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LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00004681naa a2200421 4500
001oai:lup.lub.lu.se:408e3baa-73f2-4901-a2fd-1e1db19725c9
003SwePub
008160401s1996 | |||||||||||000 ||eng|
024a https://lup.lub.lu.se/record/11101482 URI
024a https://doi.org/10.1007/BF028255092 DOI
040 a (SwePub)lu
041 a engb eng
042 9 SwePub
072 7a art2 swepub-publicationtype
072 7a ref2 swepub-contenttype
100a Axelson, Janu Lund University,Lunds universitet,Kirurgi,Forskargrupper vid Lunds universitet,Surgery,Lund University Research Groups4 aut0 (Swepub:lu)kir-ja0
2451 0a The changes in the rat parotid glands following total parenteral nutrition and pancreatico-biliary diversion are not mediated by cholecystokinin
264 1c 1996
520 a CONCLUSIONS: The results of the present study suggest that the pancreas and parotid glands both respond with hypoplasia during absence of food in the digestive tract and with hyperplasia following pancreatico-biliary diversion (PBD). Factors other than cholecystokinin (CCK) are, however, involved in the effects on the parotid glands, since infusion of CCK-8S and devazepide was without influence. BACKGROUND AND AIM: Total parenteral nutrition (TPN) causes reduced pancreatic weight, whereas PBD evokes hyperCCKemia and enlargement of the rat pancreas. The pancreas and parotid glands have in part similar morphology and function. Therefore, we studied the possible presence of alterations also in the parotid glands during TPN, after PBD and during infusion of sulfated cholecystokinin (CCK-8S) and the CCK-A receptor antagonist devazepide, respectively. MATERIALS AND RESULTS: Rats either received TPN for 7 d, or were kept under otherwise identical conditions with free access to food and water. TPN markedly reduced both pancreatic and parotid wet weight and thereby also the protein and amylase contents, and pancreatic DNA content was decreased. There was a significant correlation between the pancreas and parotid glands when comparing these parameters. The concentration of plasma CCK was unaffected by TPN. PBD caused a sevenfold increase in plasma CCK and a three fold increase in the pancreatic weight compared to control rats 28 d after the operation. The protein and DNA contents in the pancreas were found to be increased. The parotid glands increased twofold in weight, but their protein and amylase contents were not affected. There was a significant correlation between the pancreas and parotid glands when comparing weight, and protein and amylase concentrations. Infusion of CCK-8S during 28 d caused a marked increase in pancreatic wet wt and protein and DNA contents. The CCK-A receptor antagonist devazepide induced a reduction in protein and DNA contents in the pancreas. The parotid glands were not affected by either treatment. No effect on the labeling index of serous and ductal cells of the parotid gland was seen at 36 h, 3, 7, and 28 d of infusion with CCK-8S or devazepide.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Kirurgi0 (SwePub)302122 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Surgery0 (SwePub)302122 hsv//eng
653 a devazepide
653 a Cholecystokinin (CCK)
653 a pancreas
653 a pancreatico-biliary diversion (PBD)
653 a parotid glands
653 a total parenteral nutrition (TPN)
653 a trophic effects
700a Fan, Bo Guang4 aut
700a Ohlsson, Bodilu Lund University,Lunds universitet,Enheten för kroniska inflammatoriska och degenerativa sjukdomar,Forskargrupper vid Lunds universitet,Chronic Inflammatory and Degenerative Diseases Research Unit,Lund University Research Groups4 aut0 (Swepub:lu)kir-boh
700a Rehfeld, Jens4 aut
700a Ekelund, Matsu Lund University,Lunds universitet,Kirurgi, Lund,Sektion V,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Surgery (Lund),Section V,Department of Clinical Sciences, Lund,Faculty of Medicine4 aut0 (Swepub:lu)kir-mek
700a Ihse, Ingemaru Lund University,Lunds universitet,Kirurgi, Lund,Sektion V,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Surgery (Lund),Section V,Department of Clinical Sciences, Lund,Faculty of Medicine4 aut0 (Swepub:lu)kir-iih
710a Kirurgib Forskargrupper vid Lunds universitet4 org
773t International Journal of Pancreatologyg 20:2, s. 109-118q 20:2<109-118x 0169-4197
856u http://dx.doi.org/10.1007/BF02825509y FULLTEXT
8564 8u https://lup.lub.lu.se/record/1110148
8564 8u https://doi.org/10.1007/BF02825509

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Axelson, Jan
Fan, Bo Guang
Ohlsson, Bodil
Rehfeld, Jens
Ekelund, Mats
Ihse, Ingemar
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