Shijo H, Sasaki H, Miyajima Y, Okumura M
First Department of Internal Medicine, School of Medicine, Fukuoka University, Japan.
Chest. 1991 Sep;100(3):873-5. doi: 10.1378/chest.100.3.873.
We treated a 68-year-old man with cirrhosis of the liver associated with moderate hypoxemia. Contrast-enhanced echocardiography revealed late opacification of the left ventricle, and pulmonary perfusion imaging with 99mTc macroaggregated albumin showed evidence of a significant uptake in both lungs and in the liver, spleen, and kidneys. Right cardiac catheterization revealed pulmonary hypotension, low pulmonary vascular resistance, and high cardiac output. We administered prostaglandin F2 alpha intravenously (0.2 microgram/kg/min for 30 minutes) and indomethacin orally (75 mg/day for three days). There was some degree of resolution of the hypoxemia and increases in both pulmonary arterial pressure and pulmonary vascular resistance. These findings suggest that the pathophysiology of hepatogenic pulmonary angiodysplasia is a reversible intrapulmonary vascular dilatation. These conditions can to some extent be modulated by vasoactive substances such as prostaglandins or other eicosanoids.
我们治疗了一名68岁患有肝硬化并伴有中度低氧血症的男性患者。对比增强超声心动图显示左心室延迟显影，用99mTc标记的大颗粒白蛋白进行肺灌注显像显示双肺以及肝脏、脾脏和肾脏均有明显摄取。右心导管检查显示肺动脉低血压、低肺血管阻力和高心输出量。我们静脉注射前列腺素F2α（0.2微克/千克/分钟，持续30分钟）并口服吲哚美辛（75毫克/天，持续三天）。低氧血症有一定程度的缓解，肺动脉压和肺血管阻力均升高。这些发现提示肝源性肺血管扩张症的病理生理学机制是一种可逆性的肺内血管扩张。这些情况在一定程度上可由前列腺素或其他类二十烷酸等血管活性物质调节。
