Compression of the coronary arteries by the fibrillating canine heart.
We performed experiments to test whether the subendocardial ischemia which reportedly accompanies elective ventricular fibrillation (VF) during cardiopulmonary bypass might be the result of mechanical compression of the coronary vessels. The left coronary artery of the open-chest, anesthetized dog was cannulated and perfused with arterial blood through an extracorporeal circuit. Coronary inflow rate was held constant with a pump and the coronary vessels were dilated maximally by infusing adenosine. Any change in perfusion pressure or the transmural distribution of flow in these hearts would have been due to changes in compression. When the hearts were stopped in diastole by vagal stimulation, infusion of microspheres 15 mum in diameter revealed a subendocardial to subepicardial (inner to outer) flow ratio (I/O) of 1.2. When the same hearts were caused to fibrillate spontaneously (not electrically maintained) the I/O fell to 0.9. Little change in coronary perfusion pressure occurred between arrest and VF. When the contractile activity during VF was attenuated by intracoronary sodium pentobarbital (120 mg) the I/O rose toward that seen during arrest. However, augmentation of muscle activity by infusion of isoproterenol during VF failed to change the I/O. Finally the I/O fell in proportion to the degree of distention in the fibrillating ventricle. The results that we observed indicate that muscular contraction during VF preferentially inhibits subendocardial flow through vascular compression.
D000241:Adenosine / Q000494:pharmacology; D000818:Animals; D003326:Coronary Circulation; D003331:Coronary Vessels / Q000503:physiopathology*; D004285:Dogs; D005260:Female; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects; D010424:Pentobarbital / Q000494:pharmacology; D010477:Perfusion / Q000379:methods; D014693:Ventricular Fibrillation / Q000503:physiopathology*
D010424:Pentobarbital; D000241:Adenosine