Key result
Sevoflurane post-conditioning decreased infarct size compared to unprotected hearts, but this cardioprotection was abolished by 20 microg/ml lidocaine.
Why the study?
Does lidocaine abolish the cardioprotective effect of sevoflurane post-conditioning in isolated rat hearts?
Does lidocaine abolish the cardioprotective effect of sevoflurane post-conditioning in isolated rat hearts?
Lidocaine at 20 microg/ml abolishes the cardioprotective effects of sevoflurane post-conditioning against ischemia-reperfusion injury in isolated rat hearts.
Answers are grounded in this paper and cite their sources.
Lidocaine may blunt sevoflurane post-conditioning in experimental ischemia-reperfusion; leaves open relevance to clinical anesthesia.
BACKGROUND: Post-ischemic administration of volatile anesthetics activates ischemia-reperfusion injury salvage process and decreases myocardial damage. However, the mechanisms underlying anesthetic post-conditioning and effects of lidocaine on it remain unclear. Here we report the cardioprotection of sevoflurane-induced post-conditioning and the effects of lidocaine on it. METHODS: Isolated perfused rat hearts were exposed to 40 min of ischemia followed by 1 h of reperfusion. Volatile anesthetic post-conditioning was induced by 15 min of 3 vol% sevourane (1.5 minimum alveolar concentration) administered at the onset of reperfusion. In some experiments, lidocaine was coadministered with sevoflurane in different concentrations (2, 10 and 20 microg/ml). Infarct size was determined by dividing the total necrotic area of the left ventricle by the total left ventricular slice area (percent necrotic area). RESULTS: Sevoflurane-induced post-conditioning signicantly improved post-ischemia functional recovery and decreased infarct size (47.3+/-5.6% in unprotected hearts vs. 18.6+/-3.1% in anesthetic post-conditioning, P<0.05). Sevourane-mediated cardioprotection was abolished by 20 microg/ml lidocaine. CONCLUSIONS: Sevourane-induced post-conditioning effectively protected myocardium against reperfusion damage and its cytoprotection was reversed by 20 microg/ml lidocaine.
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Yan et al. (2007) studied Ischemia-reperfusion injury. Sevoflurane post-conditioning vs. Unprotected hearts was evaluated on Infarct size (percent necrotic area) (p=<0.05). Sevoflurane post-conditioning decreased infarct size compared to unprotected hearts, but this cardioprotection was abolished by 20 microg/ml lidocaine.
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