1985
DOI: 10.1016/s0344-0338(85)80203-x
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Ultrastructural Changes of the Human Pancreas in Acute Shock

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Cited by 33 publications
(10 citation statements)
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“…Histological examinations demonstrate early on morphological changes of the ER during the onset of AP. Gene-profiling studies show significant alterations in ER stress key regulators and in a model of necrotizing pancreatitis all ER stress sensors (PERK, IRE1, and ATF6) become activated, an initiation of downstream signal pathways occurs initiated from the ER (1,17,18,23,25,27). It has also been observed that stimulation of isolated pancreatic acini by different secretagogues can generate an ER stress response (22).…”
Section: Discussionmentioning
confidence: 99%
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“…Histological examinations demonstrate early on morphological changes of the ER during the onset of AP. Gene-profiling studies show significant alterations in ER stress key regulators and in a model of necrotizing pancreatitis all ER stress sensors (PERK, IRE1, and ATF6) become activated, an initiation of downstream signal pathways occurs initiated from the ER (1,17,18,23,25,27). It has also been observed that stimulation of isolated pancreatic acini by different secretagogues can generate an ER stress response (22).…”
Section: Discussionmentioning
confidence: 99%
“…This includes dilatation or vacuolation of the ER and loss of membrane-bound ribosomes (1,17,25,27). ER changes seem a common reaction of acini to the induction of ER stress (18,23).…”
mentioning
confidence: 99%
“…The examination of the vascular structure of rats in our study did not show any microthrombi or vascular pathology ( Figure 1C). However, there is evidence that ischemia may be an initiating factor of pancreatic microcirculatory injury in acute pancreatitis (31)(32)(33)(34). Tissue PAF and TNF-α levels were increased in rats with acute pancreatitis but not in rats with massive hemolysis but without acute pancreatitis.…”
Section: Discussionmentioning
confidence: 99%
“…Several experimental studies have shown the particular susceptibility of the pancreas to hypoperfusion with a decrease of capillary blood flow, an increase of pancreatic proenzymes and enzyme-complexes in the general circulation and histo-pathological alterations of the pancreas [12-15, 17, 23]. Similar findings have been made for humans with severe trauma and hypovolaemic or septic shock [6,22,35,47,50]. Splanchnic hypoperfusion and systemic inflammatory reaction contribute to pancreatic damage, with leukocyte accumulation in the pancreatic capillaries and anoxia of highly active metabolic rate cells of the exocrine pancreas.…”
Section: Introductionmentioning
confidence: 52%