论文部分内容阅读
Aim: The activation of extracellular signal-regulated kinase (ERK)1/2 protects against ischemic-reperfusion injury. Whether ERK1/2 mediates the cardioprotection of sevoflurane postconditioning is unknown. We tested whether sevoflurane postconditioning produces cardioprotection via an ERKl/2-depen- dent mechanism. Methods: In protocol 1, Langendorff-perfused Sprague-Dawley rat hearts (n=84, 12 per group), with the exception of the Sham group, were sub- jected to 30 min ischemia followed by 90 min reperfusion and were assigned to the untreated (control) group, followed by 4 cycles of ischemic postconditioning (25 s of each), 3% (v/v) sevoflurane postconditioning (for 5 rain and 10 min of washout), and the PD98059 solvent DMSO (0.05). After reperfusion, compared with the control group, sevoflurane postconditioning and ischemic postconditioning sig- nificantly (P<0.05) improved functional recovery and largely (P<0.05) de- creased myocardial infarct size (22.9%±4.6% and 21.2%±3.8%, vs 39.4%± 5.7%, both P<0.05). Sevoflurane-mediated protection was abolished by PD98059. Conclusion: Anesthetic postconditioning by sevoflurane effectively protects against reperfusion damage by activating ERK1/2 in vitro.