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Protein kinase C expression following remote ischemic preconditioning in cardiac surgery


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Objective: To evaluate cardioprotective effects of remote ischemic preconditioning (RIPC) in cardiac surgery patients undergoing aortic valve replacement depending on the type of anesthesia and investigate the level of myocardial protein kinase C epsilon (PKC-ε) expression after RIPC. Methods: In prospective randomized trial, forty eight patients aging from 50 to 75 years old (64 (56 ;69)) were included. All patients were scheduled for aortic valve replacement using cardiopulmonary bypass (CPB). The patients were randomized into 4 groups: 1) RIPC applied during propofol anesthesia (RIPC prop, n=12), 2) RIPC applied during sevoflurane anesthesia (RIPC sev, n=12), 3) propofol anesthesia without RIPC (CONTROL prop, n=12), 4) sevoflurane anesthesia without RIPC (CONTROL sev, n=12). There was no difference found between the groups as to the baseline patient’s data. RIPC protocol consisted of 3 simultaneous ischemic episodes of both lower limbs (5 minutes) with 5-min reperfusion intervals. PKC-ε expression in right atrial myocardium was assessed using Western blotting. Troponin I (cTnI) was estimated before anesthesia induction, after 30 min, 6, 12, 24, 48 hours after CPB completion. Also we calculated area under curve of cTnI (cTnI AUC). According to nonparametric distribution, data were assessed by the Mann-Whitney U-test and Newman-Keuls method for multigroup comparison. p < 0.05 was considered significant. The data are presented as median (25th; 75th percentile). Results: Cardioprotective effects of RIPC were observed only after sevoflurane anesthesia: cTnI AUC was 134,8 (122,3; 232,4) ng/ml/48 h in CONTROL sev group and only 74,3 (64,7; 85,0) ng/ml/48 h in RIPC sev group (p<0,05). RIPC applied during propofol anesthesia was not associated with cTnI AUC decrease: 93,8 (74,1; 246,8) ng /ml/48 h in CONTROL prop group and 122,5 (74,1; 185,0) ng/ml/48 h in RIPC prop group (p = 0,37). RIPC applied during sevoflurane anesthesia significantly increased PKC-ε expression: 1221 (921;1438) U in CONTROL sev group vs 1882 (1564;2131) U in RIPC sev group (p < 0,05). RIPC implication during propofol anesthesia was not associated with any significant difference in PKC- ɛ expression in comparison with control group: 620 (436; 782) U in CONTROL prop group versus 788 (574;1063) U in RIPC prop group. In control groups, PKC-ε expression was significantly higher in sevoflurane anesthesia in comparison with propofol anesthesia. Conclusion: RIPC was only effective when it was applied during sevoflurane anesthesia. This was confirmed by PKC-ε expression increase and lower value of cTnI. There were no evidence of preconditioning and cardioprotection when RIPC was initiated during propofol anesthesia.

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