血红素氧合酶-内源性一氧化碳对感染性休克大鼠死亡率的影响

Effects of heme oxygenase-endogenous carbon monoxide on mortality during septic shock in rats

目的探讨血红素氧合酶-内源性一氧化碳（HO-CO）对感染性休克大鼠死亡率的影响。方法80只健康清洁级Sprague-Dawley大鼠随机分为4组（n=20）对照（C）组，感染性休克（SS）组，LPS＋ZnPP-IX（LZ）组和ZnPP-IX（Z）组。连续监测MAP；记录大鼠7h内的死亡率；检测血中COHb，ALT，AST，Cr，Bun，肾、肝和肺脏MDA与SOD，肺脏Evans blue含量以及肝、肺、肾和股动脉血管组织HO-1 mRNA，HO-2 mRNA及HO-1，HO-2蛋白水平。数据比较采用方差分析：结果①SS组7h内死亡率低于LZ组（P〈0．05）。②LZ组MAP水平均高于SS组（P〈0．05）。③SS组ALT，ASF，Cr，Bun，肝、肾和肺脏MDA及肺脏Evans blue含量均分别低于LZ组（P〈0．05）；SS组肝、肾和肺脏SOD及全血COHb均分别高于LZ组（P〈0．05）。④LZ组肝、肺、肾和股动脉血管组织内HO-1 mRNA及HO-1蛋白水平均分别低于SS组（P〈0．05），4组间HO-2 mRNA及HO-2蛋白水平差异无统计学意义（P〉0．05）。结论HO-1蛋白水平的上调及随后CO的增加可减少感染性休克大鼠的死亡率，但是由于其所致的低血压并没有明显增加其死亡率。

Objective To investigate the effects of hemo oxygenase-endogenous carbon monoxide （HO-CO） on mortality of septic shock in rats Method Eight）, heahhy Sprague-Dawley rats were randomly divided into four groups （n = 20） ：group-C, group-Z, group-SS and group-LZ. MAP was monitored continuously, and deaths within 7 days were recorded. Evans blue in lung, ALT, Asr, Cr and BUN in plasma, SOD and MDA in kidney, lung and liver, and HO-1 mRNA, HO-2 mRNA, HO-1 protein and HO-2 protein in kidney, lung, femoral artery and liver were measured. Data were analyzed usiny ANOVA. Results （1） Mortality in group-SS was lower than that in group-LZ （ P 〈 0.05）. （2）MAP in group-LZ was greater than that in group-SS （ P 〈 0.05）. （3） Plasma ALT, AST, Cr and BUN, and MDA contents of liver, kidney and lung, and Evans blue content of lung in group-SS were lower than those in group-LZ （ P 〈 0.05）. Contrarily, the plasma levels of COHh and SOD activity in liver, kidney and lung in grnup-SS were greater than those in group-LZ （P 〈 0.05）. （4） HO-1 mRNA and HO-1 protein levels in liver, kidney, fenroral artery and lung tissues in group-LZ were lower than those in group-SS （P 〈 0.05）. There were no significant difference in HO-2 mRNA and HO-2 protein found between one another of four groups （ P 〉 0.05）. Conclusions The up-regulation of HO-1 protein followed by increase CO can reduce the mortality during septic shock, while the hypotension, which is partly attributed to HO- 1 protein and CO, matters little to mortality.