Mild hypothermia on reperfusion after warm ischemia improves guinea pig isolated heart function

Abstract

Application of mild hypothermia during the initial critical period of reperfusion after cardiac ischemia may slow mitochondrial and cell metabolism sufficiently to attenuate cardiac damage and better preserve mechanical function. To test this we isolated guinea pig hearts for perfusion at constant pressure with Krebs‐Ringer's solution at pH 7.4. Left ventricular pressure (LVP), coronary flow (CF), and O2 consumption were measured and continuous NADH/FAD and mitochondrial (m) [Ca2+] were assessed in the LV wall by fluorescence spectrophotometry in the absence or presence of indo 1 + MnCl2 to quench cell Ca2+. Hearts were subjected to 30 min ischemia at 37ºC, and then reperfused at either 32ºC or 37ºC for 60 min followed by additional 60 min reperfusion at 37ºC. Values up to reperfusion were similar in both groups. Developed LVP and m[Ca2+] were both lower at 32ºC vs. 37ºC. At the end of reperfusion the 32ºC group showed improved developed LVP (62 % of baseline) when compared to the non‐treatment group (50 %). There were no noticeable improvements in CF, NADH, FAD, and mCa2+ loading during later perfusion. Lower contractility and m[Ca2+] by hypothermia during the critical early reperfusion period may protect the heart during later warm reperfusion.