Axelson J, Fan B G, Ohlsson B, Rehfeld J, Ekelund M, Ihse I
Department of Surgery, University Hospital, Lund, Sweden.
Int J Pancreatol. 1996 Oct;20(2):109-18. doi: 10.1007/BF02825509.
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.
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.
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.
本研究结果表明,在消化道无食物时胰腺和腮腺均会出现发育不全,而在胰胆管转流术(PBD)后则会出现增生。然而,除胆囊收缩素(CCK)外的其他因素也参与了对腮腺的影响,因为输注CCK-8S和地伐西匹并无影响。
全胃肠外营养(TPN)会导致胰腺重量减轻,而PBD会引发高CCK血症并使大鼠胰腺增大。胰腺和腮腺在部分形态和功能上相似。因此,我们分别研究了TPN期间、PBD后以及输注硫酸化胆囊收缩素(CCK-8S)和CCK-A受体拮抗剂地伐西匹期间腮腺是否也可能存在改变。
大鼠要么接受7天的TPN,要么在其他条件相同的情况下自由获取食物和水。TPN显著降低了胰腺和腮腺的湿重,进而也降低了蛋白质和淀粉酶含量,且胰腺DNA含量减少。比较这些参数时,胰腺和腮腺之间存在显著相关性。血浆CCK浓度不受TPN影响。与术后28天的对照大鼠相比,PBD使血浆CCK增加了7倍,胰腺重量增加了3倍。发现胰腺中的蛋白质和DNA含量增加。腮腺重量增加了两倍,但其蛋白质和淀粉酶含量未受影响。比较重量、蛋白质和淀粉酶浓度时,胰腺和腮腺之间存在显著相关性。28天内输注CCK-8S导致胰腺湿重、蛋白质和DNA含量显著增加。CCK-A受体拮抗剂地伐西匹使胰腺中的蛋白质和DNA含量降低。两种处理均未影响腮腺。在输注CCK-8S或地伐西匹的36小时、3天、7天和28天,未观察到对腮腺浆液细胞和导管细胞标记指数的影响。