A perifusion system was applied for the study on stimulusenzyme secretion coupling in dispersed pancreatic acini. The system is highly simple, preserves the acini up to more than 3 hr, and makes feasible clear-cut examination on the time course of enzyme secretion caused by secretagogues. Caerulein (10-s M) and carbamylcholine (10-5 M) caused a biphasic amylase secretory pattern consisting of an initial burst secretion and a sustained one. Caerulein induced a persistent amylase release even after cessation of the stimulation, while carbamylcholine-stimulated amylase release returned to basal levels. Atropine inhibited completely carbamylcholine-stimulated amylase release and the successive stimulation by caerulein evoked the amylase secretion with a decreased initial burst secretion. In calcium free medium, caerulein and carbamylcholine induced only a slight secretion, particularly in the sustained secretion phase and a gradual increase occurred with the addition of calcium.

The role of Cat + and calmodulin in stimulation of the rat pancreatic acini induced by secretin, forskolin, and dibutyryl cyclic AMP (dbcAMP) was studied using W-7, a calmodulin antagonist, and a low Cat + medium. The time course of amylase secretion was studied in a perifusion system using dispersed rat pancreatic acini. The amylase release patterns of each secretagogue were as follows: a biphasic amylase release pattern under the stimulation of secretin, a one peak pattern during the stimulation of forskolin and a rapid response after cessation of the stimulation, and a gradual increased pattern during the stimulation of dbcAMP followed by a rapid response. The amylase release under the stimulation by forskolin and dbcAMP was slightly weaker as compared with that of secretin stimulation. The amylase secretion stimulated by secretin (5 x 10-' M), forskolin (50 µM), and dbcAMP (2 mM) was inhibited by W-7 (50 µM). In a low Cat + medium (4.7-5.1 x 10-6 M), the secretory rate did not increase during the stimulation by secretin, forskolin, and dbcAMP, and a rapid amylase response remained after cessation of the stimulation of forskolin and dbcAMP. The pretreatment with EDTA (1 mM) suppressed both the gradual amylase release and the rapid response induced by dbcAMP in a low Cat + medium. These results suggested that each secretagogue, via cyclic AMP (cAMP), induced a different amylase secretory pattern dependent on an intracellular Cat + content, and was mediated by the Cat+-calmodulin complex.

A new radioimmunological method for determination of serum rat elastase was described and serum elastase levels were measured in two different stages of acute pancreatitis: acute edematous and haemorrhagic pancreatitis were induced by PDL and PDLD technique in rats. In edematous pancreatitis, serum elastase levels showed a significant increase (P < 0.001) at one hour after induction of pancreatitis. Compared with control rats, whereas the serum amylase levels did not show a significant increase. In haemorrhagic pancreatitis, the levels of both elastase and amylase markedly increased within one hour of induction pancreatitis. These results show that the measurement of elastase level offers a more specific and sensitive parameter of diagnosis of acute pancreatitis than does amylase estimation.

In this study using radioimmunoassay for rat, the relationship between the changes of elastase levels and the histological changes of pancreas demonstrated in two different cases of experimental chronic pancreatitis induced by dl-ethionine or PDL technique, and the resulting elastase levels were compared with amylase levels. In some of the Ethionine rats, serum elastase showed a high level, whereas serum amylase exhibited a significant decrease. In PDL rats at 3 days after ligation, elastase levels were higher than in other control rats. In PDL rats at 2, 4, and 8 weeks after ligation, serum elastase levels had significantly decreased, whereas amylase levels had not changes significantly when compared with the control rats. The changes of serum elastase levels in two different cases of experimental chronic pancreatitis showed some relation to the histological changes of the pancreas, while changes in serum amylase levels were not exhibited.

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