Harden W R, Barlow C H, Simson M B, Harken A H
Adv Shock Res. 1980;3:239-50.
The etiology of myocardial damage in shock is multifactorial. Poor perfusion of the coronary bed during shock may result in areas of cellular anoxia. This study examines the response of isolated perfused rabbit hearts to low-flow ischemia utilizing a high resolution assay of ischemia, NADH fluorescence photography. The hearts were made ischemic by reducing coronary perfusion pressure to 50% for 60 seconds. Islands of ischemic anoxia appear over the surface of the ventricle. The intensity of the ischemic response increased with successive ischemic insults (P less than 0.01). The number of anoxic islands can be reduced by pretreatment with papaverine (P less than 0.01). Anoxic islands are stable up to 20 minutes of ischemic time and are not stained by fluorescein angiography. The data suggest that an intrinsic inequality exists in the perfusion of the coronary microcirculation during low-flow ischemia.