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Am J Physiol Heart Circ Physiol 286: H545-H551, 2004. First published October 9, 2003; doi:10.1152/ajpheart.00022.2003
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Responses of chronically hypoxic rat hearts to ischemia: KATP channel blockade does not abolish increased RV tolerance to ischemia

Joerg Forkel,1 Xiaochao Chen,2 Susanne Wandinger,1 Florian Keser,1 Alexey Duschin,2 Uwe Schwanke,2 Stilla Frede,3 Parwis Massoudy,1 Rainer Schulz,2 Heinz Jakob,1 and Gerd Heusch2

1Division of Cardiothoracic Surgery, Institutes of 2Pathophysiology and 3Physiology, University of Essen, 45122 Essen, Germany

Submitted 13 January 2003 ; accepted in final form 22 September 2003

Chronic hypoxia may precondition the myocardium and protect from ischemia-reperfusion damage. We therefore examined the recovery of left and right ventricular function after ischemia and reperfusion (15 min each) in isolated blood-perfused working hearts from normoxic (Norm) and hypoxic (Hypo; 14 days, 10.5% O2) adult rats. In addition, the mRNA expression of hypoxia-inducible factor (HIF)-1{alpha} and the protein expression of endothelial nitric oxide synthase (eNOS) were measured. Postischemic left ventricular function recovered to 66 ± 6% and 67 ± 5% of baseline in Norm and Hypo, respectively. In contrast, postischemic right ventricular function was 93 ± 2% of baseline in Hypo vs. 67 ± 3% in Norm (P < 0.05). Improved postischemic right ventricular function in Hypo (93 ± 2% and 96 ± 2% of baseline) was observed with 95% O2 or 21% O2 in the perfusate, and it was not attenuated by glibenclamide (5 and 10 µmol/l) (86 ± 4% and 106 ± 6% recovery). HIF-1{alpha} mRNA and eNOS protein expression were increased in both left and right hypoxic ventricles. In conclusion, postischemic right, but not left, ventricular function was improved by preceding chronic hypoxia. ATP-sensitive K+ channels are not responsible for the increased right ventricular tolerance to ischemia after chronic hypoxia in adult rat hearts.

chronic hypoxia; glibenclamide; hypoxia-inducible factor-1{alpha}; endothelial nitric oxide synthase


Address for reprint requests and other correspondence: G. Heusch, Institut für Pathophysiologie Zentrum für Innere Medizin, Universitätsklinikum Essen, Hufelandstrasse55, 45122 Essen, Germany (E-mail: gerd.heusch{at}uni-essen.de).




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