Journal of Capital Medical University ›› 2009, Vol. 30 ›› Issue (2): 222-226.

• 基础研究 • Previous Articles     Next Articles

Expression of Inducible Nitric Oxide Synthase and Heme Oxygenase-1 in Pulmonary Intravascular Macrophages of Rats with Hepatopulmonary Syndrome

GAO Jun1, WANG Yu2, ZHANG Zhong-tao2, LI Jian-she2, MA Xue-mei2, ZHAO Li-zhen3   

  1. 1. Department of Hepatobilary Surgery, Jingxi Area of Beijing Chaoyang Hospital, Capital Medical University;2. Department of General Surgery, Beijing Friendship Hospital, Capital Medical University;3. Department of Gastroenterology, First Hospital Affiliated to Baotou Medical University
  • Received:2008-02-18 Revised:1900-01-01 Online:2009-04-21 Published:2009-04-21

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Abstract: Objective To explore the role of pulmonary intravascular macrophages(PIM ) in the pathogenesis of hepatopulmonary syndrome(HPS). Methods Sprague-Dawley(SD) rats were divided into two test groups, control group and CCl4 group. Arterial blood was collected for measurement of blood gases, venous blood for hepatic function and endotoxin levels. Pathology of liver and lung was done. The mesenteric lymph nodes were dissected for bacteriology studies. Immunolocalization of macrophages was performed using monoclonal macrophage antibody ED1 on paraffin sections. Proteins of iNOS and HO-1 of lung tissue were examined by immunohistochemistry. By real-time polymerase chain reaction(PCR) using SYBR Green Ⅰ, the expression levels of iNOS and HO-1 mRNA in lung tissues were measured. Results There was no inflammation, edema, fibrosis, alveolar collapse and hyaline membrane formation in the lung control group. All the lungs from CCl4 group showed widened alveolar wall architectures, widespread dilatation of alveolar capillaries and decreased alveolar volume. PaO2(81.39±2.36)mmHg and PaCO2(30.55±2.87)mmHg decreased significantly in CCl4 group compared with(98.99±3.41)mmHg and(36.26±2.88)mmHg in the control group(P<0.05). Alveolar-arterial oxygen difference(A-aDO2) increased significantly in CCl4 group(30.79±5.73) as compared with the control(3.79±0.86) (P<0.05). Endotoxin level increased significantly in CCl4 group(0.30±0.13)ZU/L compared with control(0.05±0.02)ZU/L(P<0.05). Culture-positive mesenteric lymph nodes were found in 62.5% of CCl4 group. There were not Culture-positive mesenteric lymph nodes in the control. All lungs from CCl4 group showed accumulation of large mononuclear macrophage-like cells within the lumen of numerous small muscular and nonmuscular pulmonary vessels. Using immunohistochemical analysis, iNOS and HO-1 expressions were localized to PIM in CCl4 group. The mRNA expression of iNOS(0.03±0.01) and HO-1 (0.16±0.04) increased significantly in CCl4 group than(0.01±0.01) and(0.07±0.02) in the control(P<0.05). Conclusion Cirrhosis results in bacterial translocation from the gastrointestinal tract and endotoxemia. High concentrations of endotoxin in the pulmonary bloodstream activate PIM. PIM aggregates and expresses iNOS and HO-1. Thus the increasing amount of NO and CO released in the lungs results in HPS.

Key words: hepatopulmonary syndrome, pulmonary intravascular macrophages, inducible nitric oxide synthase, heme oxygenase-1

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