The effect of normothermic anoxic arrest and ventricular fibrillation on the coronary blood flow distribution of the pig.
Normothermic anoxic arrest of 15 and 30 minutes, repeated for up to a total of 90 minutes of anoxia was employed in 24 pigs. The purpose was to determine the effect of varying the duration of anoxia on coronary blood flow, coronary vascular resistance, and the distribution of coronary flow to the free wall of the ventricle. Five minutes of reperfusion at pressures of 50 and 100 mm. Hg with the ventricle fibrillating, was employed between each anoxic interval. Results were compared to control studies performed during ventricular fibrillation without anoxic arrest in 12 pigs. Prolonging the anoxic interval to 30 minutes served to create a maldistribution of coronary flow away from the left ventricular endocardium and to reduce the reactive hypermic response to anoxia. Increasing the perfusion pressure to 100mm. Hg accentuated these changes. Both light and electron microscopy of sections demonstrated edema and early myocardial necrosis in the subendocardial layer of the left ventricle subjected to repeated 30 minute intervals of anoxia at a high perfusion pressure. We postulate that repeated anoxic insults with inadequate repayment of oxygen debt results in subendocardial edema, a decrease in perfusion, increasing necrosis, and further edema. A myocardial infarction must result if this vicious cycle cannot be interrupted.
D000818:Animals; D001794:Blood Pressure; D001831:Body Temperature; D002315:Cardiopulmonary Bypass; D003326:Coronary Circulation; D003331:Coronary Vessels / Q000503:physiopathology; D004195:Disease Models, Animal; D004489:Edema, Cardiac / Q000473:pathology; D006323:Heart Arrest / Q000473:pathology / Q000503:physiopathology*; D000860:Hypoxia / Q000473:pathology / Q000503:physiopathology*; D008931:Mitochondria, Muscle / Q000648:ultrastructure; D009206:Myocardium / Q000648:ultrastructure; D009210:Myofibrils / Q000648:ultrastructure; D010477:Perfusion; D013552:Swine; D013997:Time Factors; D014655:Vascular Resistance; D014693:Ventricular Fibrillation / Q000473:pathology / Q000503:physiopathology*