RT Journal Article
SR Electronic
T1 Elevated exhaled nitric oxide in patients with hepatopulmonary syndrome
JF European Respiratory Journal
JO Eur Respir J
FD European Respiratory Society
SP 1883
OP 1885
DO 10.1183/09031936.95.08111883
VO 8
IS 11
A1 G Cremona
A1 TW Higenbottam
A1 V Mayoral
A1 G Alexander
A1 E Demoncheaux
A1 C Borland
A1 P Roe
A1 GJ Jones
YR 1995
UL http://erj.ersjournals.com/content/8/11/1883.abstract
AB The hypoxaemia of hepatopulmonary syndrome, seen in severe chronic liver dysfunction, occurs as a result of precapillary pulmonary arterial dilatation and arteriovenous communications. These abnormalities contribute to the mismatch between ventilation and perfusion, and the right to left blood flow shunting. Nitric oxide (NO) is a powerful vasodilator concerned with the regulation of pulmonary vascular tone in man. Using a chemiluminescence analyser, we have measured endogenously produced NO in the exhaled air of three patients with the hepatopulmonary syndrome, six normoxaemic cirrhotic patients and six healthy volunteers. The subjects breathed NO-free air throughout the measurements. The molar rate of production of exhaled NO was raised almost threefold in the patients with hepatopulmonary syndrome compared with normal volunteers and with normoxaemic cirrhotic patients. Hypoxia per se, achieved in the normal volunteers by breathing a hypoxic gas mixture, reduced rather than increased the exhaled NO. One hepatopulmonary syndrome patient received an orthotopic liver transplant and achieved normoxaemia after 3 months. The exhaled NO also returned to normal. Increased pulmonary production of NO could contribute to the development of the hepatopulmonary syndrome.