目的探讨穴位注射生脉注射液对布比卡因所致大鼠心脏毒性的影响,初步探讨其作用机制。方法选取SD雄性大鼠30只,随机分为3组,分别为空白组(Ⅰ组)、模型组(Ⅱ组)、给药组(Ⅲ组),每组大鼠10只。Ⅰ组大鼠,按2 mg/(kg·min)速度经股静脉泵入0.9%生理盐水,Ⅱ组、Ⅲ组大鼠,按2 mg/(kg·min)速度将0.5%盐酸布比卡因注射液经股静脉持续泵入制作心脏毒性模型。Ⅰ组大鼠经双侧内关穴注射生理盐水;Ⅱ组和Ⅲ组大鼠在出现心率失常时,经双侧内关穴分别注射生理盐水和生脉注射液。记录给药前大鼠的基础心率,给局麻药后大鼠出现心律失常(以QRS波延长至90 ms为标准)、心搏骤停的时间,计算出相应的局麻药的剂量;取大鼠心肌组织检测其中Na+-K+-ATP酶和乳酸脱氢酶含量。结果与Ⅱ组大鼠比较,Ⅲ组大鼠出现心律失常、心搏骤停明显延迟,对应的布比卡因用量大于Ⅱ组,差异有统计学意义(P<0.05);与Ⅱ组大鼠比较,Ⅲ组大鼠心肌组织中Na+-K+-ATP酶含量明显升高,乳酸脱氢酶含量明显下降,差异均有统计学意义(P<0.05)。结论穴位注射生脉注射液对布比卡因所致大鼠的心脏毒性有一定的预防和治疗作用,其机制可能与增强心肌组织Na+-K+-ATP酶活性、抑制乳酸脱氢酶活性有关。
ObjectiveTo investigate the effect of shengmai acupoint injection on cardiac toxicity induced by bupivacaine infusion in rats. MethodsA total of 30 SD adult male rats were randomly divided into blank group(groupⅠ), model group(group Ⅱ), medicine group(group Ⅲ), with 10 rats in each group. Normal saline 0.9% was pumped intravenously at a rate of 2 mg· kg-1 ·min-1 into the femoral vein in group Ⅰ, 0.5% bupivacaine was pumped intravenously at a rate of 2 mg· kg-1 ·min-1 into the femoral vein in group Ⅱ and group Ⅲ. Group Ⅰwas injected with saline in bilateral Neiguan-point; group Ⅱ and group Ⅲ were injected with normal saline and shengmai in bilateral Neiguan-point when arrhythmia occured. The heart rate(HR) before administration, the time of arrhythmia after received local anesthetics(as QRS extend to 90 ms) and cardiac arrest emergence were record, corresponding dosage of bupivacaine was calculated; Na+-K+-ATPase and lactate dehydrogenase of the cardiac muscle were measure. ResultsThe emergence of arrhythmia and cardiac arrest in group Ⅲ were significantly later than those in group Ⅱ, the corresponding dosage of bupivacaine in group Ⅲ was significantly larger than that in group Ⅱ(P<0.05); the level of Na+-K+-ATPase in myocardial of the group Ⅲ was significantly higher than that of group Ⅱ, and the level of lactic dehydrogenase in the group Ⅲ was significantly lower than that in the group Ⅱ(P<0.05). ConclusionsAcupoint injection with Shengmai can prevent and treat the cardiac toxicity induced by bupivacaine in rats, the mechanism may relate to enhancing myocardial tissue Na+-k+-ATPase activity and inhibiting lactic dehydrogenase activity.