vasoactive-intestinal-peptide and Hepatopulmonary-Syndrome

Hepatopulmonary syndrome (HPS) is a chronic hepatic complication characterized by defect in arterial oxygenation induced by pulmonary vascular dilatation and vasoactive substances in the setting of chronic liver disease (CLD). This study is to investigate the abnormality of hemodynamic and vasoactive substances in hepatopulmonary syndrome.. From September 2007 to September 2012, 58 patients with HPS in the General Surgery Department and Transplantation Center of Renji Hospital were enrolled for the case-control study. HPS patients enrolled were referred to as group H, CLD without HPS to as group C and case controls to as group N. Hemodynamic parameters of the systemic and pulmonary circulations as well as vasoactive substances in the radial and pulmonary arteries were measured in all patients. Univariate and multiple regression analysis were performed afterwards.. The mean pulmonary arterial pressure, pulmonary artery wedge pressure, systemic vascular resistance and pulmonary vascular resistance (PVR) in HPS patients were significantly lower than those in CLD patients without HPS (p < 0.05). The nitrite-to-nitrate ratio (NO2-/NO3-), endothelin-1 (ET-1) and tumor necrosis factor-α (TNF-α) in the radial and pulmonary arteries differed significantly among group H, group C and case controls (group N) separately (p < 0.05). The vasoactive intestinal peptide and 6-keto-prostaglandin-F1α in the radial and pulmonary arteries of group H were significantly higher than those in group N (p < 0.05). The NO2(-)/NO3(-) levels correlated negatively with PVR (r = -0.535, p < 0.05) and Endothelin-1 (r = -0.624, p < 0.05). CO (p < 0.05), CI (p < 0.05), SI (p < 0.05) and TNF-α (p < 0.05) level are considered significantly when performed with multiple regression analysis.. The CO increases and PVR decreases in HPS patients. The abnormally elevated NO2-/NO3- level in the pulmonary circulation leads to pulmonary vasodilation. ET-1 may induce nitric oxide synthesis and correlated negatively with PVR in HPS. CO, CI, SI and TNF-α level are independent risk factors for HPS patients' survival.

Topics: 6-Ketoprostaglandin F1 alpha; Case-Control Studies; Endothelin-1; Female; Hemodynamics; Hepatopulmonary Syndrome; Humans; Male; Middle Aged; Nitric Oxide; Pulmonary Artery; Pulmonary Circulation; Radial Artery; Risk Factors; Tumor Necrosis Factor-alpha; Vascular Resistance; Vasoactive Intestinal Peptide; Vasodilation

To evaluate the potential of vasoactive intestinal peptide (VIP) as a pathogenic factor of intrapulmonary vascular dilatation (IVD) in hepatopulmonary syndrome (HPS).. HPS comprises a triad comprising liver dysfunction, IVD and hypoxaemia. Although the pathogenesis of the process has not been elucidated, many vasodilating substances, such as VIP, have been implicated in the development of pulmonary vascular abnormalities. IVD can be detected by contrast-enhanced echocardiography (CEE) before the development of abnormal gas exchange.. Forty-two children (20M, 22F; mean age 4.39 +/- 4.17 y) with various liver diseases who attended the paediatric liver clinic of King Chulalongkorn Memorial Hospital between March 2000 and February 2001 were recruited to the study. Each patient was tested for transcutaneous O2 saturation, CEE (applying the agitated normal saline technique), liver function test and serum VIP level.. Fourteen of the 42 patients (33%) were CEE positive. Only one of the 14 patients had associated hypoxia and clinical cyanosis. The serum VIP levels of children with liver disease were significantly higher than those of the controls (60.21 +/- 35.04 pg/ml vs 43.71 +/- 34.61 pg/ml, p = 0.03). CEE-positive children tended to have higher serum VIP levels than CEE-negative children (72.65 +/- 40.31 vs 53.99 +/- 31 pg/ml, p = 0.3). The serum VIP levels of biliary atresia (BA) patients with favourable outcomes (serum bilirubin < or = 34 micromol/L) were not significantly different from those with unfavourable outcomes (serum bilirubin > 34 micromol/L) (42.95 +/- 14.53 pg/ml vs 66.07 +/- 32.17 pg/ml, p = 0.5).. CEE is a non-invasive test for early detection of IVD in children with liver disease. VIP is not solely responsible for the pathogenesis of IVD in HPS. Further studies are required to determine which substances cause the development of IVD.

Topics: Adolescent; Child; Child, Preschool; Dilatation, Pathologic; Echocardiography; Female; Hepatopulmonary Syndrome; Humans; Hypoxia; Infant; Male; Oxygen; Pulmonary Circulation; Vasoactive Intestinal Peptide