epidermal-growth-factor and Hypertension--Portal

A large number of growth factors have been described and their action and interaction is proving to be complex. The presence study estimated the epidermal growth factor (EGF) in portal hypertension patients with chronic liver disease due to bilharziasis or viral infection as well as in patients with peptic ulcers. The results showed different statistical values regarding liver cirrhosis, oesophageal varices, and bleeding. No doubt, the EGF was indirectly stimulated by the schistosomal and/or viral infection.

Topics: Epidermal Growth Factor; Hepatitis, Viral, Human; Humans; Hypertension, Portal; Liver Cirrhosis; Peptic Ulcer; Radioimmunoassay; Schistosomiasis

This study was designed to investigate the expression and localization of PDGF, bFGF, EGF, and TGF alpha in gastric coronary vein of cirrhotic (n = 30) and non-cirrhotic patients (n = 10) using immunohistochemical technique. The strongly positive immunostaining rate were 93%, 89%, 70% and 68% respectively in cirrhotic patients. The immunostaining was negative in non-cirrhotic patients. The damage to endothelium, hypertrophy and hyperplasia of vascular smooth muscle cells and vascular remodeling were seen in gastric coronary vein of cirrhotic patients. These results suggested that gastric coronary vein could produce growth factor during cirrhosis, the growth factor can act on the vascular function and/or structure via autocrine-paracrine mechanism.

Topics: Adult; Endothelium, Vascular; Epidermal Growth Factor; Female; Fibroblast Growth Factor 2; Humans; Hypertension, Portal; Immunohistochemistry; Liver Cirrhosis; Male; Muscle, Smooth, Vascular; Platelet-Derived Growth Factor; Stomach; Transforming Growth Factor alpha

This study was designed to evaluate the concentration and the regional distribution of TGF-alpha and EGF in normal and portal hypertensive human gastric mucosa. To this end we measured by RIA the gastric and duodenal concentration of TGF-alpha and EGF in subjects with chronic hepatitis, who had normal gastric endoscopic appearance, and in patients with liver cirrhosis with and without congestive gastropathy. Our results show that TGF-alpha concentration is significantly higher than EGF concentration in both the stomach and duodenum. No significant regional differences in the distribution of the two peptides were found. Moreover, the gastroduodenal tissue levels of TGF-alpha were comparable in subjects with and without hypertensive gastropathy. EGF gastric concentration was not altered in patients with congestive gastropathy. However, EGF duodenal tissue levels were significantly lower in patients with liver cirrhosis than in noncirrhotic subjects. We speculate that the higher level of TGF-alpha in the gastroduodenal mucosa may support the hypothesis that TGF-alpha and not EGF is the major physiological ligand for TGF-alpha/EGF receptor in the intact gut. Furthermore, the lower duodenal concentration of EGF in cirrhotics might partially explain the increased susceptibility of cirrhotic patients to duodenal ulcer.

Topics: Adult; Aged; Biopsy; Chronic Disease; Duodenum; Epidermal Growth Factor; Female; Gastric Mucosa; Humans; Hypertension, Portal; Intestinal Mucosa; Liver Diseases; Male; Middle Aged; Radioimmunoassay; Reference Values; Stomach Diseases; Transforming Growth Factor alpha

Epidermal growth factor (EGF) protects gastric mucosa against a variety of injurious agents, but the mechanism is unclear. Because the abnormal microvasculature of portal hypertensive (PHT) gastric mucosa is a major target of ischemia/reperfusion (I/R) injury, we used this model to assess EGF's protective role at the microvascular level.. Rats with PHT (staged portal vein ligation) received either EGF, 20 micrograms/kg, or saline solution intravenously, with or without indomethacin pretreatment (20 mg/kg subcutaneously). I/R was produced by withdrawing blood to systemic pressures of 30 mm Hg for 20 minutes and reinfusing it. Stomachs were excised 20 minutes later and evaluated for gross and histologic necrosis, microvascular permeability, mucosal ultrastructure and vimentin, and cyclooxygenase immunofluorescence.. In saline-treated rats, gross and histologic damage involved 46% +/- 3% of glandular mucosa and 23% +/- 3% of mucosal sections, respectively. Microvascular permeability was increased 43-fold over that of normal control rats. Vimentin immunofluorescence intensity was reduced to 36% +/- 4% that of normal control rats. EGF pretreatment reduced histologic necrosis to 2% +/- 1% (p less than 0.01). Microvascular permeability and vimentin intensity were almost normalized. Indomethacin partially reversed the mucosal protection induced by EGF.. EGF significantly reduces I/R injury to PHT gastric mucosa. Microvascular endothelia of PHT gastric mucosa are the major target of I/R injury and the site of EGF's protective action. Prostaglandins in part mediate EGF's protective action.

Topics: Animals; Capillaries; Endothelium, Vascular; Epidermal Growth Factor; Fluorescent Antibody Technique; Gastric Mucosa; Hypertension, Portal; Ischemia; Prostaglandins; Rats; Rats, Inbred Strains; Vimentin