Calcium gain during postischemic reperfusion. The effect of 2,4-dinitrophenol.
Reperfusing hearts after an ischemic episode can result in cellular Ca2+ overload. This is accompanied by the formation of contraction bands, loss of sarcolemmal integrity, and mitochondrial disruption. The present study investigated the effect of uncoupling oxidative phosphorylation with 2,4-dinitrophenol (DNP) during reperfusion after 30 or 60 minutes of ischemia on this reperfusion-induced Ca2+ gain. After 60 minutes' ischemia, reperfusion with 1 mM DNP delayed the accumulation of Ca2+ and increased the duration of reperfusion before sarcolemmal disruptions were evident. This suggested that once sarcolemmal integrity is lost, Ca2+ will freely enter the cells irrespective of whether the mitochondria are able to accumulate Ca2+. After 30 minutes ischemia, reperfusion for up to 30 minutes with 0.1 or 1 mM DNP attenuated the Ca2+ gain and maintained sarcolemmal integrity. Because the authors previously found that maintaining sarcolemmal integrity alone does not totally abolish Ca2+ gain, it is suggested that DNP must prevent the entry of Ca2+ that occurs via route(s) other than those created by the loss of sarcolemmal integrity.
Elz
J S
JS
Department of Medicine, University of Melbourne, Austin Hospital, Heidelberg, Victoria, Australia.
Nayler
W G
WG
D019297:2,4-Dinitrophenol; D000332:Aerobiosis; D000693:Anaerobiosis; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D003327:Coronary Disease / Q000378:metabolism* / Q000473:pathology; D004140:Dinitrophenols / Q000494:pharmacology*; D005260:Female; D006321:Heart / Q000187:drug effects; D066298:In Vitro Techniques; D007700:Kinetics; D008854:Microscopy, Electron; D009206:Myocardium / Q000378:metabolism* / Q000648:ultrastructure; D010477:Perfusion; D051381:Rats; D011919:Rats, Inbred Strains
D004140:Dinitrophenols; D019297:2,4-Dinitrophenol; D002118:Calcium