Impairment of mitochondrial respiratory activity of non-infarcted myocardium under severe pump failure in acute myocardial infarction.

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Abstract
We studied alterations in respiratory activity of mitochondria (Mt) in non-infarcted myocardium (NIZ) under severe pump failure complicated by acute myocardial infarction (AMI). Dogs in which AMI was induced were divided into two groups; one in which left ventricular systolic pressure (LVPs) was maintained higher than 70% of preligation level (ND group); and one in which LVPs was diminished to less than 70% (D group). Regional myocardial blood flow (MBF) in NIZ reduced significantly in proportion to decreases in LVPs and cardiac output (CO). State -III activity and RCR decreased in proportion to reductions in MBF, LVPs, and CO in Mt from NIZ of D group. Complex-I and DNP-stimulated ATPase activities were also reduced in NIZ of D group. Morphologic studies revealed slight swelling and fusion of mitochondria in NIZ cells of D group, but no changes such as the appearance of a dense deposit indicating ischemic damage were seen. Pump failure in AMI is likely to be caused partly by impaired function of Mt in NIZ induced by hypoperfusion. Improvement of metabolic impairment in NIZ is important in the treatment of pump failure.

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