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Divisions of Cardiology and Genetics and Development, Department of Pediatrics, University of Washington, Seattle 98195; and Children's Hospital and Regional Medical Center, Seattle, Washington 98105
Hypothermia improves resistance to
ischemia in the cardioplegia-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 2 h at 34°C
[ischemic group (I); n = 13] or at 30°C
before and during ischemia [hypothermic group (H);
n = 12]. Developed pressure, the maximum first
derivative of left ventricular pressure, oxygen consumption, and
pressure-rate product (P < 0.05) recovery were superior in H compared with in I during reperfusion. mRNA expression for the mitochondrial proteins, adenine translocase and the 
-subunit of F1-ATPase, was preserved by hypothermia. cDNA
arrays revealed that ischemia altered expression of 13 genes.
Hypothermia modified this response to ischemia for eight genes,
six related to apoptosis. A marked, near fivefold increase in
transformation-related protein 53 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 proapoptotic Bcl-2 homologue bak. These data
imply that hypothermia modifies signaling pathways for
apoptosis and suggest possible mechanisms for
hypothermia-induced myocardial protection.
-subunit of F1-ATPase; hypothermic
adaptation; myocardial reperfusion
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