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Extension of myo cardial necrosis into normal epi cardium following hypotension during experimental coronary occlusion


, : Extension of myo cardial necrosis into normal epi cardium following hypotension during experimental coronary occlusion. Cardiovascular Research 16(8): 423-427

In an effort to determine the manner in which hypotension following experimental coronary occlusion affects myocardial infarct size, the left anterior descending coronary artery was occluded in 22 barbiturate-anesthetized dogs, the chest was closed and the dogs allowed to recover. Thirty minutes following coronary occlusion, 7 dogs were hemorrhaged to a mean arterial pressure of 8.2 .+-. 0.3 kPa [kilopascal](62 .+-. 2 mm Hg) and maintained at this pressure; no intervention was undertaken in control dogs. At 24 h after coronary occlusion infarct size in control and hypotensive animals was determined. The hypotensive group developed larger percentages of necrosis of the left ventricles distal to the site of occlusion than did the control dogs (37.8 .+-. 2.3 vs. 30.4 .+-. 1.4 (P < 0.01)). Although the percentage of infarcted endocardium did not change significantly, the infarction of epicardium was 45% larger in the hypotensive group (34.4 .+-. 3.3 vs. 23.7 .+-. 1.9%, P < 0.01). Regional myocardial blood flow (RMBF) was determined by means of radioactive microspheres in 5 dogs following coronary occlusion before and after hypotension. RMBF following hemorrhage fell by an equal proportion, 61.9 .+-. 3.3% in normal tissue and 61.2 .+-. 2.4% in ischemic zones. Hypotension apparently caused infarct extension into the epicardium, i.e., into tissue that does not become necrotic under control conditions.

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