Departamento de Fisiología, Facultad de Medicina, Universidad Autónoma de Nuevo León, Monterrey, Nuevo León/México.
Clinics (Sao Paulo). 2013 Jul;68(7):1034-8. doi: 10.6061/clinics/2013(07)23.
It is essential to identify a serological marker of injury in order to study the pathophysiology of intestinal ischemia reperfusion. In this work, we studied the evolution of several serological markers after intestinal ischemia reperfusion injury in rats. The markers of non-specific cell damage were aspartate aminotransferase, alanine aminotransaminase, and lactic dehydrogenase, the markers of inflammation were tumor necrosis factor alpha, interleukin-6, and interleukin-1 beta, and the markers of intestinal mucosal damage were intestinal fatty acid binding protein and D-lactate. We used Chiús classification to grade the histopathological damage.
We studied 35 Wistar rats divided into groups according to reperfusion time. The superior mesenteric artery was clamped for 30 minutes, and blood and biopsies were collected at 1, 3, 6, 12, 24, and 48 hours after reperfusion. We plotted the mean ± standard deviation and compared the baseline and maximum values for each marker using Student's t-test.
The maximum values of interleukin-1 beta and lactic dehydrogenase were present before the maximal histopathological damage. The maximum tumor necrosis factor alpha and D-lactate expressions coincided with histopathological damage. Alanine aminotransaminase and aspartate aminotransferase had a maximum expression level that increased following the histopathological damage. The maximum expressions of interluken-6 and intestinal fatty acid binding protein were not significantly different from the Sham treated group.
For the evaluation of injury secondary to acute intestinal ischemia reperfusion with a 30 minute ischemia period, we recommend performing histopathological grading, quantification of D-lactate, which is synthesized by intestinal bacteria and is considered an indicator of mucosal injury, and quantification of tumor necrosis factor alpha as indicators of acute inflammation three hours after reperfusion.
确定肠缺血再灌注损伤的血清学标志物对于研究其病理生理学机制至关重要。在本研究中，我们研究了大鼠肠缺血再灌注损伤后几种血清标志物的变化。非特异性细胞损伤标志物包括天冬氨酸氨基转移酶、丙氨酸氨基转移酶和乳酸脱氢酶，炎症标志物包括肿瘤坏死因子-α、白细胞介素-6 和白细胞介素-1β，肠黏膜损伤标志物包括肠脂肪酸结合蛋白和 D-乳酸。我们采用 Chiús 分级法对组织病理学损伤进行分级。
我们研究了 35 只 Wistar 大鼠，根据再灌注时间分为不同组。夹闭肠系膜上动脉 30 分钟，分别于再灌注后 1、3、6、12、24 和 48 小时采集血液和活检标本。我们绘制平均值±标准差，并使用 Student's t 检验比较每个标志物的基础值和最大值。
白细胞介素-1β和乳酸脱氢酶的最大值出现在最大组织病理学损伤之前。肿瘤坏死因子-α和 D-乳酸的最大值与组织病理学损伤一致。丙氨酸氨基转移酶和天冬氨酸氨基转移酶的最大表达水平随着组织病理学损伤而增加。白细胞介素-6 和肠脂肪酸结合蛋白的最大表达水平与 Sham 治疗组无显著差异。
对于缺血 30 分钟引起的急性肠缺血再灌注损伤的评估，我们建议在再灌注后 3 小时进行组织病理学分级、D-乳酸（由肠道细菌合成，被认为是黏膜损伤的指标）定量以及肿瘤坏死因子-α定量，作为急性炎症的指标。
