Reintroduction of Ca(2+)or modification of internal Ca(2+)stores by caffeine results in widespread irreversible injury. The adult golden hamster, however, is immune to such insult and the present report investigates the phenomenon. Isolated Langendorff perfused hamster and rat heart were subjected to 15 min Ca(2+)-free perfusion followed by 30 min of Ca(2+)perfusion at 37 degrees C. Caffeine was introduced during Ca(2+)-free perfusion in a number of experiments. Papillary muscles were processed for the ultra-structural study. The hamster heart did not exhibit the calcium paradox state whereas rat heart did. Hamster heart treated with caffeine either throughout or 5 min after starting Ca(2+)-free perfusion showed 70%+/-8 or 65%+/-8. 42 recovery, respectively, when Ca(2+)reperfusion was performed. Ultrastructure of muscle from both groups showed relaxed myocytes with slight disorientation of the sarcomere register. This disorientation was not seen in hamster hearts undergoing the conventional calcium paradox protocol. The hamster cardiac muscle is remarkably tolerant to [Ca(2+)]()i loading either induced by Ca(2+)reperfusion or caffeine-induced sarcoplasmic reticulum Ca(2+)release. Structural and functional characterization of Ca(2+)depletion and repletion in the hamster heart have been discussed.
Copyright 2000 Academic Press.