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

Acute pancreatitis was produced in rats by a combination of dyschylic edema and short-term ischemia of the pancreas. The incidence of acute pancreatitis, reflected by peri- and extra-pancreatic fat necrosis, was found to be dependent on the duration of ischemia. Under most conditions there were no significant differences in enzyme activities between the animals with macroscopic signs and those without these. The time course of alpha-amylase and lipase release was investigated within 24 hours postoperatively. Additionally the quantitative correlation was estimated of the enzyme activities released from the pancreatic tissue and the activities determined in rat serum. The data show that the serum enzymes represent only a small and variable portion of the total amount of enzymes effused from the pancreas.
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PMID:Influence of pancreatic edema and short-term ischemia of rat pancreas on lipase- and alpha-amylase-activities in the serum and in the pancreas. 349 5

Plasmatic immunoreactive trypsin (IRT), thromboxane and trypsin-like enzymatic activity were measured in 117 patients at risk of developing adult respiratory distress syndrome (ARDS) (53 multiple injury, 30 abdominal surgery, 17 acute pancreatitis, 12 burnt and 5 disseminated intravascular coagulation patients). 69 of these patients developed ARDS. Immunoreactive trypsin and thromboxane were measured by radio-immuno-assay and trypsin-like enzymatic activity by spectrophotometry, using a specific chromogenic substrate. Mean IRT value was 675 ng/ml in ARDS and 265 ng/ml in non ARDS patients (p less than 0.05). Mean IRT value was 685 ng/ml in septic and 170 ng/ml in non septic patients (p less than 0.01). An abnormal trypsin-like enzymatic activity was measured in 26 ARDS patients. In 60 patients (37 ARDS and 23 non ARDS), thromboxane appeared in plasma simultaneously or about 24 hours after the beginning of IRT release. The importance of thromboxane release parallels the intensity of IRT. Originating from pancreas, trypsin can appear in plasma either by absorption from gastrointestinal tract or after pancreatic ischemia.
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PMID:Trypsin-like activity and thromboxane release in adult respiratory distress syndrome. 353 5

For investigations of cell injury during pathogenesis of acute pancreatitis antisera to pancreatic acinar cells were used as experimental tool. Within one hour after intraductal injection of antiserum a strong pancreatic edema was developed. Within 24 h this edema receded to a large extent but at this time there were inflammatory cells scattered in the intra- and periductal region. As a sequel of application of antiserum pancreatic enzymes were released. At 24 h after this application serum activities of alpha-amylase and lipase were significantly increased in comparison to the control and reached that level which was found in a model of acute pancreatitis provoked by pancreatic edema plus short-term ischemia.
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PMID:Influence of antisera to pancreatic acinar cells on rat pancreas in situ. 355 41

The primary pathophysiology of acute pancreatitis is due to a low flow state mediated through the neurohumoral mechanisms. Ischemia of the microcirculation, combined with hormonal and other biochemical factors, produces destruction of cellular elements of the pancreas. These changes can be triggered by one or more stressors, including the psychic factor. Emotional stress may not only be responsible for an initial attack of pancreatitis (idiopathic) but must be considered, like any other stressor, to be responsible for exacerbations, relapses or chronicity of pancreatic disease.
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PMID:Pathogenesis of pancreatitis: a unified concept. 369 76

Few studies have been published on the ultrastructural changes which accompany human acute pancreatitis, and these have concentrated primarily on parenchyma. The present study concentrates on extraparenchymal changes, compares acute pancreatitis occurring alone with that on a background of chronic pancreatitis, and tests for similarity with observations made previously in an experimental model. Pancreatic tissue came from 16 patients undergoing surgery for pancreatic disease and five subjects without pancreatic disease. Regressive changes in parenchymal cells were consistent with ischemia, and with previously described studies. Polymorphonuclear leukocytes infiltrated into stroma and parenchyma. Platelets accumulated intra- and extravascularly. Fibrin deposits were common in the connective tissue, and could be observed in intercellular spaces at the base of acini, mingled with degenerating acinar cells and secretion product. Microthrombi occurred in blood vessels. These alterations were consistent with those in experimental acute pancreatitis. Similar changes were observed whether or not acute pancreatitis occurred on a background of chronic pancreatitis. The vascular component is important in acute pancreatitis, and altered epithelial barriers allow interaction between blood-borne material and pancreatic exocrine secretions.
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PMID:Ultrastructure of human acute pancreatitis. 369 80

For experimental analysis of pathogenesis of acute pancreatitis a suitable animal model is necessary. The pancreatic (juice) edema and an alteration of cellular energy metabolism are important pathogenetic factors. A partial intrapancreatic edema was induced by stimulating secretion against permanent or temporary obstruction by ductal ligation. Short-term ischemia was used as tool for alteration of cellular energy metabolism. 24 h postoperatively morphological changes were macro- and microscopically investigated. The data show a correlation between duration of ischemia (10-30 min) and the frequency of acute pancreatitis at preexisting juice edema (44-68 percent). With increasing ischemia the morphological alterations (e.g.: necroses of adipose tissue) were enhanced, too. A hemorrhagic necrotizing pancreatitis was rarely observed. In comparison to other experimental models the presented one is characterized by a mostly moderate and light course of acute pancreatitis offering a good tool for elucidation of the very first stages of the pathogenesis.
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PMID:Contribution of pancreatic edema and short-term ischemia to experimental acute pancreatitis in the rat. I. Procedure and pathomorphological investigations. 382 14

A large retrospective autopsy study of patients was analyzed to evaluate the major etiologic and pathologic factors contributing to fatal acute pancreatitis (AP). From an autopsy population of 50,227 patients, 405 cases were identified where AP was defined as the official primary cause of death. AP was classified according to morphological and histological, but not biochemical, criteria. Patients with AP died significantly earlier than a control autopsy population of 38,259 patients. Sixty percent of the AP patients died within 7 days of admission. Pulmonary edema and congestion were significantly more prevalent in this group, as was the presence of hemorrhagic pancreatitis. In the remaining 40% of patients surviving longer than 7 days, infection was the major factor contributing to death. Major etiologic groups in AP were chronic alcoholism; postabdominal surgery; common duct stones; a small miscellaneous group including viral hepatitis, drug, and postpartum cases; and a large idiopathic group comprising patients with cholelithiasis, diabetes mellitus, and ischemia. The prevalence of established diabetes mellitus in the AP group was significantly higher than that observed in the autopsy control series, suggesting that this disease should be considered as an additional risk factor influencing survival in AP. Pulmonary complications, including pulmonary edema and congestion, appeared to be the most significant factor contributing to death and occurred even in those cases where the pancreatic damage appeared to be only moderate in extent. Emphasis placed on the early recognition and treatment of pulmonary edema in all cases of moderate and severe AP should contribute significantly to an increase in survival in this disease.
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PMID:Death due to acute pancreatitis. A retrospective analysis of 405 autopsy cases. 389

Microcirculatory derangements in the pancreas associated with acute pancreatitis may contribute to a low-flow state and lead to pancreatic necrosis. This study investigated the effects of glucagon, a selective mesenteric arterial dilator, on pancreatic ischemia in canine bile-trypsin-induced pancreatitis (BTP). Measurements of cardiac Index (CI), total pancreatic blood flow (QP), pancreatic oxygen consumption (O2CP), and pancreatic arteriovenous shunt flow (QAVS) were obtained prior to and after inducing BTP. Bile-trypsin-induced pancreatitis was induced in 18 dogs. Nine received lactated Ringer's solution alone (LRPAN) at 6.5 mL/kg/hr, nine received lactated Ringer's solution plus continuous Intravenous (IV) glucagon hydrochloride (GLUPAN) at 1.0 micrograms/kg/min, and nine undergoing periportal dissection without BTP received IV glucagon (GLUCON). Following BTP, CI, QP, and O2CP decreased significantly and QAVS remained unchanged in crystalloid-treated animals (LRPAN). Glucagon administration (GLUPAN) transiently increased CI and QP but failed to improve O2CP and did not change QAVS. The decrease in O2CP observed after BTP in association with a constant QAVS suggests a metabolic block to oxygen uptake at the cellular level. Glucagon in pharmacologic doses does not reverse abnormalities in O2CP and is therefore of questionable physiologic benefit in the treatment of acute pancreatitis.
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PMID:Efficacy of pharmacologic glucagon in acute experimental pancreatitis. 397 Jun 71

Segmental ischemic gangrene of the colon is a rare complication of acute pancreatitis. Three patients with long-segment colonic necrosis complicating acute pancreatitis are reported. At operation all three patients had extensive retromesocolic necrolysis associated with colonic arterial thrombosis. Colonic resection and intestinal exteriorization with peripancreatic drainage were performed, with survival of two patients. Although diagnosis of colonic ischemia in the presence of acute pancreatitis is difficult, operative therapy affords reasonable cure when this severe problem is recognized.
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PMID:Extensive colonic necrosis complicating acute pancreatitis. 397 49

Recent clinical studies have suggested that ischemia may be an important factor in the pathogenesis of acute pancreatitis. The effects of ischemia on the pancreas were investigated utilizing the isolated perfused canine pancreas. Six control glands were perfused with autologous blood with an arterial Po2 ranging from 250 to 350 mm Hg. During the 4-hour perfusion period, gross appearance remained normal, weight gain was minimal (7 gm), and mean amylase levels (853 Caraway units [CU]/dl) remained within normal limits (less than or equal to 1,000 CU/dl). Lowering the arterial Po2 (range 30 to 60 mm Hg) in six glands while maintaining the flow at control levels elicited no significant change. Similarly, decreasing the flow (25% of control) with the arterial Po2 at 250 to 350 mm Hg produced no significant change in gross appearance, weight gain, or mean amylase levels. Combining low flow and low arterial Po2 in six glands also elicited no significant change as compared with controls. Four glands were subjected to total ischemia for 1 hour before being perfused. The glands became hyperemic, but mean weight gain (13 gm) and mean amylase levels (740 CU/dl) wee similar to those of controls. In contrast, in six glands subjected to total ischemia for 2 hours gross edema developed during the subsequent 4-hour perfusion. Mean weight gain (52 gm) and mean amylase levels (1,825 CU/dl) were significantly higher than in controls. These experimental data demonstrate that in the isolated perfused canine pancreas severe ischemia can produced significant injury. They therefore support the hypothesis that ischemia can clinically initiate acute pancreatitis.
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PMID:The role of ischemia in acute pancreatitis: studies with an isolated perfused canine pancreas. 617 32


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