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

Samples of intestinal contents were obtained from 16 patients: 5 from the midjejunum, 10 from the distal ileum, and 1 from the cecum. The presence of pancreatic and nonpancreatic isoamylases in these fluids was evaluated by an inhibitor assay (Pharmacia Corporation) and by polyacrylamide gel electrophoresis. In every sample the inhibitor assay detected the presence of pancreatic-type isoamylase but not salivary-type isoamylase. Electrophoresis confirmed that salivary-type isoamylase was totally absent. Therefore, in intestinal disorders which disrupt the intestinal mucosal barrier (such as ischemia, perforation, ulceration, or obstruction), the amylase which escapes from the intestinal lumen and is reabsorbed into the circulation is likely to consist entirely of pancreatic-type isoamylases. In these circumstances, measurement of serum amylase isoenzymes will not distinguish acute pancreatitis from an acute intraabdominal catastrophe requiring surgery.
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PMID:Identification of amylase isoenzymes in intestinal contents. 620 Feb 78

Acute pancreatitis may be initiated in the ex vivo, perfused canine pancreas preparation by a variety of stimuli. These include oleic acid infusion (FFA), partial duct obstruction with secretin stimulation (POSS), and a 2-hour period of ischemia (ISCH). In each model, pancreatitis is characterized by weight gain, edema, and hyperamylasemia. Oxygen-derived free radicals such as superoxide, hydrogen peroxide, and the hydroxyl radical are highly reactive toxic substances that are normally produced in small amounts during oxidative metabolism. Ordinarily, these substances are detoxified by endogenous intracellular enzymes called free radical scavengers (FRS), such as superoxide dismutase (SOD) and catalase (CAT). These studies were undertaken to evaluate the possible role of oxygen-derived free radicals in the initiation of acute pancreatitis in the isolated canine model. All preparations were perfused for 4 hours with autologous blood. Controls (N = 6): these glands remained normal in appearance, gained minimal weight (6 +/- 1 g), and serum amylase remained normal (less than 1000 u/dl). FFA pancreatitis, FFA alone (N = 6): these glands became edematous, gained weight (113.5 +/- 27.0 g), and developed hyperamylasemia (2087 +/- 387 u/dl). FFA + FRS (N = 6), SOD (50 mg) and CAT (50 mg) were added to the perfusate at time zero: these glands became only minimally edematous, gained less weight (31.8 +/- 10.1 g, p less than 0.05), and amylase remained normal (p less than 0.05). POSS pancreatitis, POSS alone (N = 8): these glands became edematous, gained weight (38.6 +/- 4.6 g), and developed marked hyperamylasemia (9522 +/- 3226 u/dl). POSS + FRS (N = 6): these glands did not develop edema, gained less weight (15.1 +/- 2.6 g, p less than 0.05), and serum amylase only increased to 1815 +/- 343 u/dl, (p less than 0.05). ISCH pancreatitis, ISCH alone (N = 6): these glands became edematous, gained weight (75.8 +/- 25 g), and developed hyperamylasemia (1679 +/- 439 u/dl). ISCH + FRS (N = 6): these glands did not develop edema, gained only 18.3 +/- 9.0 g (p less than 0.005), and serum amylase remained normal (p less than 0.05). These studies demonstrate that, in this canine preparation, acute pancreatitis is significantly ameliorated by oxygen-free radical scavengers. Since this was true whether the pancreatitis was produced by FFA infusion, POSS, or ischemia, it suggests that oxygen-derived free radicals may mediate a common essential step in the pathogenesis of all forms of pancreatitis.
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PMID:The role of oxygen-derived free radicals in the pathogenesis of acute pancreatitis. 620 83

The influence of a short-term ischemia of the pancreas for the pathogenesis of a hemorrhagic necrotising pancreatitis was investigated in 28 mongrel dogs. Ischemia of the pancreas in 20 minute intervals repeated three times did not leave any macroscopic, histologic or electron microscopic changes and no alterations of the level of the alpha-amylase, the lipase, and the glucose in the serum. An ischemia of 20 minutes' duration by starvation of the celiac artery and the superior mesenteric artery produces a hemorrhagic necrotising pancreatitis under the precondition of a following pancreatic edema by ligature of the pancreatic duct and secretomotoring with secretin and pancreozymin. The necrosis starts histologically in the perilobular adipose and affects the parenchyma later. Whether the lipase is the starting enzyme for the acute pancreatitis or only conditions the early adipose necrosis should be discussed after these findings. Already a fugitive pancreatic edema produces a hemorrhagic necrotising pancreatitis after previous ischemic damage.
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PMID:[Animal experiment studies on the role of ischemia in the pathogenesis of acute pancreatitis]. 633 88

Additionally to the pancreatic edema short-time ischemia represents an essential factor in formation of an experimentally induced acute pancreatitis. The consequences of such an ischemia at the guinea pig pancreas on the cellular energy metabolism were investigated in isolated exocrine cells. It was shown that intact acinus cells can be isolated as well as from normally perfused and ischemic pretreated pancreata. The energy metabolism was characterized by the difference between resting and maximum respiration after stepwise uncoupling. This parameter represents a dynamic measure and allows an estimate of the load capacity of the cellular energy metabolism. Exocrine cells isolated after ischemia (20 minutes), had a smaller load capacity than cells from normally perfused pancreata. This indicates an alteration of energy supply after ischemia. The consequences of this reduced supply on energy dependent repairing and protective mechanisms are discussed in terms of the pathogenesis of acute pancreatitis.
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PMID:[Isolated acinus cells in the significance of ischemia in the pathogenesis of acute pancreatitis]. 648 42

Colonic involvement should be suspected in patients with severe acute pancreatitis, especially in the following clinical settings: plain abdominal radiographs suggesting bowel ischemia, colonic obstruction, acute lower gastrointestinal hemorrhage, gram-negative septicemia, enteric bacteria on Gram stain or culture of peritoneal fluid, and feculent abdominal drainage from a previously drained pancreatic abscess. Intraoperatively, the pancreas should be widely drained and the fecal stream diverted. Colonic hemorrhage and nonviable bowel require immediate resection. Broad-spectrum antibiotic administration and vigorous nutritional support also are required in these critically ill patients. Although proximal diversion and pancreatic diversion alone may suffice, colonic resection may be required later for persistent obstruction or fistulization, but in a more elective setting. Colonic anastomoses should be performed only when pancreatic inflammation and associated sepsis have resolved completely.
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PMID:Colonic complications of acute pancreatitis and pancreatic abscess. 663 61

The etiology and pathogenesis of acute necrotizing hemorrhagic pancreatitis remain controversial. Recent work has suggested that an early fall in pancreatic blood flow, causing ischemia, may be the initiating factor. Using an established rat model of hemorrhagic pancreatitis and the fractional indicator distribution technique with 86RbCl, pancreatic blood flow and tissue perfusion have been measured at various times in the condition. Six groups of ten rats were studied: control sham operation and pancreatitis groups were sacrificed at 1, 6, and 24 hr. Pancreatic blood flow (% of cardiac output) and perfusion (blood flow/g tissue) were measured. Blood flow was increased by a maximum of 53% at 1 hr (P less than 0.001) and remained elevated for 24 hr, and perfusion was increased by a maximum of 70% (P less than 0.001) at 1 hr and remained elevated at 6 hr. Pancreatic perfusion declines after 6 hr due to increasing gland edema. The results demonstrate a significant increase in pancreatic blood flow and perfusion in experimentally induced acute pancreatitis, suggesting a primary inflammatory response, and refute the ischemic etiological theory.
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PMID:Pancreatic blood flow in experimental acute pancreatitis. 707 32

In an examination of the effect of ischemia and reperfusion on the generation of active oxygen species during pancreatic cell damage, a short-term ischemia and reperfusion model was prepared by the occlusion and reperfusion of both the anterior mesenteric artery and the celiac artery in rats. Following 60 minutes of occlusion plus 7 hours of reperfusion of the anterior mesenteric artery and the celiac artery, the serum concentrations of amylase and lipase rose significantly to 7 and 6 times the respective control values. After 30 minutes of occlusion plus 7 hours of reperfusion, or after 7 hours of occlusion without reperfusion, amylase and lipase levels were not changed significantly. The continuous intravenous infusion of superoxide dismutase (3600 U/kg/hour) in rats receiving 60 minutes of occlusion plus 7 hours of reperfusion suppressed the rise in serum amylase and lipase values to 25 percent of the values in the non-injected group. These results suggest that the active oxygen species which are generated by the short-term ischemia and reperfusion method injure the endothelium and cause hyperamylasemia and hyperlipasemia. Inhibition of the rise in serum amylase and lipase concentrations by pretreatment with a scavenger of active oxygen, superoxide dismutase, suggests that the active oxygen species are involved in the pathogenesis of acute pancreatitis.
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PMID:Effect of postischemic reperfusion on the pancreas. 750 64

Extraintestinal trypsinogen activation peptides (TAP) have been shown to correlate with severity of acute pancreatitis in humans as well as in various animal models. Ischemia superimposed on experimental pancreatitis, however, increases acinar cell injury without increasing TAP in plasma. We speculated that TAP generated in the pancreas might not reach the circulation in necrotizing pancreatitis due to decreased pancreatic perfusion. To test the hypothesis that generation of TAP in plasma is related to pancreatic perfusion and that plasma TAP may therefore underestimate acinar cell injury in necrotizing disease, we correlated TAP in pancreatic tissue and body fluids with capillary pancreatic blood flow in necrotizing and edematous pancreatitis. The ratio between necrosis and TAP in tissue was similar in both models; the ratio between TAP in plasma and tissue, however, was significantly lower in necrotizing pancreatitis, indicating that a certain amount of TAP generated in the pancreas did not reach the circulation. Decreased pancreatic perfusion found in necrotizing pancreatitis was consistent with this finding. Our data suggest that TAP in tissue is most reliable to indicate severity of acute pancreatitis, whereas plasma TAP may underestimate pancreatic injury in necrotizing disease due to decreased pancreatic perfusion.
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PMID:Effect of microcirculatory perfusion on distribution of trypsinogen activation peptides in acute experimental pancreatitis. 758 86

Acinar necrosis in patients with acute pancreatitis can be due to enzymatic injury, ischemia, or both. We hypothesized that novel therapy aimed at an improvement of pancreatic microcirculation early in the course of pancreatitis may reduce the lethality and acinar damage. Forty-six dextran-resistant rats received controlled intraductal infusion of glycodeoxycholic acid (10 mmol/L), followed by intravenous cerulein (5 micrograms/kg/h) for 6 hours. Beginning 30 minutes after the induction of pancreatitis, all animals were resuscitated with Ringer's lactate (RL) (8 mL/kg/h intravenously for 9 hours). In addition, they were given intra-aortic bolus infusions (2 mL/kg at 30, 60, 90, and 150 minutes) of either RL, sodium chloride (NaCl) (7.5%) and dextran 60,000 (10%) (HHS-60), NaCl (7.5%) and dextran 500,000 (10%) (HHS-500), or NaCl (0.9%) and dextran 500,000 (10%) (DEX-500). Despite high-volume fluid resuscitation in the groups that received RL and HHS-60, 70% of the animals in each of these groups died within 24 hours. In contrast, the mortality rates in the groups of animals that received HHS-500 and DEX-500 were dramatically reduced to 0% and 10%, respectively (p = 0.005, p = 0.02). Histopathologic scores for acinar necrosis were significantly lower in the group of animals that received DEX-500 (p < 0.009) compared with those that received RL and HHS-60. Finally, total amounts of trypsinogen activation peptides in ascites were significantly lower in the animals that received HHS-500 (p < 0.004) and DEX-500 (p < 0.02) compared with those that received RL and HHS-60. Rapid bolus infusion of hyperoncotic ultrahigh molecular weight dextran solution with or without hypertonic saline but not RL or hypertonic-hyperoncotic saline-dextran significantly reduced pathologic trypsinogen activation, prevented acinar necrosis, and improved survival in acute experimental pancreatitis. We speculate that a sustained improvement of pancreatic microcirculation by ultrahigh molecular weight dextran is the mechanism of action.
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PMID:Hyperoncotic ultrahigh molecular weight dextran solutions reduce trypsinogen activation, prevent acinar necrosis, and lower mortality in rodent pancreatitis. 767 89

The early pathogenetic steps that finally lead to acinar cell necrosis in acute pancreatitis have been characterized only scarcely as yet. Among a lot of hypotheses, one concept favors disturbances of cellular energy metabolism as a major factor that contributes to preterm cell decline. To investigate, whether an experimental acute pancreatitis alters cell respiration, the respiratory capacities of acinar cells isolated from rats with acute pancreatitis were measured. Acute pancreatitis was induced using Popper's model, i.e., a combination of duct obstruction, secretory stimulation, and mesenteric short-term ischemia with subsequent reperfusion. Acinar cells were isolated using a collagenase digestion technique. The respiratory rates of the isolated cells in suspension were measured at 37 degrees C in 100% oxygen-saturated N-(2-hydroxyethyl)piperazine-N'-2-ethanesulfonic acid-buffered Eagle's-minimal essential medium. Resting respiration of the acinar cells uniformly amounted to about 60 pmol of O2/s x 10(6) cells in both the control and the pancreatitis group. Cellular respiration could significantly be stimulated by stepwise uncoupling of oxidative phosphorylation by means of 2,4-dinitrophenol in all cell suspensions investigated. The maximum rate of stimulated respiration was diminished in the cells isolated from rats with acute pancreatitis as compared with the controls (79.3 +/- 5.0 vs. 160.2 +/- 15.5 pmol of O2/s x 10(6) cells, p < .05), however. This reduced respiratory load capacity of the acinar cells in acute pancreatitis reflects the restricted ability of the cells to increase respiration on enhanced cellular demand. Since mitochondrial respiration is coupled to oxidative phosphorylation, an altered energy-transforming potential of the acinar cells in acute pancreatitis becomes evident.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acinar cell respiration in experimental acute pancreatitis. 777 97


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