Pathophysiology of Acute Myocardial Infarction in Conscious Dogs

Abstract

Experimental models of acute myocardial infarction (1–5) have usually involved anesthesia in the open- and closed-chest dog, and had several limitations, including: (1) hemodynamics could be monitored continuously only for a limited time, under anesthesia and usually thoracotomy; (2) animal mortality was very high and early; and (3) ventricular arrhythmias occurred early with potassium egress from the damaged myocardium. To avoid these limitations, several investigators devised models of acute myocardial infarction in un- anesthetized animals (6–8). In the model devised by Khouri et al (6), coronary insufficiency was induced by gradually reducing circumflex coronary flow to zero over several days. However, the gradual reduction in flow permitted the coronary vascular bed, including collaterals, and the myocardium to make compensatory changes, so that when occlusion was complete, minimal infarction frequently results (6, 9). Hood, et al (7) used a similar unanesthetized dog model and gradually occluded the anterior descending coronary artery. Since their study produced a higher frequency of large infarcts, the rate of occlusion was probably faster. Another disadvantage of this preparation was the lack of coronary blood flow monitoring, so that the precise onset of occlusion was not known.