AUGMENTED ENDOGENOUS NITRIC OXIDE PRODUCTION IN PARTIAL PORTAL VEIN‐LIGATED RATS

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Abstract
SUMMARY: 1. Endothelium‐derived nitric oxide (NO) is a potent vasodilator. Because the body oxidizes it to nitrate ions, NO3‐, measurement of the serum concentration and the urinary excretion of NO3‐ may be an index for endogenous NO. We investigated the role of NO on hyperdynamic circulation in cirrhotic and partial portal vein‐ligated rats by measuring NO3.2. Liver cirrhosis was induced by administration of thioacetamide. Systemic and splanchnic haemodynamics and splenic‐systemic shunting were determined by tracer microspheres. The concentration of NO3‐ was measured by using high‐performance liquid chromatography with an anion‐column.3. We found that systemic and splanchnic hyperdynamic circulation existed to almost the same extent in cirrhotic and in portal vein‐ligated rats as compared to the controls and sham‐operated rats, respectively. Splenic‐systemic shunting was markedly greater in portal vein‐ligated rats than in cirrhotic rats.4. Serum NO3‐ levels and urinary excretion of NO3‐ in cirrhotic rats tended to increase as compared to the controls. On the other hand, the levels in portal vein‐ligated rats were significantly increased as compared to those of the sham‐operated rats, and were significantly and negatively correlated to the splanchnic arterial resistance and total vascular resistance. The amount of urinary excretion of NO3‐ significantly correlated to splenic‐systemic shunting (r = 0.61, P3‐ in portal vein‐ligated rats relate to the extensive formation of porto‐collateral vasculature or acute changes in systemic and splanchnic haemodynamics due to portal vein‐ligation.