ELEVATED EXHALED NITRIC-OXIDE IN PATIENTS WITH HEPATOPULMONARY SYNDROME

The hypoxaemia of hepatopulmonary syndrome, seen in severe chronic liv er dysfunction, occurs as a result of precapillary pulmonary arterial dilatation and arteriovenous communications, These abnormalities contr ibute to the mismatch between ventilation and perfusion, and the right to left blood now shunting, Nitric oxide (NO) is a powerful vasodilat or concerned with the regulation of pulmonary vascular tone in man. Us ing a chemiluminescence analyser, we have measured endogenously produc ed NO in the exhaled air of three patients with the hepatopulmonary sy ndrome, six normoxaemic cirrhotic patients and six healthy volunteers. The subjects breathed NO-free air throughout the measurements The mol ar rate of production of exhaled NO was raised almost threefold in the patients with hepatopulmonary syndrome compared with normal volunteer s and with normoxaemic cirrhotic patients, Hypoxia per se, achieved in the normal volunteers by breathing a hypoxic gas mixture, reduced rat her than increased the exhaled NO, One hepatopulmonary syndrome patien t received an orthotopic Liver transplant and achieved normoxaemia aft er 3 months, The exhaled NO also returned to normal. Increased pulmona ry production of NO could contribute to the development of the hepatop ulmonary syndrome.