Protection of the acutely injured heart--deleterious effects of hypothermia

This experimental study was undertaken to evaluate the hypothesis that cardioplegic arrest at 37 degrees C is superior to 10 degrees C cardioplegic arrest in the myocardial protection of an acutely injured heart. The hypothesis was tested using Sprague-Dawley rat hearts that were excised and retroperfused with Krebs-Henseleit buffer as isolated, isovolumic heart preparations. After 15 min of equilibration and baseline readings, ischemic injury of the myocardium was established by cessation of perfusion for 20 min, followed by 30 min of reperfusion to obtain cardiac measurements and verify uniformity of ventricular dysfunction. All hearts were then arrested for 30 min with continuous cardioplegia (oxygenated crystalloid cardioplegia, 4 ml/min) followed by 30 min of reperfusion. In one group (N = 12), temperature of cardioplegia was 10 degrees C. In the second group (N = 12), cardioplegia temperature was 37 degrees C. The experiments showed that in acutely injured hearts, cardioplegic arrest at 10 degrees C resulted in further deterioration in ventricular dysfunction (P < 0.01). In contrast, similarly injured hearts which underwent cardioplegic arrest at 37 degrees C showed a modest deterioration in ventricular dysfunction which did not reach statistical significance (P > 0.05). The experimental findings suggest that in the presence of acute myocardial injury, cardioplegic arrest at normothermia may provide better myocardial protection.