Reperfusion of the ischaemic myocardium: the role of calcium and perfusion pressure.
1. Our experimental findings do not support the hypothesis that myocardial injury during post-ischaemic reperfusion is caused by a sudden calcium inflow into cardiac cells. This follows from these facts: a) omission of calcium from the reperfusion medium does not prevent, only delays, injury during reperfusion unless the medium has been employed also before and during ischaemia. b) increased calcium concentration in the reperfusion medium does not enhance reperfusion injury unless this increased concentration has been achieved also before and during ischaemia. 2. Manifestation or increase of ischaemic injury during reperfusion can be prevented only with difficulty. One of the important factors which can accelerate or increase reperfusion injury, is perfusion pressure and/or coronary flow rate. The mechanism of this effect is not well understood. Judging by the rate at which it unfolds, one can assume involvement of some physical processes such as explosive cellular expansion, wall "stress", etc.
D000818:Animals; D002118:Calcium / Q000502:physiology*; D003326:Coronary Circulation; D003327:Coronary Disease / Q000201:enzymology / Q000503:physiopathology*; D066298:In Vitro Techniques; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D009206:Myocardium / Q000201:enzymology; D010477:Perfusion; D011312:Pressure; D051381:Rats
D007770:L-Lactate Dehydrogenase; D002118:Calcium