Circulation, Vol 64, 796-807, Copyright © 1981 by American Heart Association
W Flameng, W Daenen, M Borgers, F Thone, R Xhonneux, A van de Water and H van Belle
The cardioprotective effects of lidoflazine, a drug with calcium
homeostatic properties, were investigated in dogs subjected to 1 hour of
normothermic global ischemia, followed by reperfusion. None of the eight
control dogs could be weaned from the extracorporeal bypass, confirming the
severity of the ischemic model. All eight acutely pretreated dogs showed
rapid recovery from the prolonged ischemic arrest and could support their
own circulation. Recovery of preischemic values was 95% for systolic aortic
pressure, 71% for diastolic aortic pressure, 99% for left ventricular dP/dt
max and 80% for cardiac output. Light and electron microscopy and calcium
cytochemistry were performed on left ventricular biopsies taken before,
during and after ischemic arrest. In the control dogs, loss of structural
integrity of the sarcolemma and mitochondria was prominent at the end of
the ischemic period. Intracellular edema, hypercontraction of sarcomeres
and great accumulation of calcium in severely damaged mitochondria occurred
after 5 and 30 minutes of reperfusion. In the lidoflazine- treated dogs,
such lesions were largely prevented during the ischemic period and
completely reversed after reperfusion. These observations suggest that the
tolerance of ischemia is markedly augmented by lidoflazine.
ARTICLES
Cardioprotective effects of lidoflazine during 1-hour normothermic global ischemia
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