Löser C, Nustede R, Becker H J, Köhler H, Fölsch U R
I. Department of Internal Medicine, Christian-Albrechts-University of Kiel, Germany.
Int J Pancreatol. 1995 Oct;18(2):107-15. doi: 10.1007/BF02785884.
The neuropeptide neurotensin is known to play a role in the regulation of exocrine pancreatic secretion, but actually there are conflicting results as to whether or not neurotensin exerts a trophic response on the pancreas and there are no data concerning its effect on pancreatic polyamine metabolism. In the present study, acute and long-term effects of various intraperitoneal dosages of neurotensin that resulted in mildly supraphysiological and even unphysiological high plasma concentrations of neurotensin were studied. Furthermore, neurotensin was simultaneously administered with cholecystokinin (1 microgram CCK-8/kg body wt ip every 8 h) for five days. The administration of neurotensin resulted in an acute significant decrease of pancreatic amylase and trypsinogen concentrations (p < 0.001), which indirectly confirms the potent effect of neurotensin on pancreatic exocrine secretion. In contrast to that, neither during the short-term study (100 micrograms neurotensin/kg body wt ip every 8 h for 2, 4, 6, 8, 16, and 24 h) nor during the long-term study (1 microgram, 100 micrograms, or 200 micrograms neurotensin/kg body wt ip three or eight times daily for 10 d) did neurotensin administration result in any increase of the various parameters of pancreatic growth and polyamine metabolism. Simultaneous administration of neurotensin and CCK failed to alter or further increase the known stimulatory effect of CCK on pancreatic polyamine metabolism and pancreatic growth after 5 d of treatment. These data indicate that neither alone nor in combination with cholecystokinin did various dosages of neurotensin exert any significant stimulation on pancreatic growth or the parameters of pancreatic polyamine metabolism.
已知神经肽神经降压素在胰腺外分泌的调节中发挥作用,但实际上关于神经降压素是否对胰腺产生营养反应存在相互矛盾的结果,且尚无关于其对胰腺多胺代谢影响的数据。在本研究中,研究了不同腹腔内剂量的神经降压素所产生的急性和长期影响,这些剂量导致神经降压素在血浆中的浓度略高于生理水平,甚至达到非生理的高浓度。此外,神经降压素与胆囊收缩素同时给药(每8小时腹腔注射1微克CCK - 8/千克体重),持续5天。神经降压素的给药导致胰腺淀粉酶和胰蛋白酶原浓度急性显著降低(p < 0.001),这间接证实了神经降压素对胰腺外分泌的强大作用。与此相反,在短期研究中(每8小时腹腔注射100微克神经降压素/千克体重,持续2、4、6、8、16和24小时)以及长期研究中(每天腹腔注射1微克、100微克或200微克神经降压素/千克体重,共3次或8次,持续10天),神经降压素的给药均未导致胰腺生长和多胺代谢的各项参数增加。在治疗5天后,同时给予神经降压素和CCK未能改变或进一步增强CCK对胰腺多胺代谢和胰腺生长的已知刺激作用。这些数据表明,不同剂量的神经降压素单独使用或与胆囊收缩素联合使用,均未对胰腺生长或胰腺多胺代谢参数产生任何显著刺激作用。