Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An 85-year-old white woman underwent placement of an intra-aortic balloon pump for stabilization prior to planned bypass surgery. The complication of acute pancreatitis was attributed to atheroemboli or compromise of circulation to the pancreas. Ischemia as a possible etiology of pancreatitis is discussed.
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PMID:Acute pancreatitis associated with intra-aortic balloon pump placement. 885 43

Bradykinin mediates the inflammatory process of acute pancreatitis characterized by an increase of microvascular permeability, vasodilation and leukocyte activation. These phenomena are characteristic also for the ischemia/reperfusion injury of the pancreas, which in time is considered a causative factor in the pathogenesis of acute pancreatitis. The aim of this study was to investigate the influence of the bradykinin B2 receptor antagonist CP-0597. After complete ischemia/reperfusion of the pancreas in rats there is progression from postischemic acute edema to necrotizing pancreatitis over a reperfusion period of 5 days. In 8 Sprague-Dawley rats (treatment group) 18 micrograms/kg/h CP-0597 was administered intraperitoneally over 5 days with an osmotic minipump starting 15 min before release of 2 h ischemia. Animals of the placebo group (n = 8) were identically treated, but received the solvent, phosphate buffer. Animals of a control group (n = 7) underwent sham operation without ischemia. After 5 days the animals were sacrificed for histology. No morphological changes of the pancreatic gland were observed in the control group. Ischemia for 2 h resulted in necrotizing pancreatitis with high mortality (4/8 animals) during the reperfusion period of 5 days. In contrast, all animals in the treatment group survived without clinical or histological signs of necrotizing pancreatitis.
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PMID:The bradykinin antagonist CP-0597 can limit the progression of postischemic pancreatitis. 885 57

A 49-year-old male presented with atypical chest pain. Complete cardiac evaluation was normal except for cardiac catheterization, which revealed a myocardial bridge across the LAD (left anterior descending coronary artery) that caused a 50% systolic stenosis. Abdominal ultrasound revealed cholelithiasis. The patient became asymptomatic and was discharged only to return with biliary pancreatitis, which resolved over 2 weeks and laparoscopic cholecystectomy was attempted. Upon establishment of a pneumoperitoneum, he began to suffer cardiac ischemia, which immediately resolved upon desufflation. The procedure was converted to an uneventful open cholecystectomy. He did well without any further problems. This is the first report of myocardial bridging, a well-known cardiac anomaly, possibly preventing safe laparoscopy. This was possibly due to transmitted intraperitoneal pressure effect on the pericardium pushing closed that myocardial bridge.
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PMID:Myocardial bridging prevents safe laparoscopy? A case report. 887 44

Pancreatic hyperstimulation with simultaneous duct obstruction does not cause the typical features of acute pancreatitis, therefore the role of an additional challenge, such as either ethanol intoxication or short-term ischemia, was studied. Alcoholic pancreatitis was induced in 28 rats by acute ethanol intoxication (0.25 LD50) and an obstruction/hyperstimulation mechanism (clip of the biliopancreatic duct for 20 min and intravenous stimulation with 5 U of cholecystokinin and secretin each). Ischemic pancreatitis was performed by obstruction/hyperstimulation and subsequent pancreatic ischemia by clamping the supplying arteries for 40 min. The macro- and microscopic alterations were evaluated and graded by a scoring system. Additionally, the pancreas was removed in 50% of the animals and the pancreatic acini were prepared. From those acini the intracellular enzymes trypsinogen, kallikreinogen, amylase, lipase, glucuronidase, and acidic phosphatases were determined. While obstruction/hyperstimulation, 40 min of ischemia, or ethanol alone did not induce acute pancreatitis, a combination of obstruction/hyperstimulation with either ethanol or ischemia resulted in acute pancreatitis in 68 and 60% of treated rats, respectively. Similarly, both models were characterized by extrapancreatic fat necrosis and acinar necrosis at the periphery of the lobules. Almost all intracellular enzymes were elevated in both pancreatitis models compared to sham-operated controls. Both alcohol and ischemia were insults that sensitize the pancreas to develop acute pancreatitis after obstruction/hyperstimulation. Since the observed morphologic and enzymatic alterations in both models are very similar, alcohol and ischemia might have some common pathways by which they make the pancreas vulnerable to enzymatic attacks.
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PMID:Similar morphological and intracellular biochemical changes in alcoholic acute pancreatitis and ischemic acute pancreatitis in rats. 898 5

A case of preeclampsia-eclampsia leading to acute edematous pancreatitis is reported, probably related to microvascular abnormalities and splanchnic ischemia. Recovery was uneventful.
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PMID:Acute pancreatitis and preeclampsia-eclampsia: a case report. 907 33

In this study we present the technical details, adaptations and modifications of the original procedure of pancreaticoduodenal transplantation in rats described by Lee et al. in 1972. We also present the results and technical failures observed in a follow-up of 12 years. From March, 1982 to December, 1994, we performed in the Laboratory of Surgical Technique and Experimental Surgery of Faculty of Medicine, Botucatu-UNESP, Brazil, 665 duodenopancreatectomies in donor rats and 592 surgeries for revascularization of the pancreatic graft in recipient animals. The observed percentage of technical failures in donor rats was 11% due to bleeding and/or vascular complications, irregular flushing of the graft with saline and respiratory insufficiency. In recipients of grafts, we observed a percentage of technical failures of 22.5% due to porto-caval thrombosis, vascular bleeding, pancreatitis and graft ischemia. In both surgeries, the successful results are directly related to the technical performance of the surgeon and the cares in the postoperative period.
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PMID:[Microsurgical pancreatoduodenal transplantation in rats. Technique and results following 12 years of investigation]. 920 29

Incomplete ischemia of the celiac trunk due to arterial thrombosis occurred in a patient infected with the HIV. Ischemia led to infarct of the spleen and pancreatitis. Endoluminal desobstruction of the arterial trunk then medical management after exploratory laparoscopy were successful without splenectomy. The causes, diagnostic methods and treatments for splenic infarction in HIV-infected patients are discussed with a review of the literature.
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PMID:[Splenic infarction in a HIV-infected patient. Apropos of a case and review of the literature]. 929 7

It is particularly difficult to distinguish between early rejection and graft pancreatitis when early rejection produces an elevated serum amylase level. In this study we determined whether peripancreatic fluid cytology (PFC) can differentiate early acute rejection and graft pancreatitis as an alternative diagnostic tool to graft biopsy that has the potential of pancreatic fistula and hemorrhage. Sixty-two dogs received either a segmental pancreas allograft (n = 25) or autograft (n = 37) heterotopically in the neck. This study included five groups: allografts without immunosuppression (group A, n = 12), allografts with immunosuppression (group B, n = 13), autografts without immunosuppression (group C, n = 11), autografts with immunosuppression (group D, n = 12), and autografts treated by 45 minutes of pretransplant warm ischemia to induce acute graft pancreatitis (group E, n = 14). A closed suction drainage catheter was placed next to the graft to collect peripancreatic fluid daily after the transplant. PFC was performed using May-Gruenwald-Giemsa double-staining technique and compared to the corresponding histology through the observation period. In analyses of 50 functioning grafts, PFC performed on day 1 showed similar neutrophil accumulations in all groups. In sharp contrast, on days 3 and 6, group A had dramatically increased mononuclear cell concentrations in PFC, whereas groups B, C, and D showed significantly lower concentrations, the percent of mononuclear cells among total leukocytes being 47.3 +/- 23.4%, 11.8 +/- 4.9%, 4.3 +/- 1.8%, and 6.4 +/- 2.4% (day 3); and 32.7 +/- 9.8%, 10.5 +/- 4.8%, 7.2 +/- 4.2%, and 8.6 +/- 6.4% (day 6) in groups A, B, C, and D, respectively. On the other hand, in group E numerous degenerating neutrophils with a marked to moderate increase in necrotic tissue fragments were observed by PFC on days 3 and 6. In terms of graft histology on days 3 and 6, group A showed interstitial mononuclear cell infiltration indicating an acute rejection process, whereas groups B, C, and D had minimal inflammatory cell infiltration. In group E graft pancreatitis was histologically confirmed on days 3 and 6. These results suggest that PFC after pancreas transplantation could be a safe, simple, useful diagnostic tool for discriminating early graft rejection from graft pancreatitis.
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PMID:Peripancreatic fluid cytology: detection of early rejection versus graft pancreatitis after canine pancreatic transplantation. 932 82

We studied the pancreatic high-energy phosphates in two models of acute pancreatitis using 31P nuclear magnetic resonance (NMR) in rats for the first time in vivo. Alcoholic pancreatitis was induced by acute ethanol intoxication and an obstruction-hyperstimulation mechanism. Taurocholate pancreatitis was generated by intraparenchymal administration of 1 ml of 1-10% taurocholate-Na+. In addition to the obligate control groups, a simple ischemia experiment was performed. The high-energy phosphates were monitored by 31P NMR spectroscopy at 2.0 T. Additionally, by means of a scoring system, the quality and quantity of pathomorphologic parameters were quantified after 24 h. 31P spectra acquired after injection of taurocholate showed an increase in inorganic phosphate with a concomitant decrease in ATP levels, similar to pancreatic ischemia. This irreversible decrease was accompanied histologically by severe pancreatic hemorrhage. After induction of alcoholic acute pancreatitis a reversible decrease in ATP was occasionally seen. Even when alcoholic pancreatitis had been fully established at 24 h, the 31P NMR spectrum was normal in all animals. In conclusion, depletion of high-energy phosphates seems to occur as a result of pancreatic cell death rather than being a cause of pancreatic necrosis. For the first time we applied in vivo NMR in the rat pancreas to study the time course in acute pancreatitis.
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PMID:Different changes in high-energy phosphates in alcoholic acute pancreatitis and taurocholate acute pancreatitis in rats using NMR spectroscopy at 2.0 T. 936 Oct 88

We studied the effects of SMS201-995, a long-acting somatostatin analogue, on bile-induced acute pancreatitis in the dog. According to morphometrical study, parenchymal necrotic ratio, zymogen granules area and zymogen granules occupied ratio of acinus were significantly decreased in SMS-treated pancreatitis. These results suggests that SMS-treated pancreatitis showed less damage than non-treated ones and decreased secretion of pancreatic enzyme. On the other hand, pancreatic blood flow showed a stronger decrease in SMS-treated dogs than in non-treated ones, and a significant difference was observed at 15 minutes and 1 hour after induction of pancreatitis. Many clinical and experimental evidences suggest that pancreatic ischemia causes acute pancreatitis. Pancreatitis may be worsened by an early phase treatment with SMS201-995, because this substance reduces pancreatic tissue blood flow. The harmful effect of this substance on pancreatic tissue blood flow must be kept in mind when SMS201-995 is used for therapeutic purpose of acute pancreatitis.
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PMID:[Experimental study on the therapeutic effects of SMS201-995 on bile-induced acute pancreatitis in the dog]. 954 45


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