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.