Hypothesis The mechanisms underlying the 'hyperdynamic circulation' of cirrhosis remain unclear. Excess production of endogenous carbon monoxide (CO) which has recently been described as a vasodilator, may have a role in the circulatory disturbance of cirrhosis. Methods We measured carboxyhaemoglobin (COHb) and plasma cyclic guanylmonophosphate (cGMP) in 22 patients (11 M, mean age 53yr) with cirrhosis and 9 healthy controls (mean age 50yr). All were nonsmokers or abstinent for 14 days. Results COHb was elevated in patients (2.1 ± 0.3%), compared to controls (0.9 ± 0.1%; p = 0.005). Nine patients who underwent elective transjugular intrahepatic portosystemic stent shunting (TIPSS) had high initial COHB levels (3.1 ± 0.4% p = 0.002). However, two weeks after TIPSS, COHb had risen further (4.3 ± 0.3% p = 0.02). Total haemoglobin concentrations were similar in all groups. Simultaneous plasma cGMP levels correlated with COHb (r = 0.72, p = 0.003). Conclusions We have demonstrated that excess endogenous CO production occurs in the vasodilated state of cirrhosis and correlates with a marker of vasodilator tone (cGMP). This supports the hypothesis that CO may be a mediator of the vasodilatation of chronic liver disease.
|Number of pages||4|
|Publication status||Published - Dec 1998|
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