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Pathogenesis and pathophysiology of hepatopulmonary syndrome

Pathogenesis and pathophysiology of hepatopulmonary syndrome
Pathogenesis and pathophysiology of hepatopulmonary syndrome. Experimental HPS is induced by the technique of CBDL cirrhosis, which leads to pulmonary vasodilation, intravascular accumulation of activated macrophages and monocytes and angiogenesis. Pulmonary vasodilation is caused by NO production, following eNOS and iNOS activation[1-5] and CO production[6,7]. In CBDL lungs, ET-1 binding to its ET-1B receptor induces eNOS activation[2,3] while iNOS and HO activation occurs in intravascular monocytes/macrophages[4-7]. Activated monocytes and macrophages are recruited to the lungs because of bacterial translocation and endotoxaemia after CBDL[4], in which CX3CL1/CX3CR1 signalling is responsible for correct monocyte/macrophage adherence to the pulmonary endothelium[8]. In addition, increased production of VEGF-A leads to endothelial cell survival and proliferation through angiogenic Akt/ERK signalling, when it binds to its VEGFR2 on pulmonary endothelial cells[9,10]. This combination of pulmonary vasodilation, angiogenesis, pulmonary capillary proliferation and formation of intrapulmonary arteriovenous shunts results in ventilation-diffusion mismatch, right-to-left shunting and diffusion restriction[11], finally contributing to gas exchange disturbances with arterial hypoxaemia, which characterizes HPS.
CBDL: common bile duct ligation; ET-1: endothelin-1; VEGF-A: vascular endothelial growth factor A; ET-1B receptor: endothelin-1 B receptor; VEGFR2: VEGF receptor 2; CX3CL1: chemokine fractalkine; TNFa: tumor necrosis factor a; eNOS: endothelial nitric oxide synthase; Akt: protein kinase B; ERK: extracellular signal-regulated kinase; iNOS: inducible nitric oxide synthase; HO: haem oxygenase; CX3CR1: chemokine fractalkine receptor; NO: nitric monoxide; CO: carbon monoxide; HPS: hepatopulmonary syndrome.
References:
  1. Ling Y, Zhang J, Luo B, et al. The role of endothelin-1 and the endothelin B receptor in the pathogenesis of hepatopulmonary syndrome in the rat. Hepatology 2004; 39:1593.
  2. Zhang M, Luo B, Chen SJ, Abrams GA, Fallon MB. Endothelin-1 stimulation of endothelial nitric oxide synthase in the pathogenesis of hepatopulmonary syndrome. Am J Physiol 1999; 277:G944.
  3. Luo B, Liu L, Tang L, et al. Increased pulmonary vascular endothelin B receptor expression and responsiveness to endothelin-1 in cirrhotic and portal hypertensive rats: a potential mechanism in experimental hepatopulmonary syndrome. J Hepatol 2003; 38:556.
  4. Nunes H, Lebrec D, Mazmanian M, et al. Role of nitric oxide in hepatopulmonary syndrome in cirrhotic rats. Am J Respir Crit Care Med 2001; 164:879.
  5. Zhang XJ, Katsuta Y, Akimoto T, et al. Intrapulmonary vascular dilatation and nitric oxide in hypoxemic rats with chronic bile duct ligation. J Hepatol 2003; 39:724.
  6. Arguedas MR, Drake BB, Kapoor A, Fallon MB. Carboxyhemoglobin levels in cirrhotic patients with and without hepatopulmonary syndrome. Gastroenterology 2005; 128:328.
  7. Zhang J, Ling Y, Luo B, et al. Analysis of pulmonary heme oxygenase-1 and nitric oxide synthase alterations in experimental hepatopulmonary syndrome. Gastroenterology 2003; 125:1441.
  8. Zhang J, Yang W, Luo B, et al. The role of CX(3)CL1/CX(3)CR1 in pulmonary angiogenesis and intravascular monocyte accumulation in rat experimental hepatopulmonary syndrome. J Hepatol 2012; 57:752.
  9. Coulon S, Heindryckx F, Geerts A, et al. Angiogenesis in chronic liver disease and its complications. Liver Int 2011; 31:146.
  10. Dimmeler S, Zeiher AM. Akt takes center stage in angiogenesis signaling. Circ Res 2000; 86:4.
  11. Rodriguez-Roisin R, Krowka MJ, Herve P, Fallon MB. Pulmonary-Hepatic vascular Disorders (PHD). Eur Respir J 2004; 24:861.
From: Raevens S, Geerts A, Van Steenkiste C, et al. Hepatopulmonary syndrome and portopulmonary hypertension: recent knowledge in pathogenesis and overview of clinical assessment. Liver Int 2015; 35:1646. http://onlinelibrary.wiley.com/wol1/doi/10.1111/liv.12791/abstract. Copyright © 2015 John Wiley & Sons A/S. Reproduced with permission of John Wiley & Sons Inc. This image has been provided by or is owned by Wiley. Further permission is needed before it can be downloaded to PowerPoint, printed, shared or emailed. Please contact Wiley's permissions department either via email: [email protected] or use the RightsLink service by clicking on the 'Request Permission' link accompanying this article on Wiley Online Library (http://onlinelibrary.wiley.com).
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