Reduced myocardial reflow and increased coronary vascular resistance following prolonged myocardial ischemia in the dog.

Abstract

Studies were performed to determine whether an alteration in coronary vascular resistance and a reduction in the reflow phenomenon occurred in the blood-perfused, heparinized canine heart after various periods of myocaridal ischemia. Regional myocardial blood flow was measured with radioactive microspheres. Proximal left anterior descending coronary artery blood flow was measured with a periarterial flow transducer. Reduced reflow to the ischemic portion of the left ventricle and increased resistance in the left anterior descending coronary artery were present after 120 minutes of myocardial ischemia. The reduction in reflow was specific to the subendocardium of the ischemic area. Saline and isosorbide dinitrate (Isordi) did not prevent the increase in coronary vascular resistance or the significant reduction in reflow to the subendocardial portion of the ischemic area. Hypertonic mannitol given so as to increase serum osmolality 40 mosmoles/kg prevented the increase in coronary vascular resistance and modified the reduction in the reflow phenomenon to the subendocardial portion of the ischemic area. Thus, both an increase in coronary vascular resistance and a significant reduction in reflow to the subendocardial portion of the ischemic area occur in the canine heart after 120 minutes of myocardial ischemia. Moreover, the increase in coronary vascular resistance can be prevented and the reduction in reflow to the subendocardial portion of the ischemic area can be modified by the administration of hypertonic mannitol.

Ischemia-induced alterations in myocardial (Na+ + K+)-ATPase and cardiac glycoside binding.

“…First, the decrement in in vivo glycoside binding is almost certainly related in part to reduced regional blood flow to ischemic tissue. Alterations in cardiac glycoside uptake with administration after reperfusion might still result from persistent reductions in regional flow due to the no reflow phenomenon, previously demonstrated after similar periods of experimental coronary occlusion (21,22). Second, impaired digoxin binding could result from ischemia-induced alterations in the local milieu preventing optimum binding of the glycoside.…”

The time course and characterization of myocardial hemorrhage after coronary reperfusion in the anesthetized dog.

“…The severity of the no-reflow phenomenon in myocardial tissue depends on the duration of occlusion. 28 Willerson et al 29 showed a significant decrease in reflow at 2 hours compared with reperfusion after 10 minutes of occlusion. This study indicates that the amount of early reflow is not critical in determining the severity of myocardial hemorrhage, and only small quantities are needed to create the phenomenon.…”

Neutral endopeptidase 24.11 in neutrophils modulates protective effects of natriuretic peptides against neutrophils-induced endothelial cytotoxity.

“…Myocardial ischemia/reperfusion cause coronary vascular injury as well as myocardial injury (20)(21)(22)(23)(24). Although the mechanism by which coronary vascular damage from myocardial ischemia/reperfusion occurs remains unclear, endothelial injury caused by the activated neutrophils has been shown to play an important role in this process (25)(26)(27)(28).…”