1998
DOI: 10.1152/ajpgi.1998.274.1.g71
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Subcellular kinetics of early trypsinogen activation in acute rodent pancreatitis

Abstract: To investigate the debated role of intracellular trypsinogen activation and its relation to lysosomal enzyme redistribution in the pathogenesis of acute pancreatitis, rats were infused with the cholecystokinin analog caerulein at 5 μg ⋅ kg−1 ⋅ h−1for intervals up to 3 h, and the changes were contrasted with those in animals receiving saline or 0.25 μg ⋅ kg−1 ⋅ h−1caerulein. Saline or 0.25 μg ⋅ kg−1 ⋅ h−1caerulein did not induce significant changes. In contrast, 5 μg ⋅ kg−1 ⋅ h−1caerulein caused significant hyp… Show more

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Cited by 39 publications
(35 citation statements)
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“…1 Recent investigations have established that one of the earliest pathophysiologic events in pancreatitis is the colocalization of acinar cell organelles containing digestive and lysosomal enzymes, resulting in premature intracellular activation of proteases. 2,3 Numerous treatments directed at inhibiting this autodigestive process have been ineffective, 4,5 in part because patients seek medical attention long after these initiating events have occurred. The individual pancreatic cell injury becomes magnified and propagated by inducing (through incompletely defined mediators) impaired microcirculation, leukocyte adhesion, and leukocyte infiltration.…”
Section: Discussionmentioning
confidence: 99%
“…1 Recent investigations have established that one of the earliest pathophysiologic events in pancreatitis is the colocalization of acinar cell organelles containing digestive and lysosomal enzymes, resulting in premature intracellular activation of proteases. 2,3 Numerous treatments directed at inhibiting this autodigestive process have been ineffective, 4,5 in part because patients seek medical attention long after these initiating events have occurred. The individual pancreatic cell injury becomes magnified and propagated by inducing (through incompletely defined mediators) impaired microcirculation, leukocyte adhesion, and leukocyte infiltration.…”
Section: Discussionmentioning
confidence: 99%
“…The activation peptides of trypsinogen and carboxypeptidase A 1 (CPA 1 ), which are cleaved from the respective proenzyme during the process of activation, are released into the pancreatic tissue or the serum early in the course of acute pancreatitis [20,[23][24][25][26][27].…”
Section: The Mechanism and Intracellular Site Of Zymogen Activationmentioning
confidence: 99%
“…Therefore, the relevance of intracellular trypsinogen activation for the development of fulminant disease remains unclear. In addition to the aforementioned intracellular events, it has been shown by our group [23][24][25][26] and others [22,27,28] that coalescent secretory granules fuse with the basolateral membrane of the acinar cell resulting in maldirected secretion of zymogens into the pancreatic interstitium ( fig. 2).…”
Section: Rationale For Protease Inhibition In Acute Necrotizing Pancrmentioning
confidence: 99%