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Query: UMLS:C0001339 (acute pancreatitis)
 10,593 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A patient with recurrent acute pancreatitis developed pericardial effusion and cardiac tamponade. His systolic blood pressure fell to 70 mmHg and sinus tachycardia (150/min) developed. The central venous pressure rose from 3 cm H2O to 27 cm H2O. A chest radiograph showed an enlargement of the cardiac shadow. Pericardial paracentesis was performed and 300 ml fluid was aspirated. This produced rapid clinical improvement. The literature related to this uncommon complication is reviewed and possible pathogenetic mechanisms are discussed.
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PMID:Cardiac tamponade--a rare complication in acute pancreatitis. 923 91

Twenty four patients with biliary pancreatitis were divided into three groups: A (18 subjects underwent surgery on the biliary tract seven days after admission to hospital when acute signs disappeared); B (3 cases were operated two months later), and C (3 patients underwent emergency surgery for acute cholescistitis with simultaneous acute pancreatitis). A cholecistectomy-choledochostomy through a Kehr tube was performed in all patients. Pressure in the main biliary duct (MBD) was measured. Only group A was significant (18 cases). As a control, another group, group D was considered (52 biliary cholecysto-choledochal lithiasis patients without pancreatitis and without transduodenal sphincterotomy). Group A: 1) The mean pressure in MBD on the fourth postoperative day (11 days after onset of pancreatitis) was low (p < 0.0001) in relation to that of group D with Oddi's sphincter (SO) normal; 2) in group A, no significant differences (p-NS) were found in relation to positions: during fasting, 4.4 +/- 4 cm H2O in the upright position, and 5.3 +/- 2 when lying (in group D, 9.9 +/- 4.1 cm H2O upright, and 7.76 +/- 3.6 lying with p = 0.0001), and 3) a slow improvement of pressure was observed and, on the 25th day after operation, it was nearly normal (9 cm H2O upright and 7 cm lying with p < 0.001). Group B: biliary surgery at 2 months; mean pressure in MBD meartly normal. Group C: 1) 4 days after emergency surgery, the pressure in MBF (15 cm H2O upright and 11.7 lying) was higher than in subjects with normal SO, probably due to compression of the distal part of MBD by the inflamed pancreas, and 2) from the 11th day the pressure followed the same evolution as that of group A. In conclusion, in patients with acute biliary pancreatitis, operated on the biliary tract when acute signs disappeared, MBD pressure is low (p < 0.0001) in reference to normal on the fourth post-operatory day (11 days after onset of pancreatitis) and no significant differences were found in relation to positions (upright and lying). The pressure changes are transient (4-5 weeks) and most probably due to the lesions and malfunction of the SO related to pancreatitis.
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PMID:Acute biliary pancreatitis: sphincter of Oddi and choledochal pressure. 955 45

This study was designed to investigate hyperbaric oxygen (HBO) therapy as a treatment for managing animals with induced acute pancreatitis. Forty-five anesthetized male Sprague-Dawley rats were studied. A severe acute pancreatitis model was established by combining an intravenous infusion of cerulein (15 microg/kg/h) and an intraductal injection of 0.1 ml of glycodeoxycholic acid (5 mM). Pathology, serum amylase level, pancreatic malondiadehyde levels and water content of the lungs and the pancreas were used to evaluate the severity of disease. Moreover, an in vivo microscopic technique was used to investigate microcirculatory derangement in the pancreas, i.e., flow velocity and leukocytes sticking in postcapillary venules. HBO was delivered in three regimens, i.e., 100% oxygen at 2.5 absolute atmospheric pressure (AAP), 40% oxygen at 2.5 AAP, and 100% oxygen at 1 AAP, 6 h after the initiation of induction of acute pancreatitis. All animals survived until the end of the experiments. HBO significantly improved the pathologic conditions and pancreatic malondiadehyde levels. Concomitantly, it also significantly lessened the severity of lung edema and improved the microcirculatory environment in the pancreas. Our results support the findings that HBO therapy has a beneficial effect on pancreatic microcirculation and lung edema during acute pancreatitis in rats.
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PMID:Hyperbaric oxygen therapy attenuates pancreatic microcirculatory derangement and lung edema in an acute experimental pancreatitis model in rats. 966 19

Bacterial translocation leading to subsequent infectious complications is a significant determinant of outcome in acute hemorrhagic pancreatitis (AHP). The colonic ileus and impaired intestinal barrier function that often accompany AHP may predispose to translocation. Sennoside is a naturally occurring cathartic and choleretic agent that stimulates intestinal mucous secretion and has potent promotility effects. The impact of sennoside-induced intestinal motility and secretory function on bacterial translocation and survival was studied in a rat model of AHP. Severe acute pancreatitis was induced in rats by the intraductal infusion of 2% sodium deoxycholate (DCA, 0.4 ml/kg). A group of sham-operated rats (group A) received intraductal saline, whereas experimental animals were subsequently administered distilled water (group B) or sennoside solution (group C) by gavage every 8 h. After 48 h, intestinal transit of fluorescein isothiocyanate-labeled dextran, serum endotoxin, and amylase levels, and bacterial translocation to mesenteric lymph nodes (MLNs) and pancreatic tissue were determined. The pancreas and intestine were sampled for histologic study. All group A animals survived and did not develop pancreatitis or endotoxemia, whereas groups B and C all demonstrated severe hemorrhagic pancreatitis with evidence of necrosis. Mortality at 48 h was 55% in group B versus 12.5% in group C. Inhibition of intestinal motility was noted in 40% versus 20%, and endotoxin levels were 61.36+/-28.26 pg/L versus 5.41+/-3.58 pg/L in group B versus group C rats, respectively (p<0.001). Pancreatic tissue and MLN cultures were positive in 100% of group B survivors versus 14% of group C survivors (p<0.05). Histologic examination of the intestine in group C animals showed increased mucous secretion, proliferation of goblet cells, and evidence of rapid turnover/renewal of enterocytes. Treatment with the cathartic agent, sennoside, reduced translocation of endotoxin and bacteria, restored intestinal motility, increased mucous secretion, and reduced mortality in a model of acute hemorrhagic pancreatitis in the rat. Other cathartics may have similar properties and may be useful in preventing infectious complications in acute pancreatitis.
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PMID:The effect of sennosides on bacterial translocation and survival in a model of acute hemorrhagic pancreatitis. 988 59

The N2-Mercaptopropionylglycine (N2-MPG) is a potent antioxidant by inhibiting the abnormal production of xantina-oxidase. The aim of this research is to analyze the antioxidant capacity of this tiol compound by offering some protection to pancreatic tissue in the acute pancreatitis (AP). The induction of AP was obtained through two methods: a) supramaximal dose of cerulein; b) infusion of 2.5% sodium taurocholate into the biliopancreatic duct of the rat. Thirty-six male Wistar rats (220-270 g) were divided into four groups. AP with cerulein (Two parenteral doses of 20 micrograms/kg; one hour interval): in two groups: GI: nineteen rats previously treated with N2-MPG (100 mg/kg) ten minutes before AP. GII (control): seventeen animals which received saline 0.9%. AP with taurocholate (0.5 ml into the main biliopancreatic duct): in other two groups: GIII: eleven rats previously treated with N2-MPG (100 mg/kg) ten minutes before AP. GIV (control): fifteen animals which received saline 0.9%. The albumin leakage into the cell interstice as an inflammatory parameter was measured through Evans-Blue (EB) colorimetry, that links totally with serum albumin after injection into the pancreatic tissue, immediately before induction of AP. The rats were sacrificed one hour after. Water tissue content was also measured. There was a relevant reduction of EB leakage in GI (344 +/- 27 micrograms/gtissue) when compared to GII (729 +/- 84 micrograms/gtissue), p < 0.01, and in GIII (386 +/- 52 micrograms/gtissue) when compared to GIV (543 +/- 53 micrograms/gtissue), p < 0.05. There was no difference in tissue water content between GI (88.2 +/- 0.6%) and GII (87.4 +/- 0.9%), but certainly between GIII (77.7 +/- 2.1%) and GIV (82.8 +/- 1.2%), p < 0.05. The amilase levels didn't show any difference among the four groups. These results suggest that the use of the antioxidant N2-MPG offers a protective action, at least in rats, reducing the severity of AP induced by supramaximal dose of cerulein, and even in a more severe AP such as produced by sodium taurocholate at 2.5%, although apparently not interfering with its pathogenesis. It also strengthens the actual participation of free radicals of oxygen in the physiopathology of acute pancreatitis.
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PMID:[Antioxidative effect of N2-mercaptopropionylglycine (N2 MPG) in experimental acute pancreatitis]. 992 94

This study was designed to evaluate the possible role of cytokines (IL-1 and TNF-alpha) in the pathogenesis of acute pancreatitis in the early stage of the disease and to evaluate the protective effect of the cytokine suppressive agent, FR167653, against pancreatic injuries. Acute pancreatitis was induced in rats by closed duodenal loop. However, the free passage for the gastrointestinal contents was maintained by inserting the tube into the duodenum. In this model, the survival rate was significantly decreased as compared with the control sham-operated rats at 48 h after induction of pancreatitis. Marked hyperamylasemia and a significant increase in pancreatic water and trypsin contents were observed at 24 h after induction of pancreatitis. Pancreatic subcellular redistribution of lysosomal enzyme cathepsin B from the lysosomal fraction to the zymogen fraction was also observed. However, treatment with FR167653 at a dose of 1.5 mg/kg (four times, every 6 h after induction of pancreatitis) significantly prevented all these pancreatic injuries, improving the survival rate. These results indicate that cytokines such as IL-1 and TNF-alpha may be involved in the pathogenesis of acute pancreatitis in the early stage of the disease, and that a cytokine-suppressive agent might be of therapeutic value for the treatment of acute pancreatitis.
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PMID:Cytokine suppressive agent improves survival rate in rats with acute pancreatitis of closed duodenal loop. 992 44

Ten dogs with pituitary-dependent hyperadrenocorticism (PDH) received 2 mg/kg of L-Deprenyl once daily for 6 months. Monthly patient assessment consisted of evaluation of the owner's daily observation protocol, a standardized owner questionnaire, physical examination, CBC, biochemical profile, determination of the urine cortisol/creatinine ratio (UC/C), low-dose dexamethasone suppression (LDDS) test, corticotropin releasing hormone (CRH) test, and adrenal ultrasonography. At the beginning and the end of the study, an adrenocorticotropic hormone (ACTH) stimulation test and computed tomography also were performed. Two dogs developed neurologic signs and 2 dogs developed acute pancreatitis. An increase in activity, decrease in polyphagia, and decrease in panting were reported by 6, 4, and 2 owners, respectively. Seven owners believed that water intake decreased, but this was confirmed in only 3 dogs. Water intake increased in 2 dogs and remained unchanged in 5 dogs. The condition of the hair coat and skin improved in 2 dogs, worsened in 3, and remained unchanged in 5. Urine specific gravity, urine osmolality, ACTH test results, UC/C, and adrenal gland size did not change significantly throughout the study. In 4 of 8 dogs, LDDS was abnormal at the start of the study but normal at the end of the study, and in 2 dogs, the opposite occurred. Marked individual variation was noted in the CRH test, with a tendency for smaller increases in ACTH toward the end of the study. A marked increase in hypophyseal tumor size occured in 4 dogs. Treatment with L-Deprenyl resulted in improvement, deterioration, and stagnation of clinical signs in 2, 4, and 4 dogs, respectively. The results of this study indicate that L-Deprenyl cannot be recommended as the sole treatment for canine PDH.
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PMID:The efficacy of L-Deprenyl in dogs with pituitary-dependent hyperadrenocorticism. 1044 18

Oxidative stress plays a major role in the early stage of acute pancreatitis. This study assessed the effects of N-acetylcysteine (NAC), a reduced glutathione (GSH) provider and a direct scavenger of reactive oxygen intermediates, in the course of acute pancreatitis in mice. Acute pancreatitis (AP) was induced by intraperitoneal (i.p.) injections of cerulein. Mice received NAC (1,000 mg/kg, i.p.) every 3 h, starting either 1 h before the first cerulein injection (prophylactic group) or 1 h after the first cerulein injection (therapeutic group), or i.p. saline injections for controls. Severity of AP was evaluated by histology, serum hydrolase levels, and serum and intrapancreatic levels of MCP-1 and interleukin 6 (IL-6). Pancreatic conjugated dienes and intrapancreatic and intrahepatic GSH levels were measured to assess the local and systemic oxidative processes. Acute pancreatitis was also induced with a CDE diet in controls and mice receiving either both NAC ad libidum in drinking water and 1,000 mg/kg i.p. injection once daily. The severity of pulmonary lesions was assessed by arterial blood gases (pO2) and intrapulmonary myeloperoxidase (MPO content) measurements as well as the survival of mice. The severity of cerulein-induced AP was significantly decreased in the prophylactic group compared with the therapeutic and control groups. Prophylactic administration of NAC also decreased the intrapancreatic levels of conjugated dienes compared with controls. The intrapancreatic and systemic release of MCP- 1 and IL-6 was also decreased in the prophylactic group 3 and 6 hours after AP induction. In addition, NAC pretreatment also reduced hepatic IL-6 production at 3 and 6 hours after starting cerulein challenge. In CDE-induced AP, the severity of lung injury (hypoxemia, MPO content) was decreased, and survival was improved by NAC. NAC administered in a prophylactic protocol limits the severity of experimental acute pancreatitis in mice, as well as its systemic complications and related mortality.
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PMID:N-acetylcysteine decreases severity of acute pancreatitis in mice. 1070 32

In order to develop a new severe but sublethal acute pancreatitis model for the study of clinically relevant extrapancreatic multiorgan injury, we have induced acute pancreatitis in a rat model by intraductal injection with low dose and moderate concentration of bile acid under low pressure. We examined the structural and functional features in the pancreas, lung, liver and kidney. The animals were divided into two groups: the bile acid injection group and the control group. In the bile acid injection group, acute necrotizing pancreatitis was induced by intraductal administration of 0.2 ml of 2.0% bile acid under 30 cm H2O pressure, while the controls underwent the sham operation. The two groups were divided into six subgroups (8 rats for each) and sacrificed at 12, 24, 36, 48, 72 and 144 h, respectively. The pancreatitis induced hyperamylasemia, ascites, pancreatic oedema, haemorrhage, acinar cell necrosis and extensive fat necrosis without early mortality. Accompanied with the pancreatic injury, the function and histologic changes have developed continuously in the kidney and liver for 72 and 144 h in the bile acid injection animals respectively. No pancreatitis associated pulmonary changes were found. Taking into account the results with the two previously developed models of pancreatitis, we conclude that the extrapancreatic injury in acute pancreatitis is found in the liver, kidney and lung, in that order, depending on the severity of pancreatitis. The present sublethal pancreatitis model, in comparison with the two previously studied acute pancreatitis models, is perfect for pathogenetic and therapeutic study of liver and renal changes in acute necrotizing pancreatitis.
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PMID:Extrapancreatic multiorgan injury in a severe sublethal acute pancreatitis model. 1134 4

This study was designed to evaluate the protective effect of thromboxane A2 (TXA2) receptor antagonist, seratrodast, against pancreatic injuries during acute pancreatitis. Acute pancreatitis was induced in rats by intravenous infusion of a supramaximal dose of caerulein (5 microg/kg x h for 4 h). In this model, marked hyperamylasemia, a significant increase in pancreatic water content, and a significant increase in pancreatic micro-vascular leakage of Evans blue dye were observed. Pancreatic subcellular redistribution of a lysosomal enzyme, cathepsin B from the lysosomal fraction to the zymogen fraction as well as a significant increase in pancreatic trypsin content were also observed. Pretreatment with seratrodast at a dose of 2 mg/kg (twice, 8 and 4 h before caerulein infusion) significantly inhibited these pancreatic injuries including hyperamylasemia, increased pancreatic microvascular leakage, redistribution of cathepsin B and increased pancreatic trypsin content. These results suggest that TXA2 may be involved in the pathogenesis of acute pancreatitis in the early stage of the disease and that TXA2 receptor antagonist might be of therapeutic value for treatment of acute pancreatitis.
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PMID:Thromboxane A2 receptor antagonist prevents pancreatic microvascular leakage in rats with caerulein-induced acute pancreatitis. 1134 8


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