论文部分内容阅读
临床缺血-再灌注引起急性肺损伤的发病机制,主要是氧自由基和花生四烯酸衍化物产生过量。美蓝能与分子氧竞争黄嘌呤氧化酶传递的电子,从而抑制氧自由基和超氧化物生成。体外研究已证实美蓝能有效地防御氧自由基对肝、肾组织的损害。由此作者就美蓝在预防肠缺血-再灌注后肺损伤方面的作用进行了实验研究。选择120只雄性豚鼠,体重380～420g。经腹腔注射氯胺酮60mg/kg和安定2.5mg/kg麻醉。行剖腹术,其中80只用血管钳夹闭肠系膜上动脉,关腹前随机分为两组:实验组(n=40),腹腔注射美蓝2ml;对照组(n=40),腹腔注射生理盐水2ml。1h后再打开腹腔
The pathogenesis of acute lung injury induced by clinical ischemia-reperfusion is mainly due to the excessive production of oxygen free radicals and arachidonic acid derivatives. Methylene blue can compete with molecular oxygen xanthine oxidase transfer of electrons, thereby inhibiting oxygen free radicals and superoxide formation. In vitro studies have confirmed that methylene blue can effectively prevent oxygen free radicals on liver and kidney damage. The authors therefore conducted an experimental study of the role of methylene blue in preventing lung injury following intestinal ischemia-reperfusion. Select 120 male guinea pigs, weighing 380 ~ 420g. Intraperitoneal injection of ketamine 60mg / kg and diazepam 2.5mg / kg anesthesia. 80 cases were involved in the occlusion of superior mesenteric artery with vascular forceps and were randomly divided into two groups: experimental group (n = 40), intraperitoneal injection of methylene blue (2ml), control group (n = 40), intraperitoneal injection of physiology Brine 2ml. 1h and then open the abdominal cavity