Ackerman Zvi, Karmeli Fanny, Cohen Patrizia, Rachmilewitz Daniel
Department of Medicine, Hadassah University Hospital, Mount Scopus, Jerusalem, Israel.
Inflamm Bowel Dis. 2003 Jan;9(1):18-24. doi: 10.1097/00054725-200301000-00003.
Within the colonic mucosa of rats with portal hypertension and liver cirrhosis, there is an increased generation of inflammatory mediators, such as leukotriene B4 and endothelin-1, and increased generation of nitric oxide. Nitric oxide overproduction may induce tissue injury. This study was undertaken to assess whether the colonic mucosa of rats with portal hypertension and liver disease have increased susceptibility to damage by noxious agents. In this study, acetic acid colitis was induced in rats with portal vein ligation and in control groups, and iodoacetamide colitis was induced in rats with partial portal vein ligation and cirrhosis due to bile duct ligation and in control groups. Rats with acetic acid colitis and those with iodoacetamide-induced colitis were studied 24 and 72 hours, respectively, after induction of colitis. Portal hypertension alone and portal hypertension with cirrhosis were present in the portal vein ligation and bile duct ligation models, respectively. In the rats with acetic acid, colitis lesion area, colonic mucosal myeloperoxidase activity, and prostaglandin E2 generation were not different between the portal vein ligation groups with and without colitis. Nitric oxide activity was higher only in the groups with colitis, irrespective of the presence of portal hypertension. In the group of rats with iodoacetamide colitis, colonic lesion area and colonic mucosal myeloperoxidase activity were similar in all groups with colitis. Colonic mucosal prostaglandin E2 generation was lower in the portal vein ligation and bile duct ligation rats with colitis compared with a control group. We concluded that rats with experimental portal hypertension do not have increased damage when induced by either acetic acid or iodoacetamide.
在门静脉高压和肝硬化大鼠的结肠黏膜中，炎性介质如白三烯B4和内皮素-1的生成增加，一氧化氮的生成也增加。一氧化氮产生过多可能导致组织损伤。本研究旨在评估门静脉高压和肝病大鼠的结肠黏膜对有害剂损伤的易感性是否增加。在本研究中，对门静脉结扎大鼠和对照组诱导乙酸结肠炎，对部分门静脉结扎和胆管结扎致肝硬化大鼠及对照组诱导碘乙酰胺结肠炎。分别在诱导结肠炎后24小时和72小时对乙酸结肠炎大鼠和碘乙酰胺诱导的结肠炎大鼠进行研究。门静脉结扎模型和胆管结扎模型分别存在单纯门静脉高压和门静脉高压合并肝硬化的情况。在乙酸结肠炎大鼠中，有无结肠炎的门静脉结扎组之间的结肠病变面积、结肠黏膜髓过氧化物酶活性和前列腺素E2生成无差异。无论是否存在门静脉高压，一氧化氮活性仅在结肠炎组中较高。在碘乙酰胺结肠炎大鼠组中，所有结肠炎组的结肠病变面积和结肠黏膜髓过氧化物酶活性相似。与对照组相比，门静脉结扎和胆管结扎的结肠炎大鼠结肠黏膜前列腺素E2生成较低。我们得出结论，实验性门静脉高压大鼠在受到乙酸或碘乙酰胺诱导时，损伤不会增加。
