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Pancreas; pancreatitis - Polish accomplishments

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Polish accomplishments in clinical and experimental pancreatology concern acute (AP) and chronic (CP) pancreatitis. Special notice was drawn in Polish studies on hemostasis disorders in acute experimental pancreatitis (AEP), and resulting clinical implications (possibility of thrombotic-embolic complications leading to hemorrhagic defects associated with coagulation factors consumption). Studies on lysosomal hydrolases role in AEP pathogenesis were discussed. In those studies notice was drawn to initiating role of zymogen activation by lysosomal hydrolases, especially ß-glucuronidase, with smaller activity of acid phosphatase and cathepsin in this process. It was stated, that also lysosomal enzymes are released from macrophages obtained from bronchoalveolar lavage fluid in AEP. It was revealed that prostacyclin (PGI2) shows stabilizing effect on lysosomes in liver and kidneys in AEP. Platelets activating factor antagonist inhibits pulmonary lysosomal hydrolases activity in such conditions. Polish studies concerning reactive forms of oxygen role in AEP pathogenesis are one of the first in Europe. Oxidative-antioxidative balance was disturbed in acute pancreatitis course and associated multiorgan changes both under experimental conditions and in humans. Oxidative stress as an early prognostic symptom in AP in humans was also emphasized, showing correlation of oxidative stress indicators with phospholipase A serum activity and polymorphonuclear elastase in plasma of patients with different degree of this disease. In a range of clinical studies special attention should be given to studies concerning lipid disorders as an AP etiological factor in humans. Clear decrease in lipoprotein lipase activity in AP in humans was determined. Polish studies concerning importance of sphincterectomy in acute gallstone derivative pancreatitis (AGP) were presented. Polish researchers accomplishments in chronic alcoholic pancreatitis (CAP) etiopathogenesis were discussed.
This study was undertaken in order to determine the influence of chronic ethanol administration on pancreatic regeneration during acute pancreatitis (AP). Rats were pair fed with isocaloric diet containing or not ethanol. After 8 weeks of such feeding AP was induced by sc injection of caerulein (Cae). 6 h, 24 h and 5 days after first Cae dose pancreatic weight, amylase, chymotrypsin, protein, RNA, DNA contents were determined and phosphatidic acid (PA) production in isolated pancreatic acini was measured. Proliferating cells were quantified by immunochemical staining of cells incorporating bromodeoxyuridine (BrdU). Results: Pancreatic weight was significantly higher at 6 h after first Cae injection in both, ethanol fed (EF) and control groups (C), however at 24 h pancreatic weight did not differ from prior to AP induction in EF rats. Ethanol feeding (EF) did not influence significantly protein, chymotrypsin and amylase content in pancreatic tissue in groups with AP. In EF rats RNA content after 5 days of AP was higher than in control animals. Total DNA content in EF rats with AP was lower 6 h after AP induction, earlier than in control animals with AP. Immunochemistry showed higher labelling index for BrdU after 6 h, 24 h and 5 days of AP in EF rats. In contrast to this findings, in EF animals, AP induction was not able to stimulate further PA accumulation. Conclusion: We conclude that chronic ethanol feeding, while inhibiting PA accumulation in comparison to control group, does not impair pancreatic tissue regeneration during the early phase of Cae-induced AP. Stimulation of regenerative/reparative processes in EF rats during Cae-induced AP seems to be even more pronounced than in the control group.
This study was designed to assess the gastric secretory effects of ebrotidine, a novel H₂ receptor antagonist, in humans. Three groups (A, В and C) of male subjects with normal gastric mucosa were used. Group A (6 subjects) was used to determine the dose-dependency of gastric inhibitory effect of ebrotidine on basal and pentagastrin- induced maximal acid output. Group В (8 subjects) was employed to examine the duration of the inhibitory effect of ebrotidine on basal and pentagastrin-induced acid secretion. In group C (6 subjects), the 24 h pH-metry was assessed using intraluminal pH-electrode placed in the gastric corpus and connected to a portable recording unit. Single oral dose of ebrotidine (200, 400 or 800 mg) caused a dose- dependent reduction in basal and pentagastrin-induced acid secretion that at a dose of 800 mg amounted to about 89% and 93%, respectively. This inhibition was still observed after 6h and averaged 72% and 50%, respectively. After 12 and 24 h upon the drug intake, both basal and pentagastrin-induced acid secretion returned to the control values. Single oral dose of ebrotidine (800 mg) caused a significant reduction in circadian acidity and resulted in a marked and significant reduction of intragastric acidity for about 6 h upon the administration. This inhibition was accompanied by a transient increase in basal and postprandial gastrin levels. We conclude that ebrotidine is highly effective inhibitor of basal, pentagastrin-induced and circadian gastric acid secretion in humans.
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