Extension of myocardial necrosis into normal epicardium following hypotension during experimental coronary occlusion

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Abstract
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 anaesthetised dogs, the chest was closed, and the dogs allowed to recover. Thirty minutes following coronary occlusion, seven dogs were haemorrhaged to a mean arterial pressure of 8.2 ± 0.3 kPa (62±2 mmHg) and maintained at this pressure; no intervention was undertaken in control dogs. Twenty-four hours 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 (Pvs 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 haemorrhage fell by an equal proportion, 61.9 ± 3.3% in normal tissue and 61.2 ± 2.4% in ischaemic zones. In conclusion, hypotension caused infarct extension into the epicardium, ie, into tissue that does not become necrotic under control conditions.