Mild Hypothermia Is Ineffective to Protect Against Myocardial Injury Induced by Chemical Anoxia or Forced Calcium Overload.

Abstract

Although hypothermia suppresses myocardial ischemia/reperfusion injury, whether it also protects the myocardium against cellular stresses such as chemical anoxia and calcium overload remains unknown. We examined the effect of mild hypothermia (33&#xb0;C) on myocardial injury during ischemia/reperfusion, local administration of sodium cyanide (chemical anoxia), or local administration of maitotoxin (forced Ca overload) using cardiac microdialysis applied to the feline left ventricle. Baseline myoglobin levels (in ng/mL) were 237 &#xb1; 57 and 150 &#xb1; 46 under normothermia and hypothermia, respectively (mean &#xb1; SE, n = 6 probes each). Coronary artery occlusion increased the myoglobin level to 2600 &#xb1; 424 under normothermia, which was suppressed to 1160 &#xb1; 149 under hypothermia (P < 0.05). Reperfusion further increased the myoglobin level to 6790 &#xb1; 1550 under normothermia, which was also suppressed to 2060 &#xb1; 343 under hypothermia (P < 0.05). By contrast, hypothermia did not affect the cyanide-induced myoglobin release (930 &#xb1; 130 vs. 912 &#xb1; 62, n = 6 probes each) or the maitotoxin-induced myoglobin release (2070 &#xb1; 511 vs. 2110 &#xb1; 567, n = 6 probes each). In conclusion, mild hypothermia does not make the myocardium resistant to cellular stresses such as chemical anoxia and forced Ca overload.