ABSTRACT
Circulatory abnormalities arising in cirrhosis increased cardiac output and, possibly, heart rate coupled with reduced systemic vascular resistance, and possibly arterial pressure could result from peripheral vasodilatation. The locally acting vasodilator nitric oxide has recently been implicated as a possible mediator in the vasodilatation observed in cirrhosis. To investigate this hypothesis, total of 51 patients with liver cirrhosis were recruited in the present investigation, 14 had hyperdynamic circulation [HDC] and 37 had no manifestations of HDC the study also included 20 completely healthy controls. In each participant, serum and urinary nitric oxide [NO], urinary cyclic guanosine monophosphate [cGMP] excretions, serum endotoxin and C-reactive protein were determined. The study revealed significantly increased levels of serum NO, endotoxin and C-reactive protein as well as urinary excretions of NO and cGMP in patients with cirrhosis compared with controls. Patients with HDC had significant increase of all bioindices expcept C-reactive protein. Significant positive correlation existed between urinary CGMP, urinary NO, serum NO, endotoxin C-reactive protein. These findings would indicate that bacterial endotoxin rather than cytokines induce NO synthase expression in vessel walls with sustained NO release. The released NO through activation of guanylate cyclase, leads to increased intracellular cGMP concentrations and induces vasodilatation and hypotension. Inhibition of NO synthesis in these patients could be achieved by reduction of endotoxaemia through sterilization of the intestine. This would result in restoration of sensitivity to vasoconstrictors and reverse the haemodynamic abnormalities in liver cirrhosis