Examinations of plastic function changes in myocardial cells (MC) from 36 patients with chronic ischemic heart disease were carried out before, during and soon after cardioplegic ischemia. The initial mean number of silver grains in nucleoli varied greatly showing some difference between groups of the patients with (9.5 +/- 0.48) or without (11.0 +/- 0.5) myocardial infarction. During the myocardial arrest this index of MC plastic activity was decreased in all but 7 patients. In contrast to this, it was elevated in most patients tested during subsequent reperfusion. On the basis of these data and parallel histochemical photometric assessment of DNA, RNA and succinate dehydrogenase activity, a hypothesis was suggested which explains the non-standard elevation of ribosomal cistron activity during both myocardial arrest and reperfusion by their compensatory reaction to myocardial injury.
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