Total Coronary Resistance Research Articles

Changes in coronary and collateral flows and adequacy of perfusion in the dog following one and three months of circumflex occlusion.

We investigated changes in circumflex, left anterior descending (LAD), and right coronary artery flows as well as changes in collateral flows to these vessels after long-term circumflex occlusion. Coronary and collateral flows of each vessel were determined simultaneously in an isolated heart preparation in which the vasculature was maximally dilated with dipyridamole. The resistances as related to total heart weight of the circumflex, LAD, and right coronary arteries of 16 control dogs were found to be 0.59 +/- 0.06, 0.93 +/- 0.09, and 2.37 +/- 0.17 (mean +/- SEM) mm Hg/[(ml/min)/100 g], respectively. Total minimal coronary resistance was 0.21 +/- 0.01. In 10 dogs subjected to occlusion for 1 month no significant change in circumflex coronary resistance was observed, but the resistance of the unimpaired vessels decreased significantly. The resistances of the LAD and right coronary arteries were 0.66 +/-0.04 and 1.72 +/- 0.13, respectively. Both values were considerably less (P less than 0.01) than control. In nine dogs subjected to occlusion for 3 months the resistance of the unimpaired LAD and right arteries, as well as the circumflex coronary resitance, were not significantly different from control. We also found that retrograde flows for all vessels increased 7-fold after 1 month and 10.5-fold (relative to control) after 3 months of occlusion. From these data we conclude that vascular adaptations, which occurred in response to an ischemic stimulus, are responsible for the long-term regulation of the metabolic needs of the myocardium.

The active and passive components of extravascular coronary resistance.

Intramyocardial stresses compress the coronary arteries raising their resistance to flow. The present study measures the relative contribution of ventricular pressure and the contractile state of the myocardium to this extravascular component of the coronary resistance. The extravascular resistance, which was found to be as much as one third of the total coronary resistance at normal ventricular and perfusion pressures, consists of two components. The major component, which persists when myocardial tension development is prevented, is attributed to passive stresses which are in equilibrium with the ventricular pressure. It accounts for 75% of the extravascular resistance. The remaining 25% is due to a modification of these passive stresses by active contraction of the myocardium. Massive increases in contractility resulted in only an additional 19% increase in the extravascular resistance. It is concluded that changes in contractility per se have only a slight effect on the amount of compression experienced by the coronary arteries and that ventricular pressure is the major determinant of the extravascular resistance.

Effects of intracoronary temperature variation on the coronary circulation

The effects of temperature on coronary pressure-flow relationships were studied in intact dogs using a controlled perfusion technique. Temperature variation did not affect left ventricular performance or total coronary resistance but did significantly alter vasomotor tone in the subepicardial vessels as estimated from the responses of post-occlusive reactive hyperaemia. Vasodilation was noted with heating while vasoconstriction occurred with cooling. Metabolic suppression with practolol did not modify these results.

The effects of dopamine on cardiogenic and endotoxin experimental shock.

Studies on dogs show that dopamine improves cardiac performance and increases renal and mesenteric flow. This paper investigates the cardiovascular effects of dopamine on narcotized dogs. 0.2 ml. of mercury was administered into the circumflex branch of the left coronary artery of 2 groups of anesthetized dogs to induce myocardial infarction. 1-3 mg/lg of Eschrichia coli endotoxin was injected in 2 other groups of dogs to induce endotoxin shock. Dopamine was administered intravenousely in one group with cardiogenic shock and in the other group with endotoxin shock; noradrenaline was administered in the other 2 groups. Coronary resistances increased after induction of shock and declined towards normal after dopamine was injected. The effect of dopamine on mesenteric and renal resistance was not signficant. Noradrenaline's effect on cardiac performance was similar to that of dopamine, although unlike dopamine, it contributed to a significant increase of total peripheral, coronary, mesenteric, renal and femoral resistances. The effects of dopamine on the dog's hemodynamics were less evident in endotoxin than in cardiogenic shock on account of the fact that in endotoxin shock, circulatory blood volume declines to a higher extent than in cardiogenic shock, and greater blood alterations develop, mainly acidosis. In such conditions, dopamine alone will not help the hemodynamic parameters return to normal levels. Lotto et al. reports that in shocked humans with serious metabolic acidosis, dopamine is effective only when bicarbonate solutions are infused to adjust blood PH.

Coronary sinus outflow and O2 content in anterior cardiac vein blood at different levels of right ventricle performance.

Previous investigations have demonstrated that 60–70% of myocardial venous blood returns from the coronary sinus and that this percentage increases by experimentally raising right ventricle systolic pressure. The experiments described were performed in anesthetized open chest dogs and showed that the increase in coronary sinus outflow is not due to a change in the distribution of venous blood between the coronary sinus and the deep venous system, but is secondary to the increased left coronary artery inflow. A possible explanation of this might be that the increase in intramyocardial right ventricular pressure brings about some release of certain catecholamines which may induce a persisting increase in coronary artery inflow. Beta-blockade can in effect prevent any change in coronary blood flow arising from overdistension of the right ventricle. The O2 content of the coronary sinus blood (returning mainly from the left ventricle) is constantly lower than that of the anterior cardiac and Thebesius veins (flowing mainly out of the right ventricle). This difference is very probably the result of mechanical factors which play an active role in regulating coronary flow. As is well known, total coronary resistances are the sum of two components i.e., a) extravascular compression during ventricular systole and b) active vasomotor tone in the coronary bed. Vasomotility in the right and left coronary arteries is virtually identical, whereas myocardial compression is considerably lower in the right side of the heart than in the left. Right coronary flow is therefore less impaired than the flow in the left coronary artery; the ratio between coronary flow and O2 myocardial extraction should thus be better in the right than in the left ventricle.

Effects of protoveratrine on coronary blood flow of the renal hypertensive dog.

In renal hypertension, protoveratrine decreased coronary blood flow, cardiac oxygen consumption, arterial and venous oxygen saturation, coronary arteriovenous oxygen difference, mean arterial blood pressure, cardiac output, cardiac work, cardiac efficiency, cardiac rate, total peripheral resistance, coronary resistance, respiratory rate, and minute volume. The decrease was significant in all functions except coronary blood flow, coronary venous oxygen saturation, and cardiac output. The results of these experiments indicate that in the renal hypertensive animal, a therapeutically beneficial effect was derived from protoveratrine on the circulation by its ability to decrease the work of the heart (lowering the elevated mean arterial pressure) and the coronary vascular resistance while maintaining coronary blood flow and cardiac output within normal levels. The less advantageous effect of protoveratrine on circulation resulted from its respiratory inhibiting effect which reduced the arterial blood oxygen saturation. Although a small decline in coronary venous oxygen saturation was noted, the coronary flow and oxygen delivery in face of the reduced arterial oxygen saturation was apparently adequate to maintain a normal cardiac activity.

Effect of heart rate and intracoronary isoproterenol, levarterenol, and epinephrine on coronary flow and resistance.

The effect was determined of changes in heart rate and of intracoronary isoproterenol, levarterenol, and epinephrine on coronary flow in the stopped and beating heart. It was possible by this means to estimate the relative action of these variables on the extravascular and intravascular resistance of the coronary bed in a heart perfused at constant pressure. As heart rate was increased extravascular resistance rose, but intravascular resistance fell to a greater extent indicating a fall in net coronary resistance. Isoproterenol had the greatest and epinephrine the least effect in decreasing the total coronary resistance. The three drugs tested caused only a small fall in extravascular resistance. Since the effect was small, it was concluded that extravascular resistance can be ignored in determining the direct effect of these drugs upon the coronary vasculature.