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作 者:唐燕华[1] 陈朋[1] 胡大仁[1] 邓根英[1]
机构地区:[1]江西医学院第二附属医院心胸外科,江西南昌330006
出 处:《中国危重病急救医学》2001年第10期604-606,共3页Chinese Critical Care Medicine
基 金:江西省卫生厅科研基金资助项目 ( No.981 58)
摘 要:目的 :观察山莨菪碱 ( 654 2 )对体外循环 ( CPB)心肌缺血再灌注损伤的保护作用。方法 :将 2 4例心脏瓣膜置换术患者随机分为 654 2组 ( 1 3例 )和对照组 ( 1 1例 ) ,654 2组患者术中心肌灌注液中加入 654 2( 1 5mg/50 0 ml) ,对照组则常规用冷晶体停搏液。通过右心房插管分别于手术开始前、转流后 3 0分钟、主动脉开放后、停机、手术结束、术后 1日及术后 3日抽血测定血中超氧化物歧化酶 ( SOD)和丙二醛 ( MDA)的含量 ,并观察 2组患者术中心脏复跳情况和术后正性肌力药物的使用情况。结果 :2组术中血 SOD均明显下降 ,以对照组更为显著 ( P<0 .0 5) ,术后 1日 654 2组血 SOD含量接近术前水平 ,而对照组于术后 3日才恢复术前水平。 2组术中血 MDA含量则较术前上升 ,仍以对照组为明显 ( P<0 .0 5) ,手术结束时开始下降 ,术后 3日降至术前水平。术中主动脉开放后 654 2组心脏自动复跳率较对照组高 ,术后对照组正性肌力药物 (多巴胺等 )的使用量较 654 2组增多。结论 :654 2可保护缺血再灌注损伤心肌细胞 SOD活性 ,减少心肌细胞 MDA产生 ,有效地保护心肌功能。Objective:To observe the protective effect of anisodamine (6542) on myocardial ischemic and reperfusion injury in patients during cardiopulmonary bypass (CPB).Methods:Twentyfour patients underwent valve replacement were randomly divided into two groups.Patients in 6542 group ( n =13) received 6542 in addition to conventional cardioplegic treatment (15 mg/500 ml),and received conventional cardioplegic treatment during operation in control group ( n =11).The blood samples were taken at seven different intervals to determine the levels of superoxide dismutase (SOD) and malondialdehyde (MDA).Cardiac resuscitation and use of positive inotropic drugs were observed.Results:The activity of SOD decreased in two groups,and it was much lower in control group during CPB.SOD activity returned to baseline values one day after operation in 6542 group and three days after operation in control group,respectively.The level of MDA increased in two groups with more marked elevation in control group during CPB ( P <0 05),and it restored until three days after operation.The incidence of active cardiac resuscitation in 6542 group was higher than that in controls.The doses of positive inotropic drugs in control group were higher than that in 6542 group.Conclusions:This study suggests that 6542 can improve the activity of SOD and decrease the production of MDA,thereby attenuating myocardial ischemic and reperfusion injury.
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