Abstract
To evaluate the efficiency of isoflurane-induced anesthetic preconditioning and the role of mitochondrial manganese superoxide dismutase (MnSOD) in hypertensive hypertrophied hearts. A prospective animal investigation. Medical center hospital research laboratory. Male spontaneously hypertensive rats (SHRs) and normotensive control Wistar-Kyoto (WKY) rats. All pentobarbital-anesthetized open-chest rats were subjected to a 45-minute left coronary artery occlusion followed by a 120-minute reperfusion. Before ischemia, both SHR and WKY rats were assigned randomly to receive a 30-minute exposure to 0.9% saline or 1.0 minimum alveolar concentration isoflurane. The myocardial infarct size, assessed as a percentage of the area at risk, was significantly greater in the hypertrophied SHRs than in the WKY rats (65.3%±8.7% v 51.8%±7.2%, p<0.05). Isoflurane preconditioning appreciably reduced the infarct size in the WKY hearts (30.9%±10.5%, p<0.05) but not in the SHR hearts. MnSOD protein expression and enzymatic activity were increased drastically in response to isoflurane exposure in the hearts of the WKY rats (p<0.05) but not in the SHRs. Isoflurane-induced anesthetic preconditioning is attenuated in hypertensive hypertrophied hearts. This impairment may be associated with the loss of MnSOD augmentation during ischemia and reperfusion.
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