SUMMARY The applicability of classic fluid dynamic equations to tapering stenoses in vasoactive, flexible coronary arteries in vivo and the validity of quantitative coronary arteriography was tested by comparing experimentally measured and x-ray-predicted pressure gradients at equal flows for left circumflex stenoses in five dogs chronically instrumented with a balloon. occluder, flow probe, and proximal and distal catheters for.injection of contrast media or recording distal coronary pressure. Arterial borders on cut-film orthogonal arteriograms were digitized and computer processed into a three-dimensional reconstruction of the stenosis. The total pressure gradient was calculated from stenosis dimensions using classic fluid dynamic equations. Over the full range of flow, the correlation of x-ray-predicted and experimentally measured pressure gradient for 51 separate stenoses was y = 1. Five male field hounds that weighed 22-28 kg were anesthetized with i. v. sodium thiopental and a mixture of nitrous oxide and methoxyfluorane. The left circumflex coronary artery was dissected free through a sterile left thoracotomy. A small, tapered, Tygon catheter was implanted at the origin of the left circumflex artery for injection of contrast medium in order to obtain coronary arteriograms and to measure proximal coronary perfusion pressure. A Doppler flow velocity transducer was placed around the left circumflex coronary artery distal to the proximal coronary catheter tip.Two millimeters distal to the Doppler transducer, a saline-filled circumferential balloon constrictor was sutured in place. A

SUMMARY Recent studies from this laboratory have indicated that sympathetic a-receptor-mediated coronary vasoconstriction can compete with local metabolic vasodilation to reduce the oxygen supply to the myocardium. In vitro studies from other laboratories on isolated coronary vessel strips suggest that large epicardial vessels are the dominant site of adrenergic a-receptor activity. In this study we used anesthetized, open-chest dogs to test the hypothesis that a-receptor-mediated vasoconstriction occurs predominantly in epicardial vessels, which are partially removed from the metabolic milieu in the myocardium. Adrenergic jS-receptor blockade was achieved by propranolol (3 mg/kg, iv). The circumflex coronary artery was pump-perfused at constant pressure to minimize passive changes in large vessel resistance. Pressure was measured at the tip of the perfusion cannula sealed in the circumflex artery, and in an apical branch of the circumflex artery. Large vessel resistance was calculated as the pressure gradient along the vessel segment divided by the coronary flow. Intracoronary injections of nitrogly cerin were used as an independent measure of the vasomotor responsiveness of the large vessel segment. Adrenergic a-receptor activation was produced by intracoronary bolus injections of norepinephrine and by electrical stimulation of the left stellate ganglion. Alpha-receptor stimulation caused an increase in total coronary vascular resistance; however, the relative increase in the resistance of the large vessel was only about 60% of that seen for the entire coronary bed. These data suggest that, contrary to the proposed hypothesis, adrenergic a-receptor-mediated vasoconstriction in the large coronary vessels is not proportionally greater than that observed in the total coronary vascular bed.DIRECT sympathetic coronary vasoconstriction is well recognized 1 " 15 and is of the a-receptor type. 45 ' 10 ' 16 Zuberbuhler and Bohr, 17 using in vitro isolated coronary vessel strips, found that adrenergic a-receptor-stimulated contractions were observed more often in strips from large (1.5-2.4 mm in diameter) than from small (0.25-0.50 mm) arteries. This finding has been confirmed in other in vitro studies. 18 " 20 Recent studies from this laboratory have indicated that sympathetic a-receptorinduced coronary vasoconstriction is capable of limiting oxygen delivery to the heart and decreasing myocardial oxygen tension, thus competing with local metabolic coronary vasodilation. 21 ' 22 These findings suggested the hypothesis that the principal site of a-receptor coronary vasoconstriction might be the large epicardial coronary vessels; since the large upstream epicardial vessels presumably are somewhat removed from the metabolic milieu surrounding small vessels within the myocardium, this hypothesis could explain sympathetic coronary vasoconstriction overriding local metabolic vasodilation. The purpose of the present study was to test the hypothesis that a-receptor vasoconstriction occurs predominantly in epicardial vessels by...

It has been suggested that vasodilation distal to a stenosis may cause a profound decrease in perfusion pressure and adversely affect regional left ventricular function. This phenomenon could explain the clinical concept of reversal of regional dysfunction by coronary revascularization. To evaluate the hypothesis that regional myocardial function parallels regional coronary blood pressure in the absence of changes in coronary flow, dogs chronically instrumented with left circumflex coronary artery flow probes, cuff occluders, pressure catheters and segmental function sonomicrometers were studied. By decreasing regional coronary vascular resistance with selective intracoronary dipyridamole and controlling blood flow with a proximal coronary cuff occluder, the mean left circumflex artery pressure was reduced from 83 +/- 3 to 38 +/- 2 mm Hg while circumflex coronary blood flow was maintained constant. Regional contractile function as measured by circumflex sonomicrometers was unchanged at constant circumflex subendocardial blood flow as measured by radioactive microspheres. These findings suggest that regional contractile function is dependent on subendocardial blood flow and is independent of coronary perfusion pressure.

No abstract

Depressed left ventricular function during the early part (first third) of both systole and diastole in the resting state have been reported to be sensitive indicators of coronary artery disease in patients with normal global function at rest. To evaluate the possible mechanisms of these findings, 11 dogs were chronically instrumented with segmental function sonomicrometers in the left circumflex and left anterior descending coronary artery distribution, circumflex coronary flow probes and cuff occluders, aortic flow probes and ventricular pressure transducers. Percent segmental function during the first third of systole and diastole was measured in the control state and with graded circumflex artery flow reductions. Significant decreases in early systolic function with ischemia in the circumflex artery distribution were partially offset by compensatory augmented shortening in the left anterior descending artery distribution. With ischemia in the circumflex distribution, there was prolonged contraction into diastole manifested as impaired relaxation. Simultaneously, in the left anterior descending artery distribution, there was minimal compensatory enhanced relaxation. These results suggest that early systolic dysfunction in ischemic segments may be offset by enhanced function in nonischemic segments, rendering minimal, if any, change in global systolic function. Early diastolic dysfunction in ischemic segments exceeds compensatory changes in nonischemic areas by two-to-four-fold. Hence, early diastolic functional indexes may be more sensitive indicators of ischemia at rest than early systolic functional indexes.