Abstract
Objectives: The present study aimed to investigate whether ischemic or sevoflurane-induced preconditioning exerts infarct size limiting effects and depresses ischemia-reperfusion arrhythmias through opening of mitochondrial KATP channels in rabbits in vivo. Methods: Rabbits anesthetized with ketamine and xylazine given intramuscularly underwent 30 min of left anterior descending coronary artery (LAD) occlusion followed by 3 hrs of reperfusion. Before this, rabbits were randomized into one of five groups. Control rabbits received no intervention before 30 min LAD occlusion and 3 h reperfusion (Group-C). The ischemia-preconditioned (IP) rabbits underwent 5 min LAD occlusion followed by 10 min of reperfusion before prolonged ischemia-reperfusion (Group-IP). In the sevoflurane (S)–preconditioned group, 30 min of sevoflurane exposure at a 1.5% end-tidal concentration was followed by 15 min of washout before prolonged ischemia-reperfusion (Group-S). The selective mitochondrial KATP channel blocker, 5-hydroxy-decanoate (5-HD, 5 mg/kg) was given intravenously 10 min before ischemic preconditioning and sevoflurane exposure, respectively (Group-5-HD-IP, Group-5-HD-S). An electrocardiogram was recorded throughout the experiment via lead 2 of the standard electrocardiogram. At the end of the 3 hrs reperfusion period, area at risk (R) and infarct size (I) were measured. Results: RPP decreased in Group-5-HD-IP and Group-5-HD-S compared with Group-S at 30 min after ischemia. The ratio of R to left ventricular mass showed no significant difference among all groups. I/R values of each group were 51.6 ± 3.0% in Group-C, 33.3 ± 4.7% in Group-IP, 36.6 ± 4.8% in Group-S, 48.9 ± 5.2% in Group-5-HD-IP, 54.8 ± 4.2% in Group-Group-5-HD-S. There was no significant difference in duration of arrhythmias during myocardial ischemia and reperfusion among 5 groups. Conclusion: Ischemic preconditioning and sevoflurane-induced preconditioning exert infarct size limiting effects through opening of mitochondrial KATP channels. However, ischemic preconditioning and sevoflurane-induced preconditioning do not have antiarrhythmic effects. This suggests that the opening of mitochondrial KATP channels does not cause antiarrhythmic effects.
Highlights
Lethal injury to the heart can be dramatically blunted by brief conditioning periods of ischemia and reperfusion: a phenomenon called ischemic preconditioning [1,2]
Adenosine triphosphatesensitive potassium (KATP) channels have long been considered as essential components of cardioprotection by both ischemic and anesthetic preconditioning [7,8]
As for the role for mitochondrial KATP channels in anesthetic preconditioning, our laboratory demonstrated that the protective effects by sevoflurane as well as brief ischemia may be mediated by mitochondrial rather than sarcolemmal KATP channel opening [4]
Summary
Lethal injury to the heart can be dramatically blunted by brief conditioning periods of ischemia and reperfusion: a phenomenon called ischemic preconditioning [1,2]. Brief exposure to a volatile anesthetic agent such as isoflurane [3] and sevoflurane [4,5] protects the heart against subsequent ischemia–reperfusion injury. This phenomenon has been recognized as anesthetic preconditioning [6]. Adenosine triphosphatesensitive potassium (KATP) channels have long been considered as essential components of cardioprotection by both ischemic and anesthetic preconditioning [7,8]. As for the role for mitochondrial KATP channels in anesthetic preconditioning, our laboratory demonstrated that the protective effects by sevoflurane as well as brief ischemia may be mediated by mitochondrial rather than sarcolemmal KATP channel opening [4]
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