摘要:

We examined whether pancreas grafts preserved by the two-layer method maintained adenine nucleotides pool as substrates for ATP synthesis before reperfusion and had the ability to recover pancreatic tissue perfusion and synthesize ATP promptly after reperfusion. After preservation by the two-layer cold storage method using EC for 48 h (group 1) or simple cold storage in EC for 48 h (group 2), canine pancreas grafts were autotransplanted. In controls (group 3), canine pancreas grafts were autotransplanted without preservation. Tissue adenine nucleotide concentrations were measured using high-performance liquid chromatography, and pancreatic tissue perfusions were measured using the hydrogen gas clearance method. Graft survival rates were five of five, zero of five, and five of five in groups 1, 2, and 3, respectively. Total adenine nucleotide levels before reperfusion in group 1 were almost the same as in group 2. Furthermore, ATP tissue levels in group 1 before reperfusion were also the same as in group 2. However, tissue ATP levels in group 1 after 2 h of reperfusion (6.71 ± 1.19 μmol/g dry weight) were significantly higher than group 2 (4.51 ± 0.51 μmol/g dry weight;p< 0.05). On the other hand, pancreatic tissue perfusions in grafts preserved by the two-layer method (group 1) after 2 h of reperfusion were significantly higher than in group 2. We conclude that oxygenation of pancreas grafts during preservation by the two-layer method allows for ATP synthesis and leads to maintenance of the grafts' ability to recover ATP levels and tissue perfusions after reperfusion.

ISSN:0885-3177    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

The respective cellular distribution of glucagon-like peptide-1 (GLP-1) immunoreactivity and mRNA expression of the GLP-1 receptor was compared in rat pancreas by means of immunohistochemistry and in situ hybridization. GLP-1 immunoreactivity was present in the marginal zone of rat pancreatic islets. In contrast, GLP-1 receptor mRNA signals were confined to the central part of pancreatic islets. Neither GLP-1 immunoreactivity nor GLP-1 receptor mRNA signals were detected in the exocrine pancreatic acinar cells or duct cells. The differential distribution of GLP-1 immunoreactivity and GLP-1 receptor mRNA signals indicates that the GLP-1 amino acid sequence is present in the α-cell zone of pancreatic islets, whereas the GLP-1 receptor is expressed mainly by α cells. Thus, our data by in situ hybridization demonstrates the significant expression of GLP-1 receptors on β cells but makes a significant expression on α cells rather unlikely.

ISSN:0885-3177    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

In adult rats, cholecystokinin (CCK) binds to pancreatic CCK-A receptors and stimulates exocrine secretion and pancreatic growth. In newborn rats there is very little mature intestinal CCK and few pancreatic CCK-A receptors. However, there is an abundant source of the related peptide gastrin, and in addition, there are pancreatic CCK-B/gastrin receptors. In this study, we have explored the hypothesis that gastrin may “deputise” for CCK in the neonate and cause pancreatic exocrine secretion, growth, and maturation. Newborn rats were injected intraperitoneally with the gastrin antagonist, CI-988, or placebo for 5 days and sacrificed on day 6. Body weight (CI-988, 8.25 ± 0.48 g; placebo, 10.17 ± 0.93 g) and pancreatic weight (19.41 ± 1.5 vs. 21.58 ± 1.72 mg) were the same. Protein (1,202 ± 78 vs. 1,254 ± 56 μg), amylase (22.3 ± 0.9 vs. 19.2 ± 1.00 U), RNA (117 ± 7 vs. 126 ± 5 μg), and DNA (95 ± 8 vs. 100 ± 7 μg) contents of the pancreas were similar in the two groups. The weight of the stomach was reduced (p= 0.04) in the treated group (50.8 ± 2.5 mg) compared to the placebo group (59.8 ± 3.7 mg). In both neonates and adults, CCK-8 was ∼1,000 times more potent than gastrin-17 in stimulating amylase release from isolated pancreatic acini. This suggests that enzyme release is probably mediated by the same receptors in both adults and neonates, and in adults previous work has shown this to be the CCK-A receptor. In conclusion, these data show that gastrin has very weak effects on neonatal pancreatic exocrine secretion, and furthermore, gastrin is not essential for growth and maturation of the neonatal pancreas. The role of gastrin and CCK-B/gastrin receptors in the neonatal pancreas remains speculative.

ISSN:0885-3177    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

Recent studies have suggested the involvement of phospholipase A2(PLA2) in pancreatic amylase secretion. The present study was designed to investigate the secretory role of arachidonic acid (AA) in carbachol (Cch)-stimulated rat pancreatic acini and its origin. From enzymatic assays, PLA2and diacylglycerol (DAG) lipase were activated by Cch and respectively inhibited by the PLA2inhibitors, mepacrine and aristolochic acid, and by the DAG lipase inhibitor, RHC 80267. Melittin-activated PLA2activity was also inhibited by the PLA2inhibitors. Cch-stimulated endogenous AA release from pancreatic acini was partially inhibited by 150 μMRHC 80267 and by 150 μMmepacrine or 200 μMaristolochic acid and totally inhibited by a combination of the two enzyme inhibitors. Exogenous AA caused amylase release in a concentration-dependent manner. Eicosatetraynoic acid (a cyclooxygenase and lipoxygenase inhibitor), significantly increased basal and Cch-induced AA release and amylase secretion. RHC 80267 and the PLA2inhibitors separately and partially suppressed Cch-stimulated amylase secretion, with an additive effect observed when the DAG lipase and the PLA2inhibitors were combined. A combination of RHC 80267, mepacrine, or aristolochic acid and the phospholipase C (PLC) inhibitor U73122 completely inhibited Cch-stimulated amylase secretion. Finally, the PLA2activator melittin-stimulated amylase secretion was blocked by the two PLA2inhibitors. We conclude that exogenous and endogenous AA can induce amylase secretion. Therefore, AA released from either PLC-DAG lipase or PLA2pathways can be considered an additional and important intracellular mediator of amylase secretion.

ISSN:0885-3177    

出版商:OVID    

年代:1997

数据来源: OVID

ISSN:0885-3177    

出版商:OVID    

年代:1997

数据来源: OVID

ISSN:0885-3177    

出版商:OVID    

年代:1997

数据来源: OVID

ISSN:0885-3177    

出版商:OVID    

年代:1997

数据来源: OVID

ISSN:0885-3177    

出版商:OVID    

年代:1997

数据来源: OVID

ISSN:0885-3177    

出版商:OVID    

年代:1997

数据来源: OVID