Niu Chun-yu, Li Ji-cheng, Zhao Zi-gang, Chen Rui-hua, Zhang Jing, Liu Yan-kai, Zhang Yu-ping, Jiang Hua
Department of Pathophysiology, Hebei North University, Zhangjiakou 075029, Hebei, China.
Zhongguo Wei Zhong Bing Ji Jiu Yi Xue. 2006 Sep;18(9):527-30.
To observe the effect of mesenteric lymph duct ligation on nitric oxide (NO) and its expression in lung in rats with serious hemorrhagic shock at different periods, and explore the role of intestinal lymphatic pathway in acute lung injury (ALI).
Seventy-eight male Wistar rats were randomly divided into the sham operation group (n=6), shock group (n=42), and ligation group (n=30). The model of serious hemorrhagic shock was reproduced in shock group and ligation group. Mesenteric lymph was diverted by ligating mesenteric lymph duct in ligation group after resuscitation. All rats were executed and their lungs were harvested. NO and nitric oxide synthase (NOS) were determined in lung homogenate 90 minutes after shock, and 0, 1, 3, 6, 12 and 24 hours after resuscitation. The expression of inducible nitric oxide synthase (iNOS) mRNA was detected by reverse transcription-polymerase chain reaction (RT-PCR).
The content of NO, activity of NOS and expression of iNOS mRNA in lung tissue in shock group were increased 3 hours after transfusion and resuscitation, and they became higher 6-12 hours after resuscitation. The values were significantly higher than those in sham operation group, 90 minutes after shock and 0 hour after transfusion and resuscitation (P<0.05 or P<0.01). The values were only increased 3 hours and 6 hours after transfusion and resuscitation, and all the values on 6, 12 and 24 hours after resuscitation were significantly lower in the ligation group compared with those in shock group at the same time points (P<0.01 or P<0.05).
The results demonstrate that the ligation of mesenteric lymph duct could reduce the NO and expression of iNOS mRNA in the lung tissue, thus ameliorate ALI in rats with serious hemorrhagic shock. Mesenteric lymph might play an important role in the pathogenesis of ALI.
观察肠系膜淋巴管结扎对严重失血性休克大鼠不同时期肺组织中一氧化氮(NO)及其表达的影响,探讨肠道淋巴途径在急性肺损伤(ALI)中的作用。
78只雄性Wistar大鼠随机分为假手术组(n = 6)、休克组(n = 42)和结扎组(n = 30)。休克组和结扎组复制严重失血性休克模型。结扎组在复苏后通过结扎肠系膜淋巴管引流肠系膜淋巴。处死所有大鼠并取肺组织。于休克后90分钟以及复苏后0、1、3、6、12和24小时测定肺匀浆中的NO和一氧化氮合酶(NOS)。采用逆转录-聚合酶链反应(RT-PCR)检测诱导型一氧化氮合酶(iNOS)mRNA的表达。
休克组肺组织中NO含量、NOS活性及iNOS mRNA表达在输血复苏后3小时升高,复苏后6 - 12小时更高。这些值显著高于假手术组、休克后90分钟以及输血复苏后0小时(P < 0.05或P < 0.01)。结扎组仅在输血复苏后3小时和6小时升高,复苏后6、12和24小时的所有值与休克组同时点相比均显著降低(P < 0.01或P < 0.05)。
结果表明,结扎肠系膜淋巴管可降低肺组织中NO含量及iNOS mRNA表达,从而改善严重失血性休克大鼠的ALI。肠系膜淋巴可能在ALI发病机制中起重要作用。