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生脉对罗哌卡因致大鼠心肌毒性的保护作用 被引量:3

Protective effect of shengmai on myocardial toxicity induced by ropivacaine in rats
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摘要 目的探讨生脉对罗哌卡因致大鼠心肌毒性的保护作用。方法SD雄性大鼠20只随机均分为两组:罗哌卡因组(R组)以0·5ml/min静脉输注0·75%罗哌卡因,生脉+罗哌卡因组(SR组)在输注罗哌卡因前10d每天预注生脉3ml/kg,然后以同样方法输注罗哌卡因。连续监测MAP、ECG。记录QRS波异常、HR减慢50%、MAP下降70%及心跳停止时罗哌卡因用量及其输注时间。在注药前、QRS波异常和MAP下降70%时测定动脉血血气及乳酸。心跳停止即刻,取心肌组织作电镜显像。结果与注药前相比,MAP下降70%时两组乳酸明显增多、pH下降、PaO2下降(P<0·05或P<0·01)。QRS波异常、HR减慢50%、MAP下降70%及心跳停止时SR组罗哌卡因的用量显著高于R组(P<0·05),输注时间长于R组(P<0·05)。SR组在MAP下降70%时乳酸明显低于R组(P<0·05)。电镜下SR组的心肌细胞形态学损害较R组明显减轻。结论生脉对罗哌卡因引起的心肌毒性具有保护作用。 Objective To explore the protective effect of shengmai on rats myocardial toxicity induced by ropivacaine infusion. Methods Twenty male SD rats were randomly divided into ropivacaine group(R ) and shengmai plus ropivacaine groups (SR) with 10 animals each. Both groups were given an intravenous infusion of 0.75% ropivacaine in a dose of 0.5 ml/min until cardiac arrest occurred. Before ropivacaine infusion the rats in group SR had been given shengmai 3 ml · kg^-1 · d^-1 for 10 days. MAP and ECG were monitored continuously. The amount of ropivacaine used,the time of ropivacaine infusion,blood lactic acid and arterial blood gas analysis were recorded before ropivacaine infusion(T0 ), at the time of abnormal QRS wave appearance (T1), and the time of 70% reduction of MAP(T2 ). The myocardium was examined by electromicroscopy. Results There was a significant increase of lactic acid and decrease of pH and PaO2 at T1 and T2 compared to those at T0 (P〈0.01). The amount of ropivacaine used was greater and the time of hemodynamic changes was later in group SR than those in group R (P〈0.05). Blood level of lactic acid at T2 was lower in group SR than that in group R (P〈0.05). The mophologic changes of the myocardium were more severe in group R than those in group SR. Conclusion Shengmai has a protective effect on rats myocardial toxicity induced by ropivacaine infusion.
出处 《临床麻醉学杂志》 CAS CSCD 2008年第4期331-333,共3页 Journal of Clinical Anesthesiology
关键词 生脉 罗哌卡因 心肌霉性 Shengmai Ropivacaine Myocardial toxicity
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