Influence of tachycardia on regional myocardial flow in chronic experimental coronary occlusion

The influences of tachycardia on regional myocardial flow was studied in normal dogs and in dogs with chronic coronary artery occlusions. Coronary vasodilation was induced by coronary occlusion and subsequent release, i.e. by reactive hyperemia. Local myocardial blood flow was determined with the tr...

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Bibliographic Details
Published in:Basic research in cardiology 1976-05, Vol.71 (3), p.243-251
Main Authors: Pasyk, S, Flameng, W, Wüsten, B, Schaper, W
Format: Article
Language:English
Subjects:
Animals
Chronic Disease
Coronary Circulation
Coronary Disease - physiopathology
Dogs
Heart Ventricles
Oxygen Consumption
Tachycardia - physiopathology
Time Factors
Vascular Resistance
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Summary:The influences of tachycardia on regional myocardial flow was studied in normal dogs and in dogs with chronic coronary artery occlusions. Coronary vasodilation was induced by coronary occlusion and subsequent release, i.e. by reactive hyperemia. Local myocardial blood flow was determined with the tracer microspheres technique. In normal hearts atrial pacing produced a slight but significant increase in coronary resistance in the subendocardial layers of the left ventricle. The coronary resistance of the subepicardium remained unaffected. In the right ventricle atrial pacing had no influence on the resistance to flow. In hearts with multiple coronary occlusions tachycardia-induced changes of coronary resistance were more pronounced. In the collateral dependent subendocardium coronary resistance increased from 0.4-2.2 resistance units when the heart rate was raised to 200 beats/min. Perfusion of the right ventricular myocardium became also rate-dependent when the right coronary artery was chronically occluded. We conclude that regional perfusion dependes upon the relationship between the effective perfusion pressure, which is reduced in chronic coronary occlusion, and the integral of effective tissue pressure, which is increased with tachycardia. The results cannot be explained by assuming excessive O2-demand but rather by a rate-induced lowered O2-supply.
ISSN:0300-8428
DOI:10.1007/BF01906449