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作 者:车晋伟[1] 胡森[1] 耿世佳[1] 吴静[1] 王磊[1] 杜颖[1] 田易军[1] 盛志勇[1]
机构地区:[1]中国人民解放军总医院第一附属医院全军烧伤研究所休克与多器官功能障碍实验室,北京市100037
出 处:《世界华人消化杂志》2008年第8期900-903,共4页World Chinese Journal of Digestology
基 金:军队十一五专项课题基金;No.06Z055~~
摘 要:目的:研究拟胆碱药卡巴胆碱(carbachol,CAR)对大鼠烫伤休克期肠内补液时肠组织氧自由基损伤的影响.方法:38只♂Wistar大鼠,采用沸水法(100℃,10s)造成35%TBSAⅢ度烫伤.随机分为不复苏组(单烫组,n=8)、葡萄糖.电解质溶液(glucose electrolyte solution)复苏组(GES组,n =10)、单纯卡巴胆碱治疗组(CAR组,n=10)和GES+CAR复苏组(GES/CAR组,n=10).两液体复苏组在伤后30 min将GES经十二指肠造口匀速泵入,按Parkland公式设定补液速率,CAR组和GES/CAR组在伤后30 min将CAR以60μg/kg溶于0.5mL生理盐水中一次注入十二指肠.所有大鼠在伤后4h处死,取空肠组织测定脂质过氧化物丙二醛(malondialdehyde,MDA)含量、黄嘌呤氧化酶(xanthine oxidase,XOD)和髓过氧化物酶(myeloperoxidase,MPO)活性,并观察肠组织病理学变化.结果:烫伤后GES组肠组织XOD、MPO活性和MDA含量分别高于单烫组13.2%、21.3%和21.1%,并有统计学意义(P<0.05);GES/CAR组XOD,MPO和MDA均较GES组明显下降(1.36±0.37 vs 2.51±0.56:0.47±0.14 vs 0.83±0.21;3.97±1.57 vs 6.59±1.50,P<0.01);CAR组各指标数值最低.肠组织病理损伤也表现为CAR组和GES/CAR组最轻,单烫组次之,GES组损伤最重.结论:卡巴胆碱能有效减轻烫伤休克大鼠肠内复苏时的肠道氧自由基损伤,机制可能与其抗炎作用和抑制黄嘌呤氧化酶活性、减少氧自由基生成有关.AIM: To investigate the effects of carbachol on oxygen free radical injury in gut during enteral resuscitation of burn shock in rats. METHODS: A 35% TBSA full thickness scald injury was induced in 38 Wistar rats. The rats were divided randomly into four groups: scald with no therapy (scald alone, n= 8), scald with enteral infusing either a glucose electrolyte solution (GES, n = 10) or GES containing carbachol (60 μg/kg, GES/CAR, n = 10), and scald with enteral infusing only carbachol (CAR, n = 10). GES was infused into intestine through a duodenal stomy according to Parkland formula (4 mL·1%TBSA/kg) 30 min after scald and carbachol was administered simultaneously through the same path. Four hours after injury, the initial jejunum was collected for evaluation of xanthine oxidase (XOD), malondialdehyde (MDA), myeloperoxidase (MPO) and assessment of the pathologic damages. RESULTS: The activity of XOD and MPO, and the MDA level were 13.2%, 21.3% and 21.1% higher in the GES containing carbachol treatment groups than in the scald alone group (P 〈 0.05). Resuscitation with GES/CAR resulted in significantly lower levels of XOD (1.36 ± 0.37 vs 2.51 ±0.56, P 〈 0.01), MDA (3.97 ± 1.57 vs 6.59 ± 1.50, P 〈 0.01) and MPO (0.47 ± 0.14 vs 0.83 ± 0.21, P 〈 0.01) than resuscitation with GES. The parameters in the CAR group were the lowest. The gut lesions were mild in the CAR and GES/CAR groups, severe in the CAR alone group, and most severe in the GES group. CONCLUSION: Carbachol can alleviate gut oxygen free radical injury during enteral resuscitation of burn shock, which might be associated with its anti-inflammation effects, inhibition of XOD activity and generation of oxygen free radicals in gut tissue.
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