Institute of Microcirculation, Hebei North University, Hebei, Zhangjiakou 075029, China.
Ren Fail. 2010 Jun;32(5):584-91. doi: 10.3109/08860221003778031.
The kidney is a common target in multiple organ dysfunction syndrome (MODS). The aim of this study is to determine the role of intestinal lymphatic pathway on renal injury in hemorrhagic shock rats.
Wistar rats were divided into sham, shock, and ligation groups. The hemorrhagic shock model was induced in the shock and ligation groups. After resuscitation, the mesenteric lymph ducts were ligated in the ligation group. Blood from the carotid artery was taken to determine renal functional indices. The kidneys were used to observe histomorphological changes at 6 h after resuscitation. In addition, kidney homogenate was used to determine malondialdehyde (MDA), superoxide dismutase (SOD), tumor necrosis factor alpha (TNFalpha), interleukin-6 (IL-6), and myeloperoxidase (MPO) levels at 90 min after shock and 0, 1, 3, 6, 12, and 24 h after resuscitation. And the survival rate of 24 h was recorded.
The survival rate in shock group was obviously lower than sham and ligation groups. The urea and creatinine contents in the serum of shock and ligation groups were significantly higher than the sham group; the indices in the ligation group were significantly lower than the shock group. Histological studies showed various degrees of renal injury in the shock and ligation groups with a lesser severity in the ligation group. MDA, TNFalpha, IL-6, and MPO in renal homogenate of the shock group were raised, and the activity of SOD was lower in comparison to the sham group. Further, MDA, TNFalpha, IL-6, and MPO in renal homogenate of the ligation group at 6, 12, and 24 h were lower, and the SOD activity was higher than that of the shock group at the same time points.
The mesenteric lymph duct ligation could be used to attenuate renal injury in shock rats. Its mechanism might be related to reducing the polymorph nuclear (PMN) and decreasing inflammatory mediator and free radical.
肾脏是多器官功能障碍综合征(MODS)的常见靶器官。本研究旨在确定肠淋巴途径在出血性休克大鼠肾损伤中的作用。
将 Wistar 大鼠分为假手术组、休克组和结扎组。休克组和结扎组诱导出血性休克模型。复苏后,结扎组结扎肠系膜淋巴管。从颈总动脉取血,测定肾功能指标。复苏后 6 h 观察肾脏组织形态学变化。此外,还测定了肾匀浆丙二醛(MDA)、超氧化物歧化酶(SOD)、肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)和髓过氧化物酶(MPO)水平,分别在休克后 90 min 和复苏后 0、1、3、6、12 和 24 h 时。并记录 24 h 的存活率。
休克组的存活率明显低于假手术组和结扎组。休克组和结扎组血清尿素氮和肌酐含量明显高于假手术组;结扎组指标明显低于休克组。组织学研究表明,休克组和结扎组均有不同程度的肾损伤,结扎组损伤程度较轻。休克组肾匀浆 MDA、TNF-α、IL-6 和 MPO 升高,SOD 活性降低,与假手术组比较。进一步的,在相同时间点,结扎组肾匀浆 MDA、TNF-α、IL-6 和 MPO 在 6、12 和 24 h 时较低,SOD 活性较高。
肠系膜淋巴管结扎可减轻休克大鼠的肾损伤。其机制可能与减少多形核白细胞(PMN)和减少炎症介质和自由基有关。