Expression of Inducible Nitric Oxide Synthase mRNA in Esophageal Varix and Congestive Gastropathy Secondary to Portal Hypertension

Roe, Im Hwan; Song, Il Han; Chin, Young Joo; Lim, Chang Young; Kim, Jung Weon; Choi, Jeong

Abstract

BACKGROUND AND AIMS: Chronic portal hypertension is associated with hyperdynamic splanchnic circulation, leading to collateralization of portal system and bleeding of gastrointestinal tracts. Nitric oxide (NO) induced by NO synthase (NOS) is endothelium-derived relaxing factor. Constitutive NOS (cNOS) is normally present in vascular endothelia and produces NO in response to physiologic stimuli. On the other hand, inducible NOS (iNOS) induces NO in response to bacterial endotoxins and cytokines. In addition, the endotoxemia is frequently observed in portal hypertension. Thus, to clarify the role of NO in development of esophageal varix and congestive gastropathy in patients with portal hypertension by measuring the expression of iNOS mRNA, we carried out this study.
METHODS
We compared the expression of iNOS mRNA in esophageal variceal and congestive gastric mucosa of 16 patients with portal hypertension with that in distal esophageal and gastric mucosa of 10 normal controls. The expression of iNOS mRNA was measured using reverse transcription-polymerase chain reaction (RT-PCR) in biopsied esophageal variceal and congestive gastric mucosa after endoscopic variceal ligation.
RESULTS
There was no expression of iNOS mRNA in distal esophageal and gastric mucosa of normal controls. In the 16 patients with portal hypertension, the expression of iNOS mRNA of esophageal variceal and congestive gastric mucosa was observed in 9 (56.3%) and 8 (50%) patients, respectively. Additionally, in all cases except one, iNOS gene was concurrently expressed in both variceal and congestive gastric mucosa. There was no difference in biochemical data and endoscopic finding between the patients with or without iNOS mRNA expression.
CONCLUSIONS
The iNOS mRNA was activated in some patients with portal hypertension. Thus, we suggest that NO induced by iNOS may be associated with hyperdynamic circulation and development of collaterals in these patients.