| Autor: |
Tanaka, Masaru, Earnhardt, Richard C, Murry, Charles E, Richard, Vincent J, Jennings, Robert B, Reimer, Keith A |
| Zdroj: |
Cardiovascular Research; Jan1991, Vol. 25 Issue 1, p7-16, 10p |
| Abstrakt: |
Study objective – Although timely reperfusion limits myocardial infarct size, it has been postulated that reperfusion itself may lull some myocytes which were alive at the end of an episode of ischaemia (lethal reperfusion injury). The aim of this study was to test the hypothesis that ischaemic catabolites may “prime” myocardium for such injury and that preliminary hypoxic washout of such catabolites, prior to arterial reperfusion, would limit myocardial infarct size.Design – Dogs underwent a 40 min occlusion of the left circumflex coronary artery, followed by 4 d reperfusion. In a treated group, a 5 min episode of coronary artery perfusion with hypoxic buffer was instituted at the end of this ischaemic episode, before blood reperfusion was restored. Control dogs received a similar volume of hypoxic buffer intravenously. Systemic fluid overload was attenuated by haemofiltration. The effect of this preliminary hypoxic washout on myocardial infarct size was assessed.Experimental material – 18 anaesthetised, open chest dogs were used. After the acute study they recovered from surgery for 4 d and were then killed for further study.Measurements and main results – Infarct size, determined by microscopic evaluation, was not significantly different in the two groups, at (control) 31.3 (SEM 6.2)% v (hypoxic reperfusion) 25.8(3.9)% of the vascular area at risk. In control dogs, infarct size was inversely related to the amount of collateral blood flow (measured using microspheres); hypoxic reperfusion did not shift this relation (analysis of covariance, F = 0.236, NS).Conclusions – The washout of ischaemic catabolites by hypoxic perfusate prior to reoxygenation did not limit infarct size. [ABSTRACT FROM PUBLISHER] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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