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Hepatopulmonary syndrome is a disease with abnormal gas exchange caused by liver diseases, with the feature of abnormal oxygenation caused by intrapulmonary vasodilation. This article introduces the pathogenesis, natural course, clinical manifestations, diagnostic methods, and therapeutic measures of this disease and discusses potential therapeutic measures besides liver transplantation.

Objective: To explore the mechanism of tanshinol on alleviate the inflammatory injury of lung tissue in rat hepatopulmonary syndrome (HPS)., Methods: SD rats were randomly divided into normal control group (n = 8), hepatopulmonary syndrome (HPS) group (n = 11) and tanshinol intervention group (n = 9). HE staining was used to observe the histopathology changes of pulmonary and hepatic tissues, and to count the number of macrophages in lung tissues. The activity of alanine transferase (ALT) and concentrations of endotoxin, tumor necrosis factor-a (TNF-alpha) and homocystein (Hcy) in plasma were detected. The concentrations of TNF-alpha, nitric oxide (NO) and malondialdehyde (MDA) and the activity of inducible nitric oxide synthase (iNOS) in the lung tissues were measured, respectively., Results: Thickened alveolar septum and increased macrophages were observed in lungs in HPS rat. After administered with tanshinol, the pulmonary pathological changes were alleviated and the number of macrophages in lung tissue was decreased compared with HPS group. The activity of ALT and the concentrations of endotoxin, TNF-alpha and Hcy in plasma ,and TNF-alpha, iNOS, NO and MDA in lung tissue in HPS group were higher than those of normal control group; meanwhile, those tanshinol group were less those that of HPS group., Conclusion: Tanshinol may play an important role in delaying the development of HPS through protecting liver or directly antagonizing the effect of intestinal endotoxemia so as to alleviate the inflammatory reaction in lung tissue.

Objective: To describe the clinical features and to highlight the main criteria for diagnosis of hepatopulmonary syndrome (HPS)., Methods: Twenty-three patients with HPS were retrospectively investigated., Results: Twenty-two cases had cirrhosis while one had acute hepatitis. The male to female ratio was 1.3:1, with an mean age of (42 +/- 21) years. 82.6% (19/23) of the patients were complicated with portal hypertension. The liver function of 78.2% of the cases was Child-Pugh grade B and C. The main clinical manifestations were dyspnea (91.3%), cyanosis (91.3%), liver palms (69.5%), clubbing fingers (65.1%), telangiectasis on face (56.5%), and spider angiomata (56.5%). The mean PaO(2) was (50.8 +/- 14.1) mm Hg (1 mm Hg = 0.133 kPa). Incidence of orthodeoxia was 85.7% (12/14). Mean diffusing capacity of lung function test was 43.1%. Chest X-ray was abnormal in 9 of the 39.1 (9/23) patients. Faint "mottled" shadows, nodular or reticulonodular opacities on bilateral lower zones were shown. All the 23 cases were diagnosed by radionuclide lung perfusion scanning technetium-labled macroaggregated albumin particles ((99m)Tc-MAA) and the mean shunt ratio was 36.3%., Conclusion: HPS is often associated with advanced Child-Pugh grade or portal hypertension. When "unexplained" hypoxaemia, portal hypertension, spider angiomata (or telangiectasis on face), or clubbing finger are present in these patients, HPS should be highly suspected. The presence of orthodeoxia is suggestive of HPS. (99m)Tc-MAA lung perfusion scanning is able to determine the presence of intrapulmonary shunting and the diagnosis of HPS.

Objective: To investigate the expression of ET-1 mRNA in the lung of rats with hepatopulmonary syndrome., Methods: Male Sprague-Dawley rats were divided into four groups: SO, IHPH, PHPH and PCS. Two weeks after production of rat models, all measurements were performed. Arterial blood gas was analyzed. The concentrations of NO and ET-1 in lungs were measured by using radioimmunoassay. In situ hybridization, ET-1 mRNA expressions were detected in lung tissue sections with digoxin-labeled ET-1 oligonucleotide probes. Liver and lung tissues and all the results of in situ hybridization were analyzed by one pathologist. At a magnification of 10 x 40, percent areas of positive stains were detected to indicate the expressions of ET-1 mRNA in the arteries, capillaries and branches., Results: Arterial blood gas analysis showed that PaO(2) (mmHg) decreased more significantly in IHPH (73.85 +/- 6.51) rats than in PHPH (97.39 +/- 1.33), PCS (95.23 +/- 2.22) and SO rats (99.05 +/- 0.75). Alveolar-arterial oxygen gradient (A-aG) (mmHg) increased more significantly in IHPH rats (32.99 +/- 6.57) than in PHPH (4.98 +/- 1.69), PCS (6.51 +/- 2.04) and SO rats (3.23 +/- 0.81). Changes of vascular active substance in plasma and lung indicated that the level of lung NO of IHPH (19.78 +/- 5.33) was increased significantly more than that of PHPH (13.21 +/- 3.99) and PCS (13.89 +/- 3.16). These levels in lung homogenate increased more significantly than those SO (8.71 +/- 1.68). The levels of ET-1 in IHPH rats (195.1 +/- 36.2) was significantly lower than in PHPH (234.8 +/- 71.0), PCS (240.4 +/- 66.5) and SO rats (271.8 +/- 40.6). ET-1 mRNA in situ hybridization showed that there was no significant difference in positive expression of ET-1 mRNA in alveolar arteries and small bronchi. The expression of ET-1 mRNA was significantly lower in alveolar capillary endothelia (5.12 +/- 1.27) than in PHPH (7.43 +/- 0.83), PCS (7.07 +/- 0.86) and SO (7.81 +/- 1.98) rats., Conclusion: The low expressions of ET-1 mRNA in HPS rat alveolar capillary endothelia accompanied by decreased ET-1 levels in lung may play an important role in the mechanism of HPS.