Johnston T D, Fischer R, Chen Y, Reed R L
Department of Surgery, University of Texas Medical School at Houston 77030.
J Trauma. 1993 Oct;35(4):508-11.
Gut ischemia/reperfusion (I/R) appears to produce pulmonary vascular injury through endotoxin release and cytokine activation. The ability of hepatic reticuloendothelial cells to clear bacterial products may also be impaired during I/R. To test this, diversion of the splanchnic blood flow from the liver into the systemic circulation was performed via a microsurgical portacaval transposition in anesthetized Sprague-Dawley rats (275-375 g). Shunted animals underwent portacaval transposition and were allowed to recover for 7-10 days; sham animals underwent exploration but no shunt was created. The I/R animals were subjected to 60 minutes of reperfusion. All shunts were patent at autopsy. Pulmonary vascular permeability was assessed by measuring tissue retention of Evans blue dye. Gut I/R produced significant increases in pulmonary vascular permeability (46.2% +/- 11.0% vs. 16.4% +/- 3.8% [I/R vs. control]; p < 0.05) regardless of the presence of hepatic bypass (32.7% +/- 9.0% vs. 10.0% +/- 1.4% [I/R vs. control]; p < 0.05). These data indicate that a mediator or mediators of gut origin are responsible for pulmonary vascular permeability changes following gut I/R and are not appreciably modulated by the liver.
肠缺血/再灌注（I/R）似乎通过内毒素释放和细胞因子激活导致肺血管损伤。在I/R期间，肝网状内皮细胞清除细菌产物的能力也可能受损。为了验证这一点，通过显微手术门静脉-腔静脉转位，将内脏血流从肝脏转移至体循环，实验对象为麻醉状态下的Sprague-Dawley大鼠（体重275 - 375克）。分流组动物接受门静脉-腔静脉转位手术，并恢复7 - 10天；假手术组动物仅进行探查，但不进行分流。I/R组动物接受60分钟的再灌注。尸检时所有分流均通畅。通过测量伊文思蓝染料在组织中的潴留量评估肺血管通透性。无论是否存在肝分流，肠I/R均显著增加肺血管通透性（46.2%±11.0% vs. 16.4%±3.8% [I/R组 vs. 对照组]；p < 0.05）（32.7%±9.0% vs. 10.0%±1.4% [I/R组 vs. 对照组]；p < 0.05）。这些数据表明，肠道来源的一种或多种介质是肠I/R后肺血管通透性变化的原因，且不受肝脏的明显调节。
