【摘要】 目的观察肠道内给予卡巴胆碱对兔肠部分缺血再灌注(I/R)损伤后心脏炎症反应的防治作用。方法大白兔75只,随机分为肠部分I/R组(n=25)、卡巴胆碱组(n=25)、假手术组(n=25);阻断肠系膜上动脉(SMA)血流50%,维持4小时,造成肠部分I/R损伤;卡巴胆碱组于SMA阻断后1小时经肠内注入3%卡巴胆碱(3μg/kg),阻断后2、6小时、1、2、3天测定心脏、肠道组织内肿瘤坏死因子-α(TNF-α)、白细胞介素-10(IL-10)的变化,血浆肌酸激酶同工酶(CK-MB)含量,并行病理组织学检查。结果肠部分I/R损伤可导致心脏、肠道组织内TNF-α等炎症介质明显增加;肠内给予卡巴胆碱后肠黏膜血流量增加,心脏炎症反应减轻,心肌组织内促炎介质TNF-α含量下降,但抗炎介质IL-10无明显变化。结论肠道部分I/R损伤可诱发心脏炎症反应和功能障碍;肠内给予卡巴胆碱可减轻心脏炎症反应,改善心肌功能,其机制可能是抑制TNF-α等促炎介质分泌,而非增加抗炎介质IL-10的释放。更多还原

【Abstract】 Objective To observe influence of enteral administration of carbachol on heart inflammation induced by partial ischemia/reperfusion injury to intestine.Methods Seventy five rabbits were randomized into three groups: intestine I/R group,carbachol group,sham operation group,the superior mesenteric artery(SMA) were occluded to 50% for 4h in intestine I/R group.In carbachol group,carbachol(3mg/kg) was injected into duodenum 1h after occlusion of SMA.Changes of TNF-α,IL-10 in heart and intestine were measured at 2,6h,1,2,3d after SMA occlusion.Results Levels of TNF-αin heart and intestine were increased dramatically after intestine I/R injury.Enteral administration of carbachol increased the blood flow of intestinal mucosa,decreased the level of TNF-αand inflammation in heart.Conclusion Partial ischemia/reperfusion injury to intestine could induce heart inflammation and dysfunction;Enteral administration of carbachol could inhibit the release of pro-inflammatory factors as TNF-α,but not increase the release of anti-inflammatory factors as IL-10.更多还原