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

Acetaldehyde (AA), the first product of ethanol metabolism, has been suggested as an important mediator in alcoholic pancreatitis, but experimental evidence has not been convincing. Prior work using the isolated perfused canine pancreas preparation has suggested that toxic oxygen metabolites generated by xanthine oxidase (XO) may mediate the early injury in pancreatitis. Xanthine oxidase is capable of oxidizing AA, and during this oxidation free radicals are released. The hypothesis that acute alcoholic pancreatitis may be initiated by AA in the presence of active XO (converted from xanthine dehydrogenase [XD]) was tested in the authors' experimental preparation by converting XD to XO by a period of ischemia, and infusing AA. Control preparations remained normal throughout the 4-hour perfusion (weight gain, 7 +/- 4 g; amylase activity, 1162 +/- 202 U/dL). One hour of ischemia or infusion of AA at 25 mg/hr or at 50 mg/hr without ischemia did not induce changes in the preparation. Acetaldehyde at 250 mg/hr induced minimal edema and weight gain (16 +/- 4 g; p less than 0.05), but not significant hyperamylasemia. Changes also were not observed when 1-hour ischemia was followed by a bolus of ethanol (1.5 g) or sodium acetate (3.0 g), or by infusion of 25 mg/hr of AA. One hour of ischemia followed by infusion of AA at 50 mg/hr or at 250 mg/hr induced edema, hemorrhage, weight gain (22 +/- 7 g [p less than 0.05] and 26 +/- 17 g [p less than 0.05]) and hyperamylasemia (2249 +/- 1034 U/dL [p less than 0.05] and 2602 +/- 1412 U/dL [p less than 0.05]). Moreover infusion of AA at 250 mg/hr after 2 hours of ischemia potentiated the weight gain (62 +/- 20 g versus 30 +/- 14 g [p less than 0.05]), but not the hyperamylasemia (3404 +/- 589 U/dL versus 2862 +/- 1525 U/dL) as compared with 2 hours of ischemia alone. Pancreatitis induced by 1 hour of ischemia followed by AA at 50 mg/hr could be inhibited by pretreatment with the free radical scavengers superoxide dismutase and catalase and ameliorated with the XO inhibitor allopurinol. The authors conclude that AA, in the presence of active XO, can initiate acute pancreatitis in the isolated canine pancreas preparation and may be important in the initiation of acute alcoholic pancreatitis in man. Toxic oxygen metabolites appear to play an important intermediary role.
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PMID:The role of acetaldehyde in the pathogenesis of acute alcoholic pancreatitis. 172 Jun 11

Vascular mechanisms play an important but controversial role in the pathogenesis of acute pancreatitis. In experimental animals, injection of wax, powder, air, mercury, and microspheres into the pancreatic artery causes pancreatitis by end artery occlusion with resulting cellular infarction. Larger microspheres do not cause pancreatitis because collateral blood flow is preserved. Clinical evidence, such as microthrombi and atheromatous emboli in the pancreatic artery of patients with pancreatitis, supports pancreatic infarction as an etiologic agent. Experimental and clinical studies have suggested that pancreatic ischemia may also cause pancreatitis, but these studies have not been conclusive. We have compared five hours of total occlusion of the pancreaticoduodenal artery along with four hours of reperfusion to bile injection into the pancreatic duct as causes of pancreatitis. Bile injection caused a significant increase in serum amylase, activation of trypsin in pancreatic exudate, and histologic evidence of necrotizing pancreatitis. Pancreatic blood flow decreased as pancreatitis developed. Ischemia for five hours did not cause a significant increase in serum amylase or activation of trypsin in pancreatic exudate. Only edema was seen histologically, but there was no necrosis. Pancreatic blood flow increased with reperfusion. We believe ischemia aggravates, but does not initiate pancreatitis. Ischemia does not induce inflammation and necrosis in the pancreas, although infarction does.
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PMID:Mechanisms of acute pancreatitis. Vascular etiology. 174 44

In order to examine the toxic effects on the pancreas of oxygen free radicals which are generated at reperfusion after ischemia, a short term-ischemia/reperfusion model was prepared in rats. Both the anterior mesenteric artery and the celiac artery were ligated and then released to restore blood flow. In a group where the anterior mesenteric and the celiac arteries were ligated for 60 minutes, the serum levels of amylase and lipase rose 7 and 6 times, respectively, 7 hours after reperfusion. In a group ligated for 30 minutes, both levels remained unchanged. Histologically, vacuolization of the pancreatic acinar cells was observed, only in a group rats ischemic for 7 hours. In rats ligated for 60 minutes with a continuous venous infusion of superoxide dismutase (SOD) (3600 U/Kg/hour), the secretion of amylase and lipase decreased to 25 percent of that in the non-injected group. These results confirm that the oxygen free radicals, which are generated by the short term-ischemia/reperfusion method, injure the pancreas. This may lead to pancreatitis with hyperamylasemia and hyperlipasemia. Pretreatment with an active oxygen scavenger, SOD, markedly reduces the rise in serum amylase and lipase levels. This suggests that active oxygen free radicals are involved in the pathogenesis of acute pancreatitis.
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PMID:[Effect of short-term-ischemia and reperfusion on the rat pancreas]. 182 5

In pathogenic studies on acute pancreatitis the importance of a temporary ischemia on induction of autodigestion was demonstrated. Because of the involvement of oxygen-derived free radicals in the ischemia/reperfusion injury of other tissues we have investigated the influence of artificial oxidants, as FeCl3 and H2O2, on pancreatic tissue and isolated pancreatic acinar cells. Lipid peroxidation was determined as thiobarbituric-acid-reactive substances (TBRS). In these experiments the TBRS concentration was elevated within the first min of incubation with FeCl3. The exposure of pancreas homogenates and intact acinar cells to H2O2 had no remarkable effect on formation of TBRS. Under this condition the survival of cells was strongly reduced, while cells exposed to FeCl3 revealed a remarkably slower rate of cytolysis. The missing correlation between cell lysis and elevation of TBRS suggests that lipid peroxidation might not be essential process in pancreatic acinar cell damage.
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PMID:Studies on lipid peroxidation in pancreatic tissue. In vitro formation of thiobarbituric-acid-reactive substances (TBRS). 191 59

Previous studies using the isolated ex vivo perfused canine pancreatitis preparation showed that during a 4-hour perfusion pancreatitis (edema, weight gain, hyperamylasemia) can be induced by four different stimuli. The stimuli include the intra-arterial infusion of oleic acid (FFA), a 2-hour period of ischemia before perfusion (ISCH), partial obstruction of the pancreatic duct with secretin stimulation (POSS), and the intra-arterial infusion of cerulein at supramaximal doses (CER). In the present study, changes in high-energy phosphate metabolism, as determined by nuclear magnetic resonance spectroscopy, and changes in cellular structure, determined by light and electron microscopy, were documented for all four models of acute pancreatitis. The control preparations remained stable for the 4-hour perfusion period, with no decrease in adenosine triphosphate (ATP) levels. In the FFA preparations, ATP decreased to 36% of baseline levels during the 4-hour perfusion (p less than 0.001). In the ISCH preparations, ATP decreased to undetectable levels during the 2-hour period of ischemia, but recovered rapidly and remained at baseline levels during the perfusion. ATP levels remained stable in the remaining two models of pancreatitis (POSS, CER). Microscopy demonstrated that the initial injury was located chiefly in the capillaries (swollen endothelium, intravascular thrombi) in the FFA and ISCH preparations. In the POSS and CER preparations, capillary changes were minimal and the injury was located chiefly in the acinar cells (swollen endoplasmic reticulum, zymogen granule depletion, vacuolization). The POSS preparations also showed striking dilation of centroacinar lumens reflecting duct obstruction. In additional studies it was shown that the ATP decline in the FFA preparations could be significantly reduced by pretreatment with free radical scavengers. The morphologic changes could be reduced by free radical scavengers in the FFA and ISCH preparations. Any amelioration of morphologic injury in the POSS preparations was obscured by dilatation of centroacinar lumens in both treated and untreated groups. The morphologic changes in the CER preparations were reduced by treatment with a cholecystokinin inhibitor.
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PMID:Changes in high-energy phosphate metabolism and cell morphology in four models of acute experimental pancreatitis. 200 16

Plain film of the abdomen is widely used in the diagnostic evaluation of intestinal occlusion. Even though this technique can yield a panoramic and high-resolution view of gas-filled intestinal loops, several factors, such as type and duration of occlusion, neurovascular status of the intestine and general patient condition, may reduce the diagnostic specificity of the plain film relative to the organic or functional nature of the occlusion. From 1987 to 1989, fifty-four patients with intestinal occlusion were studied combining plain abdominal film with abdominal ultrasound (US). This was done in order to evaluate whether the additional information obtained from US could be of value in better determining the nature of the ileus. US evaluation was guided by the information already obtained from plain film which better demonstrates gas-filled loops. The results show that in all 27 cases of dynamic ileus (intestinal ischemia, acute appendicitis, acute cholecystitis, acute pancreatitis or blunt abdominal trauma) US demonstrates: intestinal loops slightly increased in caliber, with liquid content, or loops containing rare hyperechoic particles, intestinal wall thickening and no peristalsis. In 27 cases of acute, chronic or complicated mechanical ileus (adhesions, internal hernia, intestinal neoplasm, peritoneal seedings) US shows: 1) in acute occlusion: hyperperistaltic intestinal loops containing inhomogeneous liquid; 2) in chronic occlusion: liquid content with a solid echogenic component; 3) in complicated occlusion: liquid stasis, frequent increase in wall thickness, moderate peritoneal effusion and inefficient peristalsis. In conclusion, based on the obtained data, the authors feel that the combination of plain abdominal film and abdominal US can be useful in the work-up of patient with intestinal occlusion. The information provided by US allows a better definition of the nature of the ileus.
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PMID:[Plain radiographic examination and abdominal echography in intestinal occlusion syndrome. Preliminary note]. 201 34

Five patients with severe acute pancreatitis (AP) underwent subtotal pancreatectomy, and six patients with advanced chronic pancreatitis (CP) were subjected to pancreatic resection. Microangiography and histological studies were performed on the resected pancreata. All patients with AP had histologically verified necrotizing pancreatitis. Pancreatic ducts in the necrotic areas had severe inflammation in their walls and a decrease in their vascularity. The ductal walls of CP patients were indistinguishable from the surrounding fibrosis and the vascular supply of the ducts was markedly diminished. The vessels were reduced in number, and their calibers varied considerably. Ductal ischemia in connection with AP and CP is discussed.
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PMID:Vascular changes of pancreatic ducts and vessels in acute necrotizing, and in chronic pancreatitis in humans. 203 15

Thoracoabdominal aortic aneurysmectomy with a temporary bypass from left axillary to right common iliac artery was successfully performed in a 57 year-old-female with an aneurysm involving celiac, superior mesenteric and renal arteries. An elevation of serum amylase level with a peak value on 7 POD was observed and ultrasonography revealed acute pancreatitis resulting from seventy minutes ischemia of celiac artery during the procedure. The patient was treated conservatively and discharged. It seems to be important to prevent pancreatic ischemia in thoracoabdominal aortic aneurysmectomy as well as to maintain renal and hepatic circulation.
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PMID:[Postoperative pancreatitis following thoracoabdominal aortic aneurysmectomy--a case report]. 226 48

The early lesions induced in the pancreas of dogs by the intraductal injection of bile-trypsin were studied. Histological, histochemical and electron microscopic techniques were used. The primary lesions analyzed thirty three minutes after the induction of pancreatitis consisted in cell alterations, blood stasis and oedema. At first, the affected acinar cells showed enlargement of the rough endoplasmic reticulum cisternae, later they were disrupted and then appeared vesicles with ribosomes adhering to the external surface. Mitochondria were swelled and showed cristae disrupted which finally appeared destroyed. The zymogen granules lost density, decreased in size and number and later disappeared, Ducts maintained the normal structure and their cells were still observed in areas where the tissue was greatly destroyed. the results obtained suggest that: 1) The experimental acute pancreatitis induced by bile-trypsin is characterized by primary and severe damage in the acinar cells, with secondary ischemia due to stasis and intravascular coagulation. 2) Cellular rests and probably endogenous enzymes invade the periacinar spaces, then would penetrate into the vascular system producing the generalization of lesions.
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PMID:[Acute pancreatitis induced by bile trypsin: structural and ultrastructural study]. 227 10

Viable acinar cells were isolated from normal rat pancreas as well as from pancreata pretreated in situ by a short-term ischemia without and with reperfusion, induction of a pancreatic juice edema, and acute pancreatitis (AP), respectively. The isolated cells were incubated at 37 degrees C in an oxygenated Krebs-Henseleit bicarbonate buffer lacking any nutrient. As an analog to in vivo acinar cell necrosis, the decline of the isolated cells was followed up in vitro. During the first 5-6 h of incubation, the percentage of damaged cells increased only slightly. A second phase of about 30 min followed, during which nearly all residual cells died. The mean half-life (t50) of the cells in all experimental groups ran to about 330 min, with the exception of the AP group (t50 = 132 min). The importance of an intact energy metabolism to prevent premature cell killing was underlined indirectly by the diminished t50 (about 120 min in all groups) of the cells exposed to excess 2,4-dinitrophenol, an uncoupler of oxidative phosphorylation. The results suggest that experimental AP induced by a combination of biliary-pancreatic duct obstruction, stimulation of pancreatic secretion, and short-term pancreatic ischemia with subsequent reperfusion finds a reflection within the acinar cells themselves and that these effects are not clouded by the isolation procedure. Thus, the application of acinar cells isolated from pancreatic glands pretreated in situ may offer a new tool for pathophysiological research into AP at the cellular level.
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PMID:Decreased survival rate of pancreatic acinar cells isolated from rats with acute pancreatitis. 239 82


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