Myocardial recovery from global ischemia and reperfusion: effects of pre- and/or post-ischemic perfusion with low-Ca2

The effects of brief (5 min) pre- and/or post-ischemic treatment with low-Ca2+ (10(-4)M) on cardiac mechanical performance during and after increasing periods of total global ischemia were investigated on isolated perfused rat heart. Mechanical parameters studied were changes in diastolic resting le...

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Veröffentlicht in:Journal of molecular and cellular cardiology 1983-06, Vol.15 (6), p.383-392
Hauptverfasser: Koomen, J M, Schevers, J A, Noordhoek, J
Format: Artikel
Sprache:eng
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Zusammenfassung:The effects of brief (5 min) pre- and/or post-ischemic treatment with low-Ca2+ (10(-4)M) on cardiac mechanical performance during and after increasing periods of total global ischemia were investigated on isolated perfused rat heart. Mechanical parameters studied were changes in diastolic resting length (delta DRL), ventricular contraction amplitude, its first derivative dL/dtmax, and cardiac responsiveness to variations in extracellular Ca2+. The results demonstrate that pre-ischemic low-Ca2+ may completely prevent: (a) the development of myocardial contracture during 45 min ischemia, (b) the occurrence of post-ischemic contracture and (c) a loss in myocardial contractile activity after 30 min of total ischemia. Post-ischemia low-Ca2+ was clearly less effective in protecting the heart against ischemia-induced loss in contractile function and offered no additional benefit when combined with pre-ischemic low-Ca2+. Post-ischemic mechanical recovery appeared to correlate letter with (end-)reperfusion-contracture than with (end-)ischemic contracture. Cardiac responsiveness to perfusate-Ca2+ decreased with increasing duration of the ischemic period (greater than 30 min), but was not significantly altered by the low-Ca2+-treatments. It was concluded from the results that the protective effect of a pre-ischemic low-Ca2+ treatment is superior to that of a similar post-ischemic treatment. The mechanism of protection and the role of Ca2+ in the ischemic process are discussed in terms of changes in the availability of intracellular free-Ca2+.
ISSN:0022-2828
DOI:10.1016/0022-2828(83)90322-X