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.
The effect of increased coronary flow on transmural ventricular repolarization was investigated in six pentobabital-anesthetized sheep. Fresh blood at 10 ml/min was injected into the left circumflex coronary artery (LCX) in addition to the normal coronary flow. Unipolar electrocardiograms were simultaneously registered from epicardium, mid-myocardium and endocardium with fine plunge needles. Activation-recovery interval (ARI) was measured from the unipolar electrocardiograms and was used for estimating the ventricular repolarization duration. It was found that intracoronary blood injection (n=3) prolonged ARI in the epicardium, mid-myocardium and endocardium by an average of 34 ± 16, 28 ± 18 and 25 ± 13 ms, respectively (p<0.01). Pretreatment with nitro-L-arginine (n=3), a nitric synthase inhibitor, diminished the flow-induced ARI prolongation across the ventricular wall. In conclusion, an increase in coronary flow lengthens the duration of transmural ventricular repolarization. These effects appear to be mediated by nitric oxide from the coronary endothelium., Y.-Z. Zhang, B. He, L.-X. Wang., and Obsahuje bibliografii a bibliografické odkazy