DIAGNOSTIC & PROGNOSTIC VALUE OF \: RENAL RESISTIVE INDEX AND SERUM NITRIC OXIDE LEVEL IN CIRRHOTIC PATIENTS WITH ASCITES

Abstract

The existence of cirrhosis causes marked structural abnormalities in the liver which results in a severe disturbance in the hepatic and splanchnic circulation. (I) Cirrhosis of the liver is a process of progressive destruction and ' regeneration of the hepatic parenchyma characterized by increased connective tissue deposition and marked distortion of parenchyma and vascular architecture and hence hepatic venous outflow obstruction. 2

Portal Hypertension

Portal hypertension in cirrhosis is a pathological increase in portal pressure. This increase is due to an increased portal blood flow together with an increased intrahepatic resistance. (3

The resistance in the liver is increased by two main mechanisms: 1. An obstructive process; nodules, fibrosis, or thrombosis whose site may be sinusoidal and/or postsinusoidal. 3

2. An increase in vascular tone, which is reversible. ( 4

Hepatic stellate cells

may contribute to the regulation or modulation of intrahepatic resistance. (S) Vascular biology is centered on the vascular endothelium, which synthesizes vasoactive substances. (6) The increased vascular tone in the liver in cirrhosis could exist by any combination of decreased vasodilators, increased vasoconstrictors or both. There are some evidences for decreased nitric oxide and increased responsiveness to endothelins in cirrhotic patients. (?, S) In addition to the increase m intrahepatic resistance, there is also an increase in portosystemic collateral resistance. It is likely that nitric oxide may be the principle factor initiating collateralization of the portal system probably by increasing the splanchnic flow and this opens up pre-formed channels. < )