preserves function and signaling for mitochondrial biogenesis during subsequent ischemia. Am. J. Physiol. 274 (Heart Circ. Physiol. 43): H786-H793, 1998.-Hypothermia is known to protect myocardium during ischemia, but its role in induction of a protective stress response before ischemia has not been evaluated. As cold incites stress responses in other tissues, including heat shock protein induction and signaling mitochondrial biogenesis, we postulated that hypothermia in perfused hearts would produce similar phenomena while reducing injury during subsequent ischemia. Studies were performed in isolated perfused rabbit hearts (n ϭ 77): a control group (C) and a hypothermic group (H) subjected to decreasing infusate temperature from 37 to 31°C over 20 min. Subsequent ischemia during cardioplegic arrest at 34°C for 120 min was followed by reperfusion. At 15 min of reperfusion, recovery of left ventricular developed pressure (LVDP), maximum first derivative of left ventricular pressure (LV dP/dt max ), LV ϪdP/dt max , and the product of heart rate and LVDP was significantly increased in H (P Ͻ 0.01) compared with C hearts. Ischemic contracture started later in H (97.5 Ϯ 3.6 min) than in C (67.3 Ϯ 3.3 min) hearts. Myocardial ATP preservation and repletion during ischemia and reperfusion were higher in H than in C hearts. mRNA levels of the nuclear-encoded mitochondrial proteins adenine nucleotide translocase isoform 1 (ANT 1 ) and ␤-F 1 -adenosinetriphosphatase (␤-F 1 -ATPase) normalized to 28S RNA decreased in C hearts but were preserved in H hearts after reperfusion. Inducible heat shock protein (HSP70-1) mRNA was elevated nearly 4-fold after ischemia in C hearts and 12-fold in H hearts. These data indicate that hypothermia preserves myocardial function and ATP stores during subsequent ischemia and reperfusion. Signaling for mitochondrial biogenesis indexed by ANT 1 and ␤-F 1 -ATPase mRNA levels is also preserved during a marked increase in HSP70-1 mRNA.adenine nucleotide translocase isoform 1; ␤-F 1 -adenosinetriphosphatase; cold adaptation; inducible heat shock protein; myocardial reperfusion COLD-INDUCED STRESS is a phenomenon associated with an increase in inducible heat shock protein expression in various tissues (31,32). Particularly in brown adipose tissue, cold-induced stress or hypothermia also induces mitochondrial biogenesis (20,29,30). At the transcriptional level this is characterized by coordinated increases in expression of nuclear-and mitochondrial-encoded genes regulating mitochondrial membrane proteins (28). Although this signaling has been well characterized in brown adipose fat, it remains relatively unexplored in other mammalian tissues. This is surprising because stress responses in the heart secondary to heat shock or ischemia have been a major focus of investigation with respect to enhancement of tissue resistance to subsequent ischemia (14,21,33,35,40). Furthermore, hypothermia either singly or accompanied by cardioplegia is regularly employed in myocardial protection during heart surgery. T...

Age <1 month and longer duration of surgery were independently associated with hospitalized SSI after CV surgery in children.