• 1 January 1978
    • journal article
    • research article
    • Vol. 92  (1) , 1-22
Abstract
Occlusion of the circumflex branch of the coronary artery of rabbit hearts for 45 min elicits structural and cytochemical changes in myocytes similar to those observed in ischemic dog myocardium, which are indicative of irreversible cell injury. When methylprednisolone is administered prior to occluding the artery, myocytes are transiently protected and many of the EM signs of irreversible damage are delayed for 15 min or more. During this period, the steroid preferentially protects mitochondria, lysosomes and sarcolemma from the ischemic changes that normally develop. Some other events, including depletion of glycogen and margination of nuclear chromatin, are only minimally influenced by the therapy, if at all. In all hearts, treated and untreated, the development of severe cell damage is closely associated with cell swelling, mitochondrial dilation with concomitant appearance of amorphous osmiophilic densities, and abnormalities in and disappearance of lysosomes, suggesting that damage to cell membranes is a central event in the progression of reversible injury to irreversible infarction and that protection of membrane integrity should be a reasonable aim in efforts to ameliorate or delay ischemic injury.