摘要:

These studies were designed to investigate the ability of rats to clear subcutaneous bacterial abscesses following acute pancreatitis. Animals underwent subcutaneous injection of 1 × 109Escherichia coliandStaphylococcus aureusand, 24 h later, were randomized into four groups to receive (A) an intravenous (iv) infusion of cerulein, (B) saline iv, (C) ligation of the pancreatic head, or (D) sham ligation. After 12 h, abscess sizes were measured and blood was withdrawn for culture and assay amylase and endotoxin level assay. Animals were observed for an additional 12 h to record mortality. BothE. coliandS. aureusabscesses were larger in group C vs. group D, while only theE. colilesion was larger in group A vs. group B. Bacteremia was detected in 60% of the animals in group A, 40% in groups B and D, and 100% in group C. Mortality was 80% in group C vs. 10% in all other groups. Amylase and endotoxin levels were higher in group C vs. all groups. In the second experiment rats were injected with bacteria as above. Four, twelve, and twenty-four hours later the abscesses were removed for quantitation of bacteria and histologic evaluation. At 24 h rats underwent procedure A, B, C, or D and the abscesses were excised 12 h later. Group C had a significantly higher number of viable bacteria inside the lesion compared to group D. Histology showed tissue necrosis and cellulitis not observed in group D. It is concluded that acute pancreatitis causes failure of local and systemic bacterial clearance and that the incidence of bacteremia and mortality is proportional to the severity of the disease.

ISSN:0885-3177    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

The effect of salicylate and nonsalicylate antiinflammatory drugs and prostaglandins (PGs) on pancreatic exocrine secretion are controversial. We studied the effect of aspirin (ASA) on secretin- and cholecystokinin (CCK)- or meal-stimulated pancreatic secretion. The interrelation between ASA, PG, and pancreatic exocrine secretion was also investigated. Conscious rats with chronic duodenal, pancreatic, and biliary cannulas received secretin (5 pmol/kg/h, i.v.) and CCK (56 pmol/kg/h) or a meal with administration of cimetidine (20 mg/kg/h, i.v.), ASA (1.2, 12, or 60 μmol/h, i.v.), Salicylic acid (SA) (1.2, 12, or 60 μmol/h, i.v.), prostaglandin E2(PGE2) (10 μg/kg/h), or indomethacin (2 mg/kg) was given, respectively. Pancreatic flow volume, bicarbonate, and protein were determined every 15 min. An inhibitor, 1-(5 isoquinolinylsulfonyl)-2-methylpiperazine (H-7) (36 μg/kg/h) and an activator, phorbol ester (12-O-tetradecanoylphorbol 13-acetate, TPA) (100 ng/kg/h) were used for evaluation of the role of protein kinase C on basal and secretagogue-stimulated pancreatic secretion. ASA, but not SA inhibited the secretin- and CCK-stimulated pancreatic secretion including volume, bicarbonate, and protein in a dose-dependent manner without affecting basal pancreatic secretion. ASA and indomethacin suppressed meal-stimulated pancreatic secretion up to 83.8%. PGE2significantly inhibited the secretin- and CCK-stimulated pancreatic secretion which was further suppressed by the concomitant ASA infusion. Modulation of protein kinase C failed to affect pancreatic secretion. The data indicate that ASA inhibits both secretin- and CCK-stimulated pancreatic secretion by a mechanism independent of prostaglandin biosynthesis inhibition.

ISSN:0885-3177    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

The response of the exocrine pancreas to intraduodenal perfusion of acetic and lactic acids in normal and previously atropinized rats was studied. Secretin and vasoactive intestinal peptide (VIP) plasma levels in portal plasma were also measured. Intraduodenal perfusion of both acetic and lactic acids significantly stimulated flow rate (from 0.29 ± 0.03 μl/min to a maximum of 1.06 ± 0.08 μl/min after acetic and from 0.35 ± 0.05 μl/min to a maximum of 1.13 ± 0.12 μl/min after lactic acid perfusion) and protein output (from 11.16 ± 2.33 μg/min to a maximum of 35.1 ± 7.4 μg/min after acetic and from 8.98 ± 0.95 μg/min to a maximum of 22.5 ± 1.3 μg/min after lactic acid perfusion). Atropine treatment significantly inhibited pancreatic flow rate and protein output after acetic acid perfusion, but no inhibition of flow rate and a slight decrease in the protein output after lactic acid perfusion were seen. With respect to plasma peptide concentrations, significant increases in secretin and VIP levels were found after perfusion of both organic acids; atropine administration significantly decreased plasma secretin levels after acetic acid administration although it did not affect plasma VIP concentrations. By contrast, atropine significantly increased plasma secretin levels, but significantly lower values of plasma VIP concentrations were observed after lactic acid perfusion. Therefore, cholinergic mechanisms are involved in the release of secretin and VIP and different types of control of exocrine pancreatic secretion occur, depending on the features of the intraduodenal stimulant.

ISSN:0885-3177    

出版商:OVID    

年代:1995

数据来源: OVID

摘要:

Two cases of fibrotic stricture of the extrapancreatic common bile duct were observed 3 and 5.5 months after severe acute alcoholic pancreatitis. The diagnosis was made by endoscopic retrograde cholangiography in both cases. Although colonic or ureteric stenosis have been reported after acute pancreatitis, this is the first report of extrapancreatic biliary stricture occurring after acute pancreatitis. The strictures could have arisen by either an enzymatic or ischemic mechanism. Outcome was favorable after surgical hepaticojejunostomy.

ISSN:0885-3177    

出版商:OVID    

年代:1995

数据来源: OVID

ISSN:0885-3177    

出版商:OVID    

年代:1995

数据来源: OVID