Maouyo D, Guan D, Rivard N, Morisset J
Département de Biologie, Faculté des Sciences, Université de Sherbrooke, Québec, Canada.
Pancreas. 1995 Nov;11(4):330-40. doi: 10.1097/00006676-199511000-00003.
We demonstrated previously in ad libitum fed and fasted rats that chymotrypsinogen and amylase secretions were weakly or not at all correlated (1). However, the mechanisms controlling these correlations remain undetermined. We investigated the influences of cholinergic and cholecystokinin-related systems on the relationship between amylase and chymotrypsinogen in rats. Animals provided with pancreatic, biliary, duodenal, and jugular vein cannulas were kept in restraint cages under controlled temperature and humidity, with a regular 12-h light cycle, and divided into five groups. The first group of fed rats was constantly infused with 200 micrograms kg-1 h-1 atropine, the second with 0.5 mg kg-1 h-1 MK329, and the third with both. In the group in which both drugs were simultaneously infused, 500 micrograms kg-1 h-1 atropine was intraperitoneally administered, whereas MK329 was infused by intravenous cannula. Two groups consisted of fasted rats, of which one was also atropinized (100 micrograms kg-1 h-1). Three-day experiments were performed separately with fed rats, and 2-day experiments with fasted rats; atropine and/or MK329 infusion was constant over 48 h, in both fed and fasted rats. Atropine alone did not alter the correlation between enzymes even though the total protein and amylase outputs decreased, whereas the chymotrypsinogen output increased; MK329, slowly but significantly, increased the correlation between enzymes, whereas it decreased the outputs for all secretory parameters. When both antagonists were simultaneously infused in fed rats, correlation coefficients between amylase and chymotrypsinogen rapidly and markedly increased. In fasted rats, atropine infusion induced a tremendous decrease in total protein and amylase mean outputs but a significant increase in chymotrypsinogen output, without any significant change in the correlation between both enzymes. These results indicate that the nonparallel secretion of amylase and chymotrypsinogen is strongly modulated by a cholecystokinin-dependent mechanism and that this modulatory process is potentiated by the parasympathetic system.
我们先前在随意进食和禁食的大鼠中证明，胰凝乳蛋白酶原和淀粉酶的分泌之间相关性较弱或根本没有相关性(1)。然而，控制这些相关性的机制仍未确定。我们研究了胆碱能和胆囊收缩素相关系统对大鼠淀粉酶和胰凝乳蛋白酶原之间关系的影响。给配备有胰腺、胆管、十二指肠和颈静脉插管的动物置于可控温度和湿度的约束笼中，保持12小时规律光照周期，并分为五组。第一组喂食的大鼠持续输注200微克/千克·小时的阿托品，第二组输注0.5毫克/千克·小时的MK329，第三组同时输注两者。在同时输注两种药物的组中，腹腔注射500微克/千克·小时的阿托品，而MK329通过静脉插管输注。两组由禁食大鼠组成，其中一组也用阿托品处理(100微克/千克·小时)。对喂食大鼠进行为期三天的实验，对禁食大鼠进行为期两天的实验；在喂食和禁食大鼠中，阿托品和/或MK329的输注在48小时内持续进行。单独使用阿托品尽管总蛋白和淀粉酶输出量减少，但胰凝乳蛋白酶原输出量增加，却并未改变酶之间的相关性；MK329缓慢但显著地增加了酶之间的相关性，而它降低了所有分泌参数的输出量。当在喂食大鼠中同时输注两种拮抗剂时，淀粉酶和胰凝乳蛋白酶原之间的相关系数迅速且显著增加。在禁食大鼠中，输注阿托品导致总蛋白和淀粉酶平均输出量大幅下降，但胰凝乳蛋白酶原输出量显著增加，而两种酶之间的相关性没有任何显著变化。这些结果表明，淀粉酶和胰凝乳蛋白酶原的非平行分泌受到胆囊收缩素依赖性机制的强烈调节，并且这种调节过程被副交感神经系统增强。
