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

We investigated adrenal medullary function in acute pancreatitis with shock in dog. Pancreatitis was induced by injection of autologous bile into the main pancreatic duct. Adrenal medullary function was examined by basal adrenal catecholamine (CA) output and CA release response to the electrical stimulation of the 1t. splanchnic nerve. Animals were divided into two types--Shock type and non-shock type. In both types, basal CA output increased gradually, but, CA release response in shock type was lower than that in non-shock type. Moreover, both values of basal CA output and CA release response in shock type were lower than those oligemic shock group at the same blood pressure level. On the other hand, no significant difference was observed among these 3 groups on the increase of blood pressure by nerve stimulation, that is, low response of CA release in shock type had no relation with the nerve injury. It was concluded that adrenal medulla was injured in acute pancreatitis with shock by pancreatitis per se.
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PMID:[Adrenal medullary function in acute pancreatitis with shock in the dog]. 405 13

The long-term effects of octreotide, the synthetic analog of the hormone somatostatin, on acute experimental pancreatitis were studied. Acute pancreatitis was induced in rats by intraparenchymal injections of 0.5 ml 5% or 10% sodium taurocholate. Octreotide (10 mg/kg/day, subcutaneously), or saline injections as controls, were started four hours later, and their effects were assessed 30, 60, and 90 days after the induction of pancreatitis. Neither intrapancreatic saline injections nor octreotide administration without the induction of pancreatitis caused any biochemical or histological abnormalities. Taurocholate-induced pancreatitis was followed by remarkable hyperglycemia, which was ameliorated by octreotide. Thirty days after induction of pancreatitis, glucose levels were 269+/-21 mg/100 ml and 153+/-17 mg/100 ml in the control and octreotide treated animals, respectively (P < 0.02). Octreotide administration was associated with increased pH values after 60 and 90 days (P < 0.05 for the 90 days group). The levels of hematocrit, calcium, and amylase were already within the normal ranges after 30 days and were unaffected by octreotide. There were no signs of chronic exocrine insufficiency and all the surviving rats gained weight during the follow-up. However, the relative weights of the pancreases of the octreotide-treated animals were higher than those of the controls 30 days after IOP. Histopathological evaluation demonstrated regeneration of the pancreatic tissue, and increased number and hypertrophy of the islets of Langherhans. There were no significant differences whether the octreotide treatment was given for only 48 or 96 hr. Survival was significantly improved by octreotide; only one octreotide-treated rat (2.5%) with 10% taurocholate-induced pancreatitis died, while six (15%) of the control animals succumbed (P < 0.05). These studies provided data on the sequelae of acute pancreatitis and showed that octreotide may have long-term beneficial effects in this disease.
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PMID:Octreotide ameliorates glucose intolerance following acute experimental pancreatitis. 950 25

This study investigated the mechanistic role of group IIA phospholipase A2 (sPLA2-IIA) in the process of pancreatitis-associated adrenal injury in acute necrotizing pancreatitis. One hundred and sixty male Wistar rats were subdivided into a sham-operated group, a sodium taurocholate-induced pancreatitis group, and a pancreatitis group pretreated with sPLA2 inhibitor (pku-mdl-101). The sPLA2 inhibitor was administered by intravenous injection 30 min before induction of pancreatitis. The severity of pancreatitis was evaluated by serum amylase and pancreatic histological score. The serum corticosterone level was measured. Adrenal injury was evaluated by histological evaluation, as well as by sPLA2 activity and sPLA2-IIA protein analysis. Pancreatitis resulted in a time-related increase in serum amylase and in the pancreatic histological score. At first, serum corticosterone increased after 3h and decreased rapidly after 6h in pancreatitis. Adrenal injury aggravated during the observation period. The sPLA2 activity in the serum and adrenal glands, as well as the expression of sPLA2-IIA protein in adrenal glands increased and peaked 6h after the induction of pancreatitis. Pretreatment of sPLA2 inhibitor significantly reduced the severity of pancreatitis and adrenal histological injury, improved the 24-h serum corticosterone levels, and effectively inhibited sPLA2 activity and sPLA2-IIA expression in adrenal glands. The sPLA2 inhibitor attenuated the severity of pancreatitis and pancreatitis-associated adrenal injury. The observations indicate that sPLA2-IIA plays a crucial role in pancreatitis-associated adrenal injury in acute necrotizing pancreatitis.
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PMID:Crucial role of group IIA phospholipase A2 in pancreatitis-associated adrenal injury in acute necrotizing pancreatitis. 1936 31