Cremona G, Higenbottam T W, Mayoral V, Alexander G, Demoncheaux E, Borland C, Roe P, Jones G J
Dept of Respiratory Physiology, Addenbrookes Hospital, Cambridge, UK.
Eur Respir J. 1995 Nov;8(11):1883-5. doi: 10.1183/09031936.95.08111883.
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.
肝肺综合征的低氧血症见于严重慢性肝功能不全，是由肺前毛细血管动脉扩张和动静脉分流所致。这些异常导致通气与灌注不匹配以及右向左的血流分流。一氧化氮（NO）是一种强效血管舒张剂，参与人体肺血管张力的调节。我们使用化学发光分析仪，测量了3例肝肺综合征患者、6例血氧正常的肝硬化患者和6例健康志愿者呼出气体中内源性产生的NO。在整个测量过程中，受试者呼吸不含NO的空气。与正常志愿者和血氧正常的肝硬化患者相比，肝肺综合征患者呼出NO的摩尔生成率几乎提高了两倍。正常志愿者通过呼吸低氧混合气体造成低氧状态后，呼出的NO减少而非增加。1例肝肺综合征患者接受了原位肝移植，3个月后血氧恢复正常，呼出的NO也恢复了正常。肺内NO生成增加可能促使肝肺综合征的发生。
