高压氧防止创伤/失血性休克复苏后大鼠肠道缺血-再灌注损伤

目的 观察高压氧(HBO)对创伤/失血性休克复苏后大鼠肠道缺血-再灌注损伤的保护作用并探讨其作用机制.方法Wistar大鼠用铁块砸击左侧股骨并同时通过右颈动脉放血建立创伤/失血性休克模型,随后进行自体血和液体复苏.大鼠随机分成对照组、休克组、HBO一次和三次治疗组.结果 复苏24 h后HBO一次和三次组大鼠肠道组织乳酸含量、诱生型一氧化氮合成酶(iN0s)活性、一氧化氮(NO)和肿瘤坏死因子-α(TNF-α)水平均明显低于休克组(P<0.05);HBO一次和三次组中肠组织病理损伤评分明显低于休克组(P<0.05).电镜显示休克组肠黏膜上皮细胞肿胀,微绒毛广泛脱落;线粒体肿胀,嵴消失,形成空泡,广泛线粒体溶解;桥粒连接稀疏,细胞间紧密连接开放.HBO一次和三次组上述改变明显减轻:线粒体部分溶解,嵴部分消失,紧密连接得以保存.HBO三次组在以上所有的指标中均要好于HBO一次组,但差异无统计学意义(P>0.05).结论HBO可以减少创伤性休克后肠道组织炎性细胞因子的产生,减轻炎症反应,保护肠道组织和黏膜屏障免受创伤/失血性休克后缺血/再灌注的损伤.

Hyperbaric oxygen prevents intestinal ischemia-reperfusion injury in rats after resuscitation from traumatic/hemorrhagic shock

Objective To investigate the effects of hyperbaric oxygen (HBO) on ischemia/repeffusion (Ⅰ/R) injury of the small intestine after resuscitation from trauma and hemorrhagic shock (T/HS) in rats in order to elucidate the underlying mechanisms. Method Ninety-six male Wistar rats were randomly divided into four groups with 24 rats in each group. In shock group, rats were operated with induced T/HS. In sham group, rats operated without induced T/HS. In one HBO therapy (HBOT) group, rats with T/HS were treated with HBOT once. In three-HBOT group, rats with T/HS were treated with HBOT thrice. The Animal Care and Use Committee of China Medical University approved all animal protocols. Rats were anesthetized with amobarbital sodium (80 mg/kg, i.p.) at room temperature (25 ℃), the bloed pressure was monitored via polyethylene cannula inserted into the right femoral artery, connecting with the pressure analyzer (Multiparameter Monitor, M3046A, Boebin-gen, Germany). The left jugular vein was cannulated for administering normal saline and for resuscitation. The right carotid artery was cannulated for shedding blood. After operation, the middle part of left thigh of rat was se-lected as a site to be made of trauma by a lump of 2.5 kg iron falling upon from 20 cm height, causing the com-pound fracture of femur and crush injury of muscular tissue, then the damaged thigh was bandaged and fixed. At the same time, the blood was drawing out of fight carotid artery via cannula until the mean arterial was reduced to 30-35 mmHg within 5 minutes. The hypotension was kept constant for 60 minutes by additional drawing small amounts of blood as needed. After 60 minutes of hypotension, the rats were resuscitated by transfusing the shed blood over 5 minutes, followed by 4 -6 mL normal saline in 60 minutes to get the mean artery pressure maintained above 80 mmHg. The resuscitated rats were put into the hyperbaric chamber (10N-750, menoplace chamber, Ningho, China). The pressure inside the chamber was adjusted to 2.5 ATA and the oxygen concentration was higher than 95 %. The set pressure and oxygen concentration were maintained for 60 minutes. When the pressure within the chamber was decreased to 1 ATA, rots were taken out. The rats in one-HBOT group were given one HBO therapy immediately after resuscitation, and the rats in three-HBOT group were given one HBO therapy im-mediately after resuscitation with additional twice HBO therapy within 24 hours ((q 8 h). The one-way ANOVA and Pearson's bivariate methed were used for statistics. Results Twenty-four hours after resuscitation, the levels of lactate, induced nitric oxide synthase (iNOS), nitric oxide (NO), and tumor necrosis factor-α (TNF-α) in in-testinal tissue of rats in both HBOT groups were significantly lower than those in the rats of shock group without HBOT (P < 0.05). The histological injury grading scores of intestinal tissue in both HBOT group was significant lower than that in shock group (P < 0.05). There was positive correlation between the levels of iNOS and NO in intestinal tissue (P < 0.001). All the above-mentioned parameters in the three-HBOT group were better than those in one-HBOT group, but the difference was not significant (P > 0.05). Conclusions HBO decreases the production of inflammatory factors, inhibits the excessive inflammatory reaction to T/HS, and prevents the mucosal barrier of intestine from I/R injury after resuscitation from T/HS.