Blood flow in the left coronary artery is lower in the systole than in the diastole. This difference is attenuated in the presence of severe stenosis, which affects the flow more during the diastole than during the systole. Some explanations have been suggested: epicardial vasodilatation distal to the stenosis, a decrease in myocardial contractility and impairment of the intramyocardial pump effect. The present investigation in anaesthetized dogs showed that, in the presence of severe stenosis, the attenuation of the diastolic-systolic coronary flow differences occurs together with distal vasodilatation in the epicardial layers of the myocardium. This attenuation may be even greater if further vasodilatation is induced by increasing the heart rate. Mo evidence of reduced myocardial contractility was observed. In addition, it was found that the onset of the systolic rise of the coronary blood pressure below the stenosis occurs before that of the aortic blood pressure. This finding may serves as evidence for the role played by the intramyocardial pump mechanism in causing the systolic reduction of coronary flow. Since this mechanism is believed to propel some blood back into the aorta during the systole, the impairment of this retrograde flow caused by the stenosis could also account for the reduction of the diastolic-systolic flow differences.
In isolated rat hearts which can or cannot utilize fatty acids (FA) as substrates the coronary responses to an increase in flow were studied under three different conditions: a) control, during perfusion with glucose-enriched Tyrode solution which allowed the hearts to utilize long-chain FA from the endogenous pool, b) during forced utilization of glucose obtained with oxfenicine, an inhibitor of long-chain FA oxidation, and c) during restored utilization of FA obtained with the addition of hexanoic acid which bypasses the blockade induced by oxfenicine. A step increase in coronary flow (50 %) induced an increase in coronary perfusion pressure whose initial slope (first 60-80 s) was similar in all the conditions of buffer perfusion, thereafter the pressure tended to further increase under control conditions (buffer a), but to decrease during oxfenicine (buffer b). The addition of hexanoic acid to the perfusion solution (buffer c) abolished the effect of oxfenicine. Steady-state conditions were reached after four minutes of increased flow, when perfusion pressure increased by about 70 and 65 % under control conditions and during hexanoate, respectively, but only by 45 % during oxfenicine. In isolated rat hearts during inhibition of FA utilization, an increase in flow elicited a reduced increase in perfusion pressure that resulted in delayed coronary dilation. It follows that the resulting shear stress is substrate-sensitive.