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Articles in PresS, published online ahead of print December 21, 2001
J Appl Physiol, 10.1152/jap.01035.2001
Submitted on October 11, 2001
Accepted on December 5, 2001
1 Pediatrics, University of Washington Medical Center, Seattle, WA, USA; Pediatrics, Children's Hospital & Regional Medical Center, Seattle, WA, USA
2 Pediatrics, University of Washington Medical Center, Seattle, WA, USA
* To whom correspondence should be addressed. E-mail: xh{at}u.washington.edu.
Hypothermia improves resistance to ischemia in the cardioplegic-arrested heart. This adaptive process produces changes in specific signaling pathways for mitochondrial proteins and heat-shock response. To further test for hypothermic modulation of other signaling pathways such as apoptosis, we used various molecular techniques including cDNA arrays. Isolated rabbit hearts were perfused and exposed to ischemic cardioplegic arrest for two hours at 34°C (Ischemia, I; n-13), or at 30°C (Hypothermia, H; n=12) prior to and during ischemia. Developed pressure (DP), dP/dtmax, oxygen consumption, and pressure-rate product (P<0.05) recovery was superior in H compared with I during reperfusion. mRNA expression for the mitochondrial proteins, adenine translocase, and ß F1-ATPase, was preserved by hypothermia. cDNA arrays revealed that ischemia altered expression of 13 genes. Hypothermia modified this response to ischemia for 8 genes, 6 related to apoptosis. A marked, near five fold increase in transformation related protein 53 (p53) in I was virtually abrogated in H. Hypothermia also increased expression for the anti-apoptotic Bcl-2 homologue Bcl-x relative to I, but decreased expression for the pro-apoptotic Bcl-2 homologue, bak. These data imply that hypothermia modifies signaling pathways for apoptosis and suggest possible mechanisms for hypothermia-induced myocardial protection.
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