ABSTRACT
OBJECTIVE: to study the expression of urokinase-type plasminogen activator (uPA) and plasminogen activator inhibitor-1 (PAI-1) in the gastric mucosal (GM) vascular endothelium and epithelial cells of patients with portal hypertensive gastropathy (PHG) and those with portal hypertension (PH) without signs of PHG as compared to a control group. MATERIAL AND METHODS: GM biopsy specimens from patients with PHG, those with PH without signs of PHG, and controls with the normal gastric mucosa were immunohistochemically examined. RESULTS: Comparison of the expression of uPA in the GM vascular endothelium and epithelial vessels revealed no significant differences in the patient groups. The level of PAI-1 in the GM vessels was statistically significantly higher in the control group than in the groups of patients with PHG and PH without PHG. PAI-1 expression in the GM epithelial cells was significantly more commonly absent in the PHG group than in the control group. An analysis of an uPA and PAI-1 expression ratio showed a statistically significant predominance of the expression of uPA over its inhibitor in the GM vascular endothelium of the patients with PHG and those with PH without PHG as compared to the controls. CONCLUSION: The predominance of uPA over PAI-1 in the GM vessels and epithelial cells can play a role in the development of GM bleeding.
Subject(s)
Gastric Mucosa/metabolism , Gastrointestinal Hemorrhage/etiology , Gastrointestinal Hemorrhage/metabolism , Hypertension, Portal/metabolism , Plasminogen Activator Inhibitor 1/biosynthesis , Stomach Diseases/metabolism , Urokinase-Type Plasminogen Activator/biosynthesis , Case-Control Studies , Endothelium, Vascular/metabolism , Endothelium, Vascular/pathology , Epithelial Cells/metabolism , Epithelial Cells/pathology , Female , Gastric Mucosa/blood supply , Gastric Mucosa/pathology , Gastrointestinal Hemorrhage/pathology , Gastroscopy , Humans , Hypertension, Portal/complications , Hypertension, Portal/pathology , Immunohistochemistry , Male , Middle Aged , Portal Pressure , Severity of Illness Index , Stomach Diseases/etiology , Stomach Diseases/pathologyABSTRACT
In spite of a great number of publications, as yet there is no agreement that which of the detected morphological changes should be considered pathognomonic in portal hypertensive gastropathy (PHG). The study of the pathogenesis of PHG suggested a diversity of mechanisms involved in varying degrees in the development of this abnormality. The paper summarizes the data available in the literature on the role of endothelial dysfunction, apoptosis, damaging factors, and H. pylori infection in the development of this abnormality. A differential diagnosis was made between PHG and GAVE syndrome and histological features in both groups were revealed.
Subject(s)
Helicobacter Infections/pathology , Liver Cirrhosis/pathology , Stomach Diseases/pathology , Diagnosis, Differential , Gastric Antral Vascular Ectasia/diagnosis , Gastric Antral Vascular Ectasia/pathology , Helicobacter Infections/microbiology , Helicobacter pylori/pathogenicity , Humans , Liver Cirrhosis/diagnosis , Stomach Diseases/diagnosisABSTRACT
Portal hypertensive gastropathy (PHG) is a complex of secondary macroscopic and microscopic changes in the mucous layer of the stomach, resulting from portal hypertension of any origin. The overall prevalence of PHG ranges from 9.1 to 80%. PHG is a potential cause of an acute or chronic gastric bleeding. The presence of PHG is associated with prognosis deterioration that dictates the need for improved diagnosis and treatment strategy. The article summarizes literature on the pathological changes, diagnosis and classification of portal hypertensive gastropathy.
Subject(s)
Gastrointestinal Hemorrhage/classification , Gastrointestinal Hemorrhage/diagnosis , Hypertension, Portal/classification , Hypertension, Portal/diagnosis , Stomach Diseases/classification , Stomach Diseases/diagnosis , Acute Disease , Chronic Disease , Female , Gastrointestinal Hemorrhage/etiology , Gastrointestinal Hemorrhage/therapy , Humans , Hypertension, Portal/complications , Hypertension, Portal/therapy , Male , Stomach Diseases/etiology , Stomach Diseases/therapyABSTRACT
Effect of oxidized and reduced forms of pyridine nucleotides on activity of creatine kinase BB was studied in rat brain. NAD did not affect the enzymatic activity at concentrations of 1.0-4.0 mM, while in presence of NADH activity of creatine kinase BB was gradually decreased as the coenzyme concentration increased. The plot of 1/V against 1/S at various NADH concentrations produced a series of lines intersecting at one point (-1/Km), thus indicating the noncompetitive type of brain cytoplasmic creatine kinase inhibition by reduced pyridine nucleotides. Apparent Ki value for NADH was about 1.5 mM which was lower than the known parameter for cytoplasmic creatine kinase isozymes from skeletal and heart muscles. Dependence of brain creatine kinase BB on the rate of pyridine nucleotide reduction suggested a possible mechanism for the enzyme regulation under hypoxic conditions.
Subject(s)
Brain/enzymology , Creatine Kinase/metabolism , Pyridines/pharmacology , Animals , Brain/drug effects , Cytoplasm/metabolism , Isoenzymes , NAD/metabolism , Oxidation-Reduction , RatsABSTRACT
Results are presented of mathematical analysis of succinate dehydrogenase and NADH-dehydrogenase activities in mitochondria of rabbit brain. The type of the function describing the correlation between the enzymes is found to be independent of changes in the environments.
