Functional Changes of the Exocrine Perfused Rat Pancreas in Cerulein-Induced Pancreatitis

Abstract

Functional changes of the exocrine pancreas in cerulein-induced pancreatitis were evaluated with the isolated perfused rat pancreas. In control specimens (n = 7), baseline pancreatic juice volume was 0.23 ± 0.06 µl/min and after stimulation with CCK-8 (10^-10M) and secretin (10^-10M), it was 2.26 ± 0.45 µl/min, and in cerulein-induced pancreatitis specimens (n = 8), the corresponding values were 0.11 ± 0.03 and 0.23 ± 0.08 µl/min. The amylase content in the pancreatic juice (IU/min) was 0.73 ± 0.15 (baseline) and 7.03 ± 1.66 (stimulated) in the control specimens, and 0.012 ± 0.002 (baseline) 0.018 ± 0.004 (stimulated), in the cerulein-induced pancreatitis specimens. Amylase and lipase concentrations in the portal effluents were significantly higher in the cerulein-induced pancreatitis (481.3 ± 79.4 IU/ml, 283.7 ± 47.2 BALB U/ml) than in the control specimens (10.7 ± 1.8 IU/ml, 8.9 ± 2.9 BALB U/ml). Using the electron microscope fusion of large vacuoles with lateral plasma membrane was observed in cerulein-induced pancreatitis. In cerulein-induced pancreatitis, normal secretion was markedly decreased, and the lateral secretion was suggested to result in the elevation of pancreatic enzyme levels in portal effluents.

Enzyme load in pancreatic acinar cells is increased in the early stages of acute pancreatitis induced by duct obstruction in rats

“…The accumulation of intracellular enzymes could be explained by two possibilities : (1) the blockage of pancreatic secretion produced by acute pancreatitis, which has been observed both clinically [29] and experimentally [8,[30][31][32][33], and (2) an increase in plasma levels of cholecystokinin (CCK) as a consequence of the absence of the feedback inhibitory mechanism induced by bile [18] and pancreatic proteases [34] in the duodenum. Previous studies have reported that CCK plasma levels are increased in rats from 1 h [35] to at least 18 h [36] after pancreatic duct obstruction.…”

Substance P inhibits pancreatic exocrine secretion via a neural mechanism

“…Here, activation of sensory nerves with resultant peripheral release of SP might rapidly inhibit exocrine pancreatic secretion and protect the gland from enzymatic injury. Inhibition of pancreatic exocrine secretion has been documented by several investigators early in the course of pancreatitis induced by cerulein, a CCK analog (1,25). Future studies are needed to address the potential role of SP in the regulation of exocrine secretion under both physiological and pathophysiological conditions.…”

Vigilin and enzyme expression in isolated pancreatic acini after mellitin and gamma-interferon treatment

“…The onset of acute pancreatitis is accompanied by elevated serum levels of pancreatic amylase, lipase and elastase [3]. Although normal secretion into pancreatic juice of the inflamed pancreas is decreased, these high serum enzyme levels are considered to result from discharge of the lateral plasma membrane [4]. Premature activation of the digestive pancreatic enzymes contributes in a complex extent to severity of pancreatitis [5,6].…”