Warning: Undefined variable $zfal in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 525
Deprecated: str_replace(): Passing null to parameter #3 ($subject) of type array|string is deprecated in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 525
Warning: Undefined variable $sterm in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 530
free
Warning: Undefined variable $sterm in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 531
free free
English Wikipedia
Nephropedia Template TP (
Twit Text
DeepDyve Pubget Overpricing |
lüll Role of hydrogen sulfide in portal hypertension and esophagogastric junction vascular disease Wang C; Han J; Xiao L; Jin CE; Li DJ; Yang ZWorld J Gastroenterol 2014[Jan]; 20 (4): 1079-87AIM: To investigate the association between endogenous hydrogen sulfide (H(2)S) and portal hypertension as well as its effect on vascular smooth muscle cells. METHODS: Portal hypertension patients were categorized by Child-Pugh score based on bilirubin and albumin levels, prothrombin time, ascites and hepatic encephalopathy. Plasma H(2)S concentrations and portal vein diameters (PVDs) were compared between portal hypertension patients and control participants, as well as between portal hypertension patients with varying degrees of severity. In addition, we established a rabbit hepatic schistosomiasis portal hypertension (SPH) model and analyzed liver morphology, fibrosis grade, plasma and liver tissue H(2)S concentrations, as well as cystathionine gamma-lyase (CSE) activity and phosphorylated extracellular signal-regulated kinase (pERK)1/2, B cell lymphoma (Bcl)-2 and Bcl-XL expression in portal vein smooth muscle cells, in addition to their H(2)S-induced apoptosis rates. RESULTS: In portal hypertension patients, endogenous H(2)S levels were significantly lower than those in healthy controls. The more severe the disease was, the lower were the H(2)S plasma levels, which were inversely correlated with PVD and Child-Pugh score. Liver tissue H(2)S concentrations and CSE expression were significantly lower in the SPH rabbit livers compared with the control animals, starting at 3 wk, whereas pERK 1/2 expressions gradually increased 12-20 wk after SPH model establishment. In portal vein smooth muscle cells, increasing H(2)S levels led to increased apoptosis, while Bcl-2 and Bcl-XL expression decreased. CONCLUSION: H(2)S prevents vascular restructuring caused by excessive proliferation of smooth muscle cells via apoptosis induction, which helps to maintain normal vascular structures.|Adult[MESH]|Animals[MESH]|Apoptosis[MESH]|Case-Control Studies[MESH]|Cell Proliferation[MESH]|Cells, Cultured[MESH]|Disease Models, Animal[MESH]|Esophagogastric Junction/*blood supply/*metabolism[MESH]|Female[MESH]|Humans[MESH]|Hydrogen Sulfide/*blood[MESH]|Hypertension, Portal/*blood/parasitology/pathology[MESH]|Liver Cirrhosis, Experimental/metabolism/parasitology[MESH]|Liver/*metabolism/pathology[MESH]|Male[MESH]|Middle Aged[MESH]|Muscle, Smooth, Vascular/*metabolism/pathology[MESH]|Myocytes, Smooth Muscle/*metabolism/pathology[MESH]|Portal Vein/metabolism/pathology[MESH]|Rabbits[MESH]|Schistosomiasis/complications[MESH]|Severity of Illness Index[MESH]|Time Factors[MESH] |