Göke B, Leferink J, Göke R, Adler G
Dept. of Internal Medicine, Philipps University of Marburg, Federal Republic of Germany.
Res Exp Med (Berl). 1989;189(1):33-8. doi: 10.1007/BF01856026.
Oral administration of the proteinase inhibitor camostate to rats results in a characteristic regulation of pancreatic enzyme synthesis and release. These effects are thought to be mediated by an endogenous cholecystokinin release in answer to camostate feeding. An additional direct effect of the compound could be exerted directly on the acinar cell. We evaluated in the present study whether the acute or chronic influence of camostate alters the basal or cerulein-stimulated enzyme release from isolated rat acini. Neither basal nor cerulein-induced (10(-12) to 10(-8) M) amylase release from acini of non-pretreated donor rats were influenced in the presence of 5, 50, or 500 microM camostate. After oral feeding of camostate (200 mg/kg b.wt. daily) over 5 days pancreatic growth occurred. In experiments with acini obtained from the camostate-pretreated rats highly significant reductions of the cerulein-induced amylase release were found as compared to controls. Our findings exclude a direct effect of camostate on the secretory process of pancreatic acinar cells. However, after repeated oral pretreatment of donor rats a "desensitization" of acini against cerulein stimulation occurs. This latter effect is ascribed to elevated endogenous cholecystokinin which was released in response to camostate feeding.
给大鼠口服蛋白酶抑制剂卡莫司他会导致胰腺酶合成和释放出现特征性调节。这些作用被认为是由内源性胆囊收缩素释放介导的，以应对卡莫司他喂食。该化合物的另一种直接作用可能直接作用于腺泡细胞。在本研究中，我们评估了卡莫司他的急性或慢性影响是否会改变从分离的大鼠腺泡中基础或蛙皮素刺激的酶释放。在存在5、50或500微摩尔卡莫司他的情况下，未预处理供体大鼠腺泡的基础或蛙皮素诱导（10^(-12)至10^(-8) M）的淀粉酶释放均未受到影响。口服卡莫司他（200毫克/千克体重，每日）5天后，胰腺发生生长。在使用从经卡莫司他预处理的大鼠获得的腺泡进行的实验中，与对照组相比，发现蛙皮素诱导的淀粉酶释放显著降低。我们的研究结果排除了卡莫司他对胰腺腺泡细胞分泌过程的直接作用。然而，在对供体大鼠进行反复口服预处理后，腺泡对蛙皮素刺激出现“脱敏”。后一种作用归因于因卡莫司他喂食而释放的内源性胆囊收缩素升高。
