INTRODUCTIONThe integration of reactive oxygen species is strongly associated with important pathophysiological mechanisms that mediate myocardial ischaemia/reperfusion (I/R) damage. Pyruvate is an efficacious scavenger of reactive oxygen species and a previous study has shown that ethyl pyruvate (EP) has a myocardial protective effect against regional I/R damage in an in vivo rat model. The purpose of this study was to determine whether the myocardial protective effect of EP is associated with anti-apoptosis.
METHODSRats were allocated to receive EP dissolved in lactated Ringer's solution or lactated Ringer's solution alone, via intraperitoneal infusion one hour before ischaemia. They were exposed to 30 minutes of ischaemia followed by reperfusion of the left coronary artery territory over two hours. Anti-apoptotic effects were checked using several biochemical parameters after two hours of reperfusion. Apoptosis was analysed using measured caspase-3 activity, Western blotting of B-cell lymphoma 2 (Bcl-2) family protein cleaved by caspase-3, and assessment of DNA laddering patterns and the terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL) staining test.
RESULTSIn ischaemic myocardium, EP increased Bcl-2 expression, but reduced Bcl-2-associated X protein and cleaved caspase-3 expressions. EP reduced the expression of DNA laddering and the number of myocardial I/R-damaged TUNELpositive cells.CONCLUSION This study demonstrated that EP has an anti-apoptotic effect after regional I/R damage in an in vivo rat heart model. The myocardial protective effect of EP may be related to its anti-apoptotic effect.
Background: The aim of this study was to evaluate the effect of aging on the hemodynamic response to endotracheal intubation during the induction of anesthesia. Methods: Fifty patients with American Society of Anesthesiologists physical status classification 1 or 2 were enrolled and allocated according to age to either group N (35-44 years, not elderly, n=25) or group E (65-74 years, elderly, n=25). The patients were administered 3 minimum alveolar concentrations of sevoflurane for 5 minutes for the induction of anesthesia. Systolic arterial pressure (SAP) and heart rate (HR) were recorded before (baseline), immediately after (T0), and at 1-minute intervals during the first 4 minutes after endotracheal intubation (T1-T4). Results: SAP increased by 15.4% and 10.8% (p<0.05) from the baseline at T0 and T1, respectively, in group N, and by 21.6%, 17.8%, and 11.8% (p<0.05) from the baseline at T0, T1 and T2 respectively, in group E. The SAP increases at T0, T1 and T2 were significantly greater in group E than in group N (p<0.05). The HR increases at T0 and T1 were significantly greater for group N than for group E (p<0.05). Conclusion: We recommend that anesthesiologists vigilantly monitor and attenuate adverse hemodynamic responses for at least 5 minutes after endotracheal intubation especially in elderly patients, particularly because significant systolic hypertension can occur in this age group.
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