The mast cell integrates the splanchnic and systemic inflammatory response in portal hypertension.
Portal hypertension is a clinical syndrome that is difficult to study in an isolated manner since it is always associated with a greater or lesser degree of liver functional impairment. The aim of this review is to integrate the complications related to chronic liver disease by using both, the array of mast cell functions and mediators, since they possibly are involved in the pathophysiological mechanisms of these complications. The portal vein ligated rat is the experimental model most widely used to study this syndrome and it has been considered that a systemic inflammatory response is produced. This response is mediated among other inflammatory cells by mast cells and it evolves in three linked pathological functional systems. The nervous functional system presents ischemia-reperfusion and edema (oxidative stress) and would be responsible for hyperdynamic circulation; the immune functional system causes tissue infiltration by inflammatory cells, particularly mast cells and bacteria (enzymatic stress) and the endocrine functional system presents endothelial proliferation (antioxidative and antienzymatic stress) and angiogenesis. Mast cells could develop a key role in the expression of these three phenotypes because their mediators have the ability to produce all the aforementioned alterations, both at the splanchnic level (portal hypertensive enteropathy, mesenteric adenitis, liver steatosis) and the systemic level (portal hypertensive encephalopathy). This hypothetical splanchnic and systemic inflammatory response would be aggravated during the progression of the chronic liver disease, since the antioxidant ability of the body decreases. Thus, a critical state is produced, in which the appearance of noxious factors would favor the development of a dedifferentiation process protagonized by the nervous functional system. This system rapidly induces an ischemia-reperfusion phenotype with hydration and salinization of the body (hepatorenal syndrome, ascites) which, in turn would reduce the metabolic needs of the body and facilitate its temporary survival.
Aller
María-Angeles
MA
Surgery I Department, School of Medicine, Complutense University of Madrid, Spain. maaller@med.ucm.es
Arias
Jorge-Luis
JL
Arias
Jaime
J
D000818:Animals; D002908:Chronic Disease; D006501:Hepatic Encephalopathy / Q000276:immunology / Q000503:physiopathology; D006801:Humans; D006975:Hypertension, Portal / Q000276:immunology* / Q000503:physiopathology*; D008407:Mast Cells / Q000276:immunology*; D013152:Splanchnic Circulation / Q000502:physiology*; D018746:Systemic Inflammatory Response Syndrome / Q000276:immunology* / Q000503:physiopathology*