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Страница 1 од 40 резултати
Failure of secretin to increase sodium taurocholate-induced pancreatic necrosis in alcoholic rats.
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Recently we indicated that pancreatic secretory stimulation with pancreozymin superimposed on chronic alcohol intake increases the tissue necrosis in rat pancreas caused by intraductal bile salt administration, and proposed a new theory of the pathogenesis of acute alcoholic pancreatitis. The
Pituitary adenylate cyclase-activating polypeptide attenuates tumor necrosis factor-α-induced apoptosis in endothelial colony-forming cells.
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Endothelial colony-forming cells (ECFCs) are important in angiogenesis and vascular proliferation. Tumor necrosis factor (TNF)-α is a significant risk factor for the development of atherosclerosis and a key proinflammatory cytokine known to induce apoptosis in endothelial cells. Pituitary adenylate
Exocrine pancreatic function in patients with idiopathic necrosis of the femoral head.
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Exocrine pancreatic function after secretin and cholecystokinin stimulation was examined in a group of patients with idiopathic necrosis of the femoral head and in a normal control group. The volume output, bicarbonate and amylase concentrations in the patient group were not significantly lower than
Ceruletide-induced acute pancreatitis in the dog and its amelioration by exogenous secretin.
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Large pharmacological doses of ceruletide administered to conscious dogs by intravenous (i.v.) infusion uniformly induce a severe acute necrotizing pancreatitis within 4 h. High-dose i.v. secretin administered for a period of 24 h after cessation of ceruletide infusion resulted in a significant
Failure of secretin to exert an ameliorative effect on acute reflux pancreatitis in the rat.
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This study was undertaken to evaluate the possible ameliorative effect of secretin on acute reflux pancreatitis in the rat. Thirty days after the performance of a gastrojejunal anstomosis, in all rats (36 Sprague-Dawley, mean weight 250 g) acute pancreatitis was induced by creating a closed duodenal
Protective effects of exogenous secretin on ceruletide-induced acute pancreatitis in the rat.
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Unconscious rats given intravenous ceruletide (diethylamine salt of the decapeptide caerulein) in large pharmacologic doses consistently developed moderate acute pancreatitis by 3 h and florid pancreatitis by 6 h. Biochemical serum markers of acute pancreatitis tended to parallel the severity of the
Increased susceptibility of cholangiocytes to tumor necrosis factor-alpha cytotoxicity after bile duct ligation.
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Tumor necrosis factor (TNF)-alpha plays a critical role in epithelial cell injury. However, the role of TNF-alpha in mediating cholangiocyte injury under physiological or pathophysiological conditions is unknown. Thus we assessed the effects of TNF-alpha alone or following sensitization by
Tumor necrosis factor-α promotes bile ductular transdifferentiation of mature rat hepatocytes in vitro.
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We previously showed that mature hepatocytes could transdifferentiate into bile ductular cells when placed in a collagen-rich microenvironment. To explore the mechanism of transdifferentiation, we examined whether inflammatory cytokines affected the phenotype of hepatocytes in a three-dimensional
Influence of secretin on the course of acute experimental pancreatitis in rats.
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Inhibition of pancreatic secretion is a widely accepted therapeutical principle of acute pancreatitis. However, stimulation of water and bicarbonate secretion may be beneficial by washing out the ductular system in pancreatitis. Secretin (2 and 16 CU/kg body weight) or saline were given to rats at
Failure of secretin to prevent or ameliorate cerulein-induced pancreatitis in the rat.
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Infusion of supramaximal concentrations of the synthetic pancreozymin analog cerulein induces acute edematous pancreatitis in the rat. Vacuolization and necrosis of acinar cells is paralleled by an almost complete reduction of pancreatic secretion from the cannulated duct. Preinfusion or coinfusion
Standard and augmented secretin testing in chronic pancreatic alcoholic disease.
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Sequential standard (1.0 U./kg.) and augmented (4.0-5.0 U./kg.) secretin response to the pancreas has been briefly compared in normal subjects and in patients with combinations of alcoholism, cirrhosis and alcoholic pancreatitis. The results of sequential testing led to the conclusion that, for
Taurocholic acid feeding prevents tumor necrosis factor-alpha-induced damage of cholangiocytes by a PI3K-mediated pathway.
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Cholangiopathies, such as primary biliary cirrhosis and primary sclerosis cholangitis, are characterized at the end stage by ductopenia due to increased cholangiocyte apoptosis and decreased cholangiocyte proliferation. Although cholangiocyte proliferation is associated with an increased number of
Caerulein-induced acute necrotizing pancreatitis in mice: protective effects of proglumide, benzotript, and secretin.
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The onset, course, and regression of the biochemical and structural alterations associated with pancreatitis induced by various doses of caerulein were studied in the mouse. In addition, the protective effect of secretin was compared with that of the cholecystokinin-receptor antagonists proglumide
Combined administration of secretin and oxytocin inhibits chronic colitis and associated activation of forebrain neurons.
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BACKGROUND
The pathogenesis of inflammatory bowel disease is unknown; however, the disorder is aggravated by psychological stress and is itself psychologically stressful. Chronic intestinal inflammation, moreover, has been reported to activate forebrain neurons. We tested the hypotheses that the
Gastrin-Releasing Peptide and Glucose Metabolism Following Pancreatitis.
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BACKGROUND
Gastrin-releasing peptide (GRP) is a pluripotent peptide that has been implicated in both gastrointestinal inflammatory states and classical chronic metabolic diseases such as diabetes. Abnormal glucose metabolism (AGM) after pancreatitis, an exemplar inflammatory disease involving the
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