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Query: UMLS:C0030305 (pancreatitis)
16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Morphologic disorders in the liver during the acute pancreatitis are an important aspect of multiorgan disturbances seen in this disease. The study aimed at evaluating ultrastructural disorders in the of the experimental pancreatitis. The study involved 24 male Wistar rats. The acute experimental pancreatitis has been produced by the injection of a 5% sodium taurocholate during sterile laparotomy. Samples for examination have been taken after 1, 3, 6, and 12 hours. Collected samples have been examined systematically. Mitochondrial pleomorphism, partial RER degranulation, decrease in glycogen content, and autophagocytosis have been noted already within 1 and 3 hours. The degree of these disorders has increased within 6 hours, reaching its peak after 12 hours. Marked degeneration of mitochondria, high autophagocytosis, nearly complete disappearance of glycogen, impaired sinusal endothelium, and Kupffer's cells stimulation, in which increased phagocytic activity has been noted made a complete picture of the ultrastructural disorders. Such morphologic changes in the liver have indicated its damage in the early stages of the acute pancreatitis. It may be of importance for the development of multiorgan complications of this disease.
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PMID:[Ultrastructural changes in rat liver in early stages of experimental acute pancreatitis]. 166 89

The rat pancreas ultrastructure was examined 6, 12, and 18 h after (1) taurocholate-induced acute pancreatitis and after (2) pancreatitis preceded 6 h earlier by intragastric acute 40% ethanol ingestion (5 g/kg b.w.). Pancreatic specific trypsin activity and plasma alpha-amylase were assayed at the same time intervals. The antecedent acute ethanol ingestion resulted in the evident aggravation of pancreas ultrastructural alterations. Acute pancreatitis preceded by ethanol resulted in the increase of zymogen granules number, RER channels were more irregularly distributed, autophagosomes were more abundant and degeneration of mitochondria was more advanced when compared to acute pancreatitis without ethanol ingestion. Tryptic activity increased to higher degree in all pancreatitis groups preceded by ethanol, but this difference was statistically significant (P < 0.01) only after 18 h. These morphological (but not biochemical) differences progressed 12 h after pancreatitis induction. After 18 h of acute pancreatitis the number of zymogen granules decreased in previously alcoholized rats, but tryptic activity remained twofold higher that in animals not given ethanol. Other signs of cellular impairment were still more prominent in alcoholized rats. The obtained results suggest that even single acute ethanol abuse prior to acute pancreatitis does aggravate the morphological and biochemical lesions observed in this disease with possible negative consequences for the prognosis.
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PMID:The effect of antecedent acute ethanol ingestion on the pancreas ultrastructure in taurocholate pancreatitis in rats. 982 48