ISSN:0012-2823    

DOI:10.1159/000199857

出版商:S. Karger AG    

年代:1989

数据来源: Karger

摘要:

The lipolytic activity of Campylobacter pylori capable of gastric mucosal lipid degradation was investigated. The colonies of bacteria, cultured from antral mucosal biopsy specimens of patients undergoing endoscopy, were washed with saline and passed through a sterilization filter; the filtrate was examined for lipase and phospholipase A activities, using glycerol trioleate and dipalmitoyl phosphatidylcholine as substrates. The obtained results revealed that both enzymes are present in the C. pylori filtrate. The enzymes exhibited optimal activity at 37 °C and the pH range of 7.0–7.4. The major product of the triglyceride degradation was glycerol monoleate, while lysophosphatidylcholine resulted from the degradation of phosphatidylcholine. The lipase activity of the C pylori filtrate was inhibited by an antiulcer drug, sofalcone, which at a concentration of 200 µg/ml caused a 43 % reduction in the triglyceride hydrolysis. The sofalcone, however, showed only marginal, if any, inhibitory activity toward C pylori phospholipase A. The results suggest that C pylori infection may be detrimental to the integrity of gastric mucosal lip

ISSN:0012-2823    

DOI:10.1159/000199858

出版商:S. Karger AG    

年代:1989

数据来源: Karger

摘要:

The role of free radicals in the development of pancreatitis was evaluated by measuring the level of activities of xanthine oxidase (XOD), lipid peroxide (LPO) and superoxide dismutase (SOD). Acute pancreatitis was induced in female mice fed a choline-deficient meal containing 0.5 % DL-ethionine (CDE meal). Acute pancreatitis was confirmed by the changes in serum amylase level and other typical features observed microscopically 24 h after the meal was taken. Activity of XOD was elevated significantly (p < 0.05) from the baseline of 1.13 ± 0.19 U/g tissue to 2.34 ± 0.46, 2.59 ± 0.33 and 3.46 ± 0.70 U/g tissue, 8, 12 and 24 h, respectively, after the CDE meal. The LPO level was also increased from an undetectable amount to 1.10 ± 0.47 nmol/ml (p < 0.05), 1.03 ± 0.18 (p < 0.01) at 6 and 8 h, respectively, and then returned to an undetectable amount at 12 h. The peak level of LPO was shown at 24 h, 1.76 ± 0.40 nmol/ml (p < 0.01) and gradually decreased until 48 h, 1.17 ± 0.37 nmol/ml (p < 0.01) after the CDE meal. Changes of LPO took a biphasic pattern. SOD was decreased significantly from 47.1 ± 3.4 mU/g tissue to 30.7 ± 2.5, 24.8 ± 1.7 and 20.6 ± 1.1 mU/g tissue at 8 (p < 0.01), 12 (p < 0.01), and 24 (p < 0.01) h, respectively. These results indicate that oxygen-derived free radicals play an important role in the development of acute pancreatitis and that the imbalance of the offense system represented by XOD and LPO and the defense system reflected by SOD in the tissue might be an important cause of tissue damage induced by oxygen-derived fr

ISSN:0012-2823    

DOI:10.1159/000199859

出版商:S. Karger AG    

年代:1989

数据来源: Karger

摘要:

The effect of an oral dose of 70 μg enprostil (a prostaglandin E2 analogue) on the post-prandial hormone response to a test breakfast was examined in a double-blind, placebo-controlled, cross-over study in 10 healthy volunteers. Enprostil markedly reduced the postprandial rises in insulin and glucose-dependent insulinotropic peptide (GIP) but plasma glucose remained unchanged. To study the effects on gut motility 8 healthy volunteers ingested a liquid meal containing 75 g glucose, 20 g lactulose and 99mTc colloid after taking placebo or 70 μg enprostil. Gastric emptying, measured using a gamma camera, was unchanged but mouth-to-caecum transit time was significantly longer on enprostil; time to half maximal breath hydrogen: placebo 119 min, enprostil 200 min (p < 0.05). This delay was associated with a reduced and delayed post-prandial rise in GIP and insulin and with other changes in the gut hormone profil

ISSN:0012-2823    

DOI:10.1159/000199860

出版商:S. Karger AG    

年代:1989

数据来源: Karger

摘要:

Six patients with chronic type B hepatitis and concurrent infection with the immunodeficiency virus were treated with 600 mg azidothymidine (AZT)&slash;day and 3 × 106 units of interferon-α (IFN-α) every other day for a total of 4 months. None of the patients treated lost the hepatitis B virus (HBV). HBV-DNA concentrations were not significantly influenced by this treatment. Human immunodeficiency virus (HIV) infection was also not affected except for a transient rise in CD 4-positive cells in 2 individuals, who had initially low CD 4-positive cells. Treatment did not influence the presence of HIV-Ag in the serum. In conclusion, a combination therapy of IFN and AZT does not seem to be beneficial at the doses given and the time involv

ISSN:0012-2823    

DOI:10.1159/000199861

出版商:S. Karger AG    

年代:1989

数据来源: Karger

摘要:

The effects of the selective muscarinic M1-receptor antagonist pirenzepine and the nonselective muscarinic antagonist atropine on bombesin- and peptone-stimulated release of pancreatic polypeptide (PP) were studied in healthy subjects. To exclude any effect of changes in intraduodenal pH continuous intragastric titration was performed during all tests. Both pirenzepine (i.v. bolus 0.6 mg/kg) and atropine (i.v. bolus 15 μg/kg, followed by an infusion of 5 μg/kg·h) significantly reduced peptone-induced integrated mean rise of plasma PP from 28 ± 5 to 8 ± 4 and -2 ± 5 pmol/l, respectively (n = 4). Both drugs also reduced bombesin-induced rise of plasma PP in all 4 subjects, from 27 ± 12 to 6 ± 4 and 7 ± 1 pmol/l (0.05 < p < 0.1). It is concluded that cholinergic regulation of PP release is mediated mainly through muscarinic M1-r

ISSN:0012-2823    

DOI:10.1159/000199862

出版商:S. Karger AG    

年代:1989

数据来源: Karger

摘要:

The effect of a peripheral cholecystokinin (CCK)-receptor antagonist, CR 1409, on pancreatic growth has been studied in the rat. 1.8 nmol/kg CCK-8 or caerulein and 3.6 nmol/kg bombesin or gastrin-releasing peptide (GRP) administered subcutaneously 3 times daily for 4 successive days increased pancreatic weight and its content in protein, enzymes and RNA but not in DNA, suggesting cellular hypertrophy. CR 1409 (10 mg/kg) administered intragastrically 30 min prior to peptides prevented pancreatic growth due to CCK-8 or caerulein but not that induced by bombesin and GRP. It is concluded that bombesin and GRP act on the exocrine pancreas directly rather than through the release of CCK.

ISSN:0012-2823    

DOI:10.1159/000199863

出版商:S. Karger AG    

年代:1989

数据来源: Karger

摘要:

Exclusion of bile and pancreatic juice (BPJ) from the proximal intestine increases the release of pancreatic polypeptide (PP) from 4.4 to 14.3 pM and its increase was diminished by the intravenous infusion of atropine (100 μg/kg/h) in conscious rats. Neither intravenous bolus injection nor continuous infusion of cerulein did increase plasma PP concentration. It is suggested that the increase in plasma PP concentration produced by BPJ diversion is regulated by cholinergic mechanism, but not by cholecystokinin (CCK) released despite the known fact that BPJ diversion increases plasma CCK concentration

ISSN:0012-2823    

DOI:10.1159/000199864

出版商:S. Karger AG    

年代:1989

数据来源: Karger

摘要:

In vivo somatostatin inhibits exocrine pancreatic secretion. In in vitro experiments, such as the isolated perfused pancreas, somatostatin fails to inhibit exocrine pancreatic secretion. This suggests an indirect action of somatostatin, such as modulation of neural regulation. In the anesthetized rat we tested the inhibitory capacity of somatostatin in the presence of neural blockade in vivo. Neither the drugs given intravenously – phentolamine, propanolol, atropine and naloxone – nor vagotomy were able to prevent somatostatin-induced inhibition of exocrine pancreatic secretion. We conclude that somatostatin-induced inhibition of exocrine pancreatic secretion is not dependent on intact extrinsic innervat

ISSN:0012-2823    

DOI:10.1159/000199865

出版商:S. Karger AG    

年代:1989

数据来源: Karger

摘要:

Repeated intraperitoneal administration of compound 48/80 to rats produced gastric lesions, a decrease in connective tissue mast cells (CTMCs) and an increase in gastric mucosal mast cells (MMCs). The ratio of MMC to CTMC was significantly correlated with lesion formation. A mast cell stabilizer, MAR-99 (50 mg/kg), prevented lesion formation and changes in the mast cells. Omeprazole (20 or 60 mg/kg) significantly reduced the gastric lesions, but mast cell changes persisted. Cimetidine (50 mg/kg) could not inhibit compound 48/80-induced lesions nor a decrease in CTMCs, but did prevent an increase in MMCs. These facts suggest that in compound 48/80-induced gastric lesions chemical mediators released from CTMCs might be trigger factors, while intraluminal gastric acid might be an aggravating factor. Furthermore, the increase in MMCs might be regulated by histamine released from the CTMCs via H2 receptors and have no causal relation to lesions formation.

ISSN:0012-2823    

DOI:10.1159/000199866

出版商:S. Karger AG    

年代:1989

数据来源: Karger