Leister Ingo, Sydow J, Stojanovic T, Füzesi L, Sattler B, Heuser M, Becker H, Markus P M
Department of General Surgery, Georg August University, Robert-Koch-Strasse 40, 37099 Göttingen, Germany.
Int J Colorectal Dis. 2005 Jan;20(1):42-8. doi: 10.1007/s00384-004-0610-8. Epub 2004 Jul 27.
Alterations in microvascular perfusion of the intestine after hepatic ischemia/reperfusion have been suggested as an important cause of postoperative septic complications. We therefore investigated small bowel microcirculation and mucosal injury after liver ischemia/reperfusion in a rat model. Furthermore, we analyzed the effects of the regulatory peptides vasoactive intestinal polypeptide and gastrin-releasing peptide for their splanchnic vasoactivity.
Hepatic ischemia was induced by clamping of the left hepatic artery and vein for 40 min, followed by 60 min of reperfusion. The control group was treated similarly, but without clamping of the liver vessels. Ten minutes after clamping of the hepatic vessels, vasoactive intestinal polypeptide or gastrin-releasing peptide, respectively, were continuously infused intravenously in the experimental groups. Small bowel microcirculation and mucosal injury were assessed using intravital microscopy and the Chiu-score, respectively.
The functional capillary density of the small intestine following ischemia and reperfusion of the left hepatic lobe significantly decreased compared to normal controls in both the mucosa and the smooth intestinal muscle. Red blood cell velocity decreased, whereas leukocyte-endothelium adherence, stasis index and the mucosal injury score increased. Administration of vasoactive intestinal polypeptide resulted in an increase of functional capillary density in the mucosa and of the red blood cell velocity and a decrease in the stasis index. The mucosal injury score was significantly higher in reperfused animals without treatment. The application of gastrin-releasing peptide resulted in an isolated increase of the red blood cell velocity. Leukocyte adherences could not be altered by the regulatory peptides.
We conclude that hepatic ischemia/reperfusion injury leads to significant alterations of small bowel microcirculation and mucosal injury. Vasoactive intestinal polypeptide and gastrin-releasing peptide attenuate the damage in a different manner.
肝缺血/再灌注后肠道微血管灌注的改变被认为是术后感染性并发症的重要原因。因此,我们在大鼠模型中研究了肝缺血/再灌注后的小肠微循环和黏膜损伤。此外,我们分析了调节肽血管活性肠肽和胃泌素释放肽对内脏血管活性的影响。
通过夹闭左肝动脉和静脉40分钟诱导肝缺血,随后再灌注60分钟。对照组进行类似处理,但不夹闭肝脏血管。在夹闭肝脏血管10分钟后,分别在实验组中持续静脉输注血管活性肠肽或胃泌素释放肽。分别使用活体显微镜和Chiu评分评估小肠微循环和黏膜损伤。
与正常对照组相比,左肝叶缺血再灌注后小肠黏膜和肠平滑肌的功能性毛细血管密度显著降低。红细胞速度降低,而白细胞-内皮细胞黏附、血流淤滞指数和黏膜损伤评分增加。给予血管活性肠肽可导致黏膜功能性毛细血管密度增加、红细胞速度增加以及血流淤滞指数降低。未治疗的再灌注动物的黏膜损伤评分显著更高。应用胃泌素释放肽可使红细胞速度单独增加。调节肽不能改变白细胞黏附。
我们得出结论,肝缺血/再灌注损伤导致小肠微循环和黏膜损伤的显著改变。血管活性肠肽和胃泌素释放肽以不同方式减轻损伤。