Abstract

Objective To investigate the effects of sevoflurane on myocardial damage after cardiopulmonary resuscitation in rats. Methods The cardiac arrest model was established by asphyxia. Thirth-six male Wistar rats were assigned to three groups randomly(random number). Rats in the sham group were anesthetized with intubation, without induced cardiac arrest. Rats in the sevo group inhaled 1minimal alveolar concentration(MAC) of sevoflurane during CPR. Rats in the control group received the standard CPR. At 4 h and 24 h after ROSC , half the rats of every group received the echocardiography examination. At 4 h after ROSC, the rest of rats in every group were sacrificed with overdose anesthetics, the hearts were removed and mitochondria was isolated promptly. Determination of the status of mitochondrial permeability transition pore(MPTP) using the spectrophotometer. The level of cytosolic cytochrome C was measured by Western blot. Results After ROSC, the left ventricular posterior wall during diastolic(LVPWd) became thick and the cardiac output was decreased dramatically. At 4 h after ROSC, the mice of the sevo group had a slighter thickness of LVPWd (mm)(1.95±0.14)vs.(2.32±0.34), P<0.05 and an enhanced cardiac output(mL/min)(46.94±3.61)vs.(38.77±6.63), P<0.05 than the control group. The mitochondria swelling was triggered by the addition of CaCl2,the sevo group showed an slighter decrease in the absorbance of light compared with the control group(0.048±0.007)vs.(0.069±0.011), P<0.01. After ROSC, cytochrome C was released to cytosol, and the sevo group had a lower level of this protein than the control group(1.02±0.22)vs.(1.59±0.31), P<0.05. Conclusions After ROSC, sevoflurane can alleviate myocardial dysfunction, attenuate the MPTP opening and decrease the level of cytosolic cytochrome C. Key words: Cardiac arrest; Cardio-pulmonary resuscitation; Asphyxia; Sevoflurane; Post-resuscitation myocardial dysfunction; Mitochondrial permeability transition pore

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