myocardial perfusion (microspheres) ranged from 35 to 450 ml/100 g per min (mean 167 +/- 125). Two flow algorithms derived from characteristics of the contrast clearance curves showed a good correlation with regional myocardial flow determined by microspheres: the ratio of the peak myocardial opacification from baseline to the area under the left ventricular cavity curve (r = 0.7, p less than 0.001, SEE = 44.4 ml/min), and the ratio of the left ventricular cavity to posterior papillary muscle curve areas divided by the full width/half maximal contrast transit time in the region of the posterior papillary muscle (r = 0.82, p less than 0.001, SEE = 52.2 ml/100 g per min). The form of these two flow algorithms was derived from classical indicator dilution theory. In conclusion, indices derived from these data correlated well with regional myocardial perfusion in the posterior papillary muscle region of the dog as assessed by microspheres. This approach offers promise for the quantitation of regional myocardial perfusion and myocardial flow reserve in patients.

Algorithms↗
PubMed1987

Electrical stimulation in perifornical lateral hypothalamus decreases coronary blood flow in cats.

Based on evidence implicating the central nervous system in the regulation of coronary vascular resistance and the knowledge that the hypothalamus is a central site for integration of cardiovascular control, studies were undertaken to determine if electrical stimulation in the hypothalamus produced coronary vasoconstriction. In anesthetized cats, following beta-adrenergic receptor blockade, stimulation in perifornical lateral hypothalamus produced a transient decrease in coronary blood flow velocity (30 +/- 5%), a small pressor effect (7 +/- 2 mmHg), and an initial decrease in hindquarter blood flow velocity (51 +/- 5%). The decrease in coronary flow velocity, which had an onset latency of 1-3 s and a duration of 5-15 s, was abolished by ipsilateral stellate ganglionectomy and by intravenous and intracoronary prazosin. The coronary vasoconstriction produced by hypothalamic stimulation was not different from that produced by cardioaccelerator nerve stimulation. These results suggest that electrical stimulation of a hypothalamic site produces an alpha-adrenergic receptor-mediated decrease in coronary blood flow that is unmasked by beta-adrenergic receptor blockade, requires the integrity of ipsilateral cardiac sympathetic innervation, and mimics the coronary response to cardioaccelerator nerve stimulation.

Adrenergic beta-Antagonists↗
PubMed1987

Relative importance of hypertension after coronary occlusion in chronic hypertensive dogs with LVH.

We have shown that there was a 50% increase in infarct size and a threefold increase in the incidence of sudden death following coronary occlusion in dogs with hypertension and left ventricular hypertrophy (LVH). To further investigate this problem, we separated the effects of hypertension from those of LVH by decreasing arterial pressure either by renal anastomosis or intravenous administration of nitroprusside in dogs with chronic renal hypertension and LVH. In 123 conscious dogs, the circumflex coronary artery was acutely occluded. Hemodynamics were monitored, myocardial perfusion was measured with labeled microspheres, the risk area was defined by postmortem angiography, and infarct size was determined pathologically 48 h after occlusion. The incidence of sudden death following acute coronary occlusion decreased dramatically in dogs with LVH if the arterial pressure was decreased with either nitroprusside or renal anastomosis. In addition, if arterial pressure was decreased with nitroprusside or renal anastomosis, infarct size in dogs with LVH was not augmented. In conclusion, normotension induced by renal anastomosis or nitroprusside returned infarct size and the incidence of sudden death in dogs with chronic hypertension and LVH toward control values. Thus it is likely that hypertension, as opposed to LVH, is the critical factor responsible for the increase in infarct size and the high incidence of sudden death observed in dogs with hypertension and LVH following sudden coronary occlusion.

Animals↗
PubMed1987

Prediction of the physiologic significance of coronary arterial lesions by quantitative lesion geometry in patients with limited coronary artery disease.

Studies in animals with normal coronary arteries have shown that coronary flow reserve can be predicted by angiographic measurements of arterial stenosis. Studies in man, however, suggest that even quantitative analysis of coronary angiograms cannot predict the physiologic significance of individual coronary lesions. These studies, however, were carried out in patients with either widespread, diffuse coronary artery disease or by measurement techniques that tend to underestimate maximal coronary flow reserve. To determine the relationship between coronary arterial stenosis and coronary flow reserve (CFR) in patients with discrete limited coronary atherosclerosis, we studied 50 patients with a single discrete coronary stenosis in only one or two vessels. The minimum coronary arterial cross-sectional area (mCSA), percent area stenosis (%AS), and percent diameter stenosis in the left and right anterior oblique projections were determined by the Brown/Dodge method of quantitative coronary angiography. A No. 3F coronary Doppler catheter was placed immediately proximal to the lesion. Measurements of CFR were obtained by intracoronary administration of papaverine in doses sufficient to provide maximal arteriolar vasodilation. In 25 patients, a translesional pressure gradient was obtained with an angioplasty catheter. CFR measured in patients with coronary artery disease was compared with that in 13 patients with normal coronary vessels. In normal patients, CFR averaged 5.0 +/- 0.6 (peak/resting velocity ratio; mean +/- SEM, range 3.7 to 8.2). In patients with limited coronary artery disease, CFR was closely correlated with %AS (r = .85), mCSA (r = .79), and the translesional pressure gradient (r = .83). Additionally, the most severe percent diameter stenosis in either the left or right anterior oblique view was also highly correlated with CFR (r = .82). Importantly, all arteries with lesions producing less than 70% area stenosis and less than 50% diameter stenosis, or with greater than 2.5 mm2 mCSA had CFR of over 3.5. These results suggest that, in contrast to the poor correlation of percent area and percent diameter stenosis to CFR measured in patients with multivessel coronary artery disease, CFR measured at angiography in patients with discrete, limited coronary artery disease correlates closely with luminal stenosis determined precisely with quantitative coronary angiography. Differences in the extent of diffuse arterial narrowing may account for these discrepancies.

Blood Pressure↗
PubMed1987

The importance of the determination of the myocardial area at risk in the evaluation of the outcome of acute myocardial infarction in patients.

On the basis of animal studies, we postulated that the size of the perfusion field (risk area) of an occluded coronary artery would be an important determinant of outcome in patients with acute myocardial infarction. To test this hypothesis, we measured size of the risk area in 27 patients with acute myocardial infarction by the intracoronary injection of 99mTc-macroaggregated albumin and gated nuclear imaging. After injection of the albumin spheres (5.3 +/- 1.4 hr after the onset of chest pain) streptokinase was administered and in 16 of 27 patients (59%) effective thrombolysis was achieved. Since none of the patients had evidence of a prior acute myocardial infarction, the 3 day nuclear left ventricular ejection fraction (LVEF) was considered an index of infarct size. Response to thrombolysis was analyzed according to success or failure of reperfusion and the size of the risk area (small risk area less than 25%, large risk area greater than 25% of left ventricular surface area). Standard clinical indexes correlated poorly with size of the risk area: electrocardiographic variables (r = .37), left ventricular end-diastolic pressure (r = .23), cardiac index (r = .55), and the LVEF obtained from a right anterior oblique contrast ventriculogram (r = .31). The coronary vessel responsible for the acute myocardial infarction significantly influenced size of the risk area (left anterior descending, 38 +/- 5% [mean +/- SD] vs circumflex or right coronary artery, 17 +/- 4%). However, knowledge of the site of coronary occlusion within a vessel was not helpful in predicting the size of the area at risk.(ABSTRACT TRUNCATED AT 250 WORDS)

Female↗
PubMed1987

Methods of measurement of myocardial blood flow in patients: a critical review.

During the past decade, major progress has been made in the evolution of technology directed toward the accurate measurement of regional myocardial perfusion in patients. The deficiencies of some of the older methods (thermodilution and gas clearance) are better appreciated and improved approaches (Doppler catheters, positron-emission tomography, and digital subtraction angiography) have been developed. The new approaches should play a major role in research and for most applications the older methods will gradually be replaced. Efforts to bring these new methods to community hospitals and practicing cardiologists should be stimulated. Doppler catheters, positron-emission tomography, and digital-subtraction angiography are commercially available and Doppler catheters and digital-subtraction angiography could be easily incorporated into routine cardiac catheterization procedures. The Doppler catheter is the most inexpensive and probably the simplest to apply. In our opinion, routine measurements of coronary flow reserve will significantly improve the care of patients with coronary obstructive disease and other diseases that impair myocardial perfusion. If coronary reserve measurements are used frequently, patient selection for coronary angioplasty and bypass surgery will no longer depend entirely on visual assessment of percent diameter stenosis, a very poor criterion in many situations. Also, patients with chest pain syndromes, normal coronary vessels, and impaired coronary reserve will be identified and perhaps some effective treatment for this condition will be devised.(ABSTRACT TRUNCATED AT 250 WORDS)

Absorptiometry, Photon↗
PubMed1987

Quantitative determination of aortic regurgitant volumes in dogs by ultrafast computed tomography.

Current imaging modalities can provide only a qualitative or semiquantitative measure of the severity of aortic regurgitation. Ultrafast computed tomography (CT) has the capability of rapid imaging (17 frames/sec) coupled with high spatial resolution (1.5 mm2). Eight millimeter thick images can be acquired to interrogate simultaneously the right and left ventricles. End-diastolic and end-systolic tomograms can be reconstructed serially from apex to base by Simpson's rule to provide end-diastolic and end-systolic volumes from which the right and left ventricular stroke volumes can be derived. To determine whether the difference between left and right ventricular stroke volume measured with ultrafast CT could be used to estimate the volume of experimentally induced aortic regurgitation, we studied six dogs in which proximal aortic electromagnetic flow probes had been implanted. Varying degrees of aortic regurgitation were induced by manipulation of a basket catheter through the aortic valve. During suspended respiration in the control state in the absence of aortic regurgitation, right and left ventricular stroke volumes measured with ultrafast CT were nearly identical (mean difference 1.0 +/- 1.2 ml [mean +/- SE]). In the presence of varying degrees of aortic regurgitation, regurgitant volume derived by ultrafast CT as the difference between right and left ventricular stroke volumes correlated closely to the regurgitant volume measured by the electromagnetic flow probe (r = .99, slope = .92, y intercept = 0.98 ml, SEE = 1.02 ml, n = 16). Regurgitant fraction also correlated closely to the regurgitant fraction measured by the electromagnetic flow probe (r = .94, slope = .98, y intercept = 0.66%, SEE = 4.73%, n = 16).(ABSTRACT TRUNCATED AT 250 WORDS)

Angiography↗
PubMed1987

Dietary treatment of atherosclerosis abolishes hyperresponsiveness to serotonin: implications for vasospasm.

Diet-induced atherosclerosis in primates impairs vasodilator responses and greatly potentiates vasoconstrictor responses to serotonin. Serotonin may play an important role in the pathogenesis of vasospasm. In diet-induced regression of atherosclerosis, intimal lesions are reduced, but maximal vasodilator responses do not improve, perhaps because of vascular fibrosis. Our goal was to determine whether dietary treatment of atherosclerosis reverses the augmented vasoconstrictor responses to serotonin and thus might reduce susceptibility to vasospasm. Normal cynomolgus monkeys, atherosclerotic monkeys, and atherosclerotic monkeys that were given a normal (regression) diet for 18 months were studied. Morphometric studies indicated that the regression diet reduced lesions in the iliac and femoral artery since intimal area was reduced by about 50%. In the hind limb perfused at constant flow, residual resistance during maximal vasodilatation produced by infusion of adenosine tended to be greater in atherosclerotic monkeys than in normals and failed to improve in regression monkeys. In contrast, vasoconstrictor responses to serotonin were greatly potentiated in atherosclerotic monkeys and were restored to normal in regression monkeys. Serotonin (20 micrograms i.a.) decreased hind limb resistance (in mm Hg/ml/min) 0.34 +/- 0.06 (mean +/- SE) in normal monkeys, increased resistance 0.58 +/- 0.17 in atherosclerotic monkeys (p less than 0.05 vs. normal), and decreased resistance 0.70 +/- 0.15 in regression monkeys (p less than 0.05 vs. atherosclerotic). Thus, dietary treatment of atherosclerosis abolishes augmented vasoconstrictor responses to serotonin. It is proposed that treatment of atherosclerosis may be beneficial, even when vasodilator responses fail to improve, by reducing susceptibility to serotonin-induced vasospasm.

Animals↗
PubMed1987

Neurogenic regulation of coronary blood flow: evidence for a central nervous system pathway.

The central representation of neurogenically mediated coronary vasoconstriction produced by activation of the sympathetic nervous system was examined in anesthetized cats instrumented for continuous recording of coronary and femoral blood flows, arterial pressure, and heart rate. Electrical stimulation in a small region of perifornical lateral hypothalamus increased arterial pressure, heart rate, and coronary blood flow; following the administration of propranolol, a transient coronary vasoconstrictor response was unmasked. The response was mediated over the sympathetic nervous system since it was blocked by stellate ganglionectomy and by the alpha 1-adrenergic receptor antagonist prazosin. Projections to and from the lateral hypothalamic site were identified by using anterograde and retrograde pathway-tracing techniques. Paraventricular nucleus projected to lateral hypothalamus, which in turn made connections in periaqueductal gray with projections terminating in lateral reticular formation of medulla. Coronary vasoconstrictor responses qualitatively identical to those produced by hypothalamic stimulation were found with activation of paraventricular nucleus and lateral reticular formation. Interruption of neuronal transmission in the medullary site blocked the response produced by activation of hypothalamic site. These data demonstrate that coronary vasoconstriction mediated over the sympathetic nervous system can be elicited from an interconnected pathway that links sympathoexcitatory sites in forebrain and brainstem.

Animals↗
PubMed1987

Effects of epinephrine on coronary microvascular diameters.

This study was designed to examine the hypothesis that epinephrine has nonuniform effects on coronary microvascular diameters. Measurements of coronary microvascular diameter were completed in anesthetized, open-chest cat preparations in which the epicardial microcirculation was viewed through an intravital microscope using stroboscopic epi-illumination. Images of coronary microvessels were digitized and analyzed on a video monitor. With arterial pressure controlled, measurements in the absence and presence of beta-adrenergic blockade (propranolol 1 mg/kg) were obtained during epinephrine infusion (1-2 micrograms/kg/min). In the absence of beta-adrenergic blockade, epinephrine produced a 25% increase in myocardial perfusion. Under these conditions, coronary vasodilation was observed in all classes of coronary arterial and arteriolar vessels. In the presence of beta-adrenergic blockade, epinephrine produced a significant decrease in myocardial perfusion (-20%). Nonuniform effects on diameter were observed in arterial and venous segments of the coronary circulation. These data are consistent with the view that in the absence of beta-adrenergic blockade, the functional coronary hyperemia associated with epinephrine administration is produced by uniform coronary arterial and arteriolar dilation. In the presence of beta-adrenergic blockade, with metabolic effects controlled, epinephrine produced a decrease in myocardial perfusion, which is related to a nonuniform decrease in coronary microvascular diameters. Such heterogeneous effects on microvascular diameters result in a redistribution of coronary microvascular resistance.

Animals↗
PubMed1987

Alterations of vascular reactivity in atherosclerosis.

We have previously found that vascular relaxation to acetylcholine and thrombin is markedly impaired in vessels from monkeys with diet-induced atherosclerosis. In the present study, we found that both normal and atherosclerotic vessels relaxed completely to the calcium ionophore A23187, which stimulates release of the endothelium-derived relaxing factor by nonreceptor-mediated mechanisms. Atherosclerotic vessels, however, were less sensitive to this agent. The finding that responses to the calcium ionophore were impaired in atherosclerosis suggests that abnormal endothelium-dependent relaxation in atherosclerotic vessels is not related entirely to alterations of thrombin and muscarinic receptors but may also be due to abnormal endothelium-derived relaxing factor production or transfer from the endothelium to the underlying vascular smooth muscle. Neither normal nor atherosclerotic iliac arteries constricted in response to acetylcholine when studied in the nonpreconstricted state. Constriction to acetylcholine in these vessels was not unmasked by removal of the endothelium. Thus, the smooth muscle of iliac vessels from monkeys contains few functioning muscarinic receptors. Impaired relaxation of atherosclerotic vessels to acetylcholine is not due to enhanced muscarinic-mediated constriction or to production of an endothelium-derived constricting factor. In vivo studies were performed to determine if alpha-adrenergic coronary vascular constriction is enhanced in the presence of atherosclerosis. In anesthetized monkeys, myocardial oxygen consumption was increased by two mechanisms, aortic occlusion and phenylephrine infusion. During both aortic occlusion and phenylephrine infusion, decreases in coronary vascular resistance were similar in control and atherosclerotic monkeys.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗