Experimental study on the correlation of nitric oxide with portal hypertensive enteropathy.

To explore the role of nitric oxide (NO) in the pathogenesis of portal hypertensive enteropathy (PHE), cirrhotic portal hypertension was induced in Wistar rats by subcutaneous administration of carbon tetrachloride. At the end of 12th week, NADPH-diaphorase staining was performed on ice frozen sections with the sample of fresh colonic tissues. NO synthase (NOS) activities and NOS mRNA expression of colonic tissues were investigated with chemoluminescence method and reverse transcription-polymerase chain reaction (RT-PCR), respectively. After NADPH-diaphorase histochemical staining, the computer image analysis and paired t test showed that NOS staining intensities of submucosal vascular endothelial cells and nerve fibers were all significantly higher in PHE group than those in normal group (P < 0.01 and P < 0.05, respectively), but the intensities of superficial epithelial cells were significantly lower than those of controls (P < 0.01). Chemoluminescence method demonstrated that general NOS activity of colonic mucosa was significantly higher in PHE group than that in control group (P < 0.01). Moreover, the degree of iNOS activity increase was greater than that of cNOS (104% vs 35%). RT-PCR revealed that NOS mRNA expressions were dramatically higher in PHE group than those in control group (P < 0.01). The results suggested that NO, with its property of vasodilatation, may be involved in the pathogenesis of vascular lesions of PHE in cirrhotic rats, and may also has something to do with mucosal lesions of colon in PHE.