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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In experiments with dogs the influence of controlled respiration with positive endexpiratory pressure (PEEP) on the pancreas was investigated. The pO2 within the tissue was measured during the time of respiration. At PEEP 10 and PEEP 20 an average diminution was observed in the tissue pO2 of 27% and 37%, respectively. A pancreatic edema produced after PEEP 20 was changing into a necrotizing pancreatitis during the following 24 h. At PEEP 10, such a transition was not observed. The pancreatic edema was accompanied by the typical increase in alpha-amylase and lipase activities. After 24 h there were small changes of the enzyme activities in the serum at PEEP 10, whereas at PEEP 20 they were remarkably increased. These results demonstrate that PEEP 20 causes a shortage of oxygen supply of the pancreas. This shortage in connection with an edema can provoke an acute pancreatitis.
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PMID:[Is there a PEEP-induced pancreatitis in experiments?]. 638 40

Hyperlipemia in an acyanotic patient with diabetic ketoacidosis, alcoholism, and pancreatitis produced a falsely elevated concentration of methemoglobin (19 percent) and a lower-than-expected oxygen saturation measured with an automated spectrophotometer (IL-282 CO-Oximeter). In addition, there was a "normal" hemoglobin level despite a low hematocrit reading. In vitro studies showed that hyperlipemia corresponding to triglyceride levels of 500 mg/100 ml and greater produced erroneously high values for methemoglobin and total hemoglobin and "negative" values for carboxyhemoglobin. These abnormalities disappeared when the excessive lipids were removed by washing the erythrocytes in physiologic saline solution.
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PMID:Factitious methemoglobinemia caused by hyperlipemia. 673

Morphological changes of the lung occur frequently in fatal acute hemorrhagic pancreatitis. The pulmonary alterations are independent of mechanical ventilation and therefore not due to iatrogenic damage caused by high inspired oxygen concentrations. The histological findings are similar to those seen in the so-called shock lung syndrome. The pulmonary lesion develops progressively and three stages can be separated: early, late, and final phase. The pulmonary complications in acute hemorrhagic pancreatitis may be explained by the release of mediators such as pancreatic enzymes or free fatty acids into the blood stream. In acute hemorrhagic pancreatitis a close monitoring for shock parameters is necessary. A fall in arterial PO2 is an early indication for mechanical ventilation, including positive end-expiratory pressure.
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PMID:Pulmonary complications in fatal acute hemorrhagic pancreatitis. 682 33

Acute hemorrhagic pancreatitis (AHP) involves multiple organ failure probably caused by the toxic factor(s) released in pancreatitis-associated ascitic fluid (PAAF). We found that PAAF interferes with hepatic mitochondrial respiration resulting in severe disturbances in respiratory control (RCR) and ADP/O ratios. Pancreatitis was induced in dogs by retrograde pancreatic duct infusion and the resultant PAAF was centrifuged, filtered, and frozen until used. Two human PAAFs collected from AHP patients were treated in a similar manner. Rat liver mitochondrial oxygen uptake was measured at 30 degrees C before and after addition of ADP and PAAF. Paired control runs were made using pooled heat-inactivated dog serum. Tests with nine canine PAAFs showed a mean increase of 120% in state 4 respiration (P less than 0.0001). After exposure to PAAF, addition of ADP to previously coupled mitochondria did not induce state 3 respiration. The human PAAFs both showed significant increases in state 4 respiration (P less than 0.01) and a marked decrease in RCR. Dose-response tests with human and canine PAAFs showed a positive correlation between percentage increase in state 4 respiration and the concentration of PAAF used. These results confirm the presence in PAAF of mitotoxic substance(s) which cause irreversible mitochondrial damage. Inhibition of coupled mitochondrial respiration by PAAF with the resultant fall in ATP may be the causative agent for the tissue and organ damage observed in AHP.
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PMID:Mitochondrial dysfunction induced by pancreatitis-associated ascitic fluid. 684 50

In the last years non operative and surgical efforts could not diminish the high lethality of severe acute haemorrhagic necrotising pancreatitis. While majority of patient die in consequence of pancreatitis-shock, hyperbaric oxygen therapy (HBO) can improve all hypoxic circulation situations. Therefore the value in treatment of experimental necrotising pancreatitis in pig is examined. 5 pigs were treated with, 5 without HBO and 5 served as control. With HBO liquid sequestration was diminished and total protein loss prevented significantly, but foremost survival time was significantly prolonged. In consequence demarcation of necrosis with connective tissue was possible, but nevertheless operative treatment remain necessary. Without HBO all pigs and with HBO only 2 pigs died in consequence of necrotising pancreatitis. It is demonstrated, that HBO as additive therapy can improve the prognosis of necrotising pancreatitis.
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PMID:[Hyperbaric oxygen therapy in experimental necrotising pancreatitis (author's transl)]. 707 24

The beneficial effect of ethamsylate in maintaining the relative pancreatic blood flow in acute canine necrotizing pancreatitis has been demonstrated. This beneficial effect is a function of the action of the drug in tending to maintain pancreatic blood flow, thereby minimizing the significant decrease which normally occurs in this parameter in acute necrotizing pancreatitis. The exact mechanism of action of the drug is unclear. Concurrent measurements of oxygen consumption by the pancreas show an apparent beneficial trend in the ethamsylate-treated group, although this was not proved to be statistically significant.
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PMID:Beneficial effect of ethamsylate on the relative blood flow of the pancreas in acute canine necrotizing pancreatitis. 713 74

Fifteen patients with acute pancreatitis had 68 physiologic cardiopulmonary assessments performed, and they were compared with 61 performed on normal postoperative patients, and 113 on 41 cirrhotics. It was found that the patients with pancreatitis have an elevated cardiac index (CI), which is not due to the hyperdynamic hemodynamic state found in cirrhotics. In spite of this, the Sarnoff curves demonstrated that pancreatitis was accompanied by a myocardial depression p less than 0.03, not found in hyperdynamic cirrhotics. Cirrhotics are unable to increase their oxygen consumption in response to an increase in CI, as do normal patients or those with acute pancreatitis. In cirrhotics the hemodynamic lesion occurs at the capillary level with the opening of arteriovenous shunts which rob the tissues of their nutritive blood supply, while the patient with acute pancreatitis has a primary myocardial depression and his peripheral vasculature reacts like that of a normal person.
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PMID:Myocardial function in acute pancreatitis. 724 38

Oxygen radicals mediate an important step in the initiation of acute pancreatitis. These reactive oxygen metabolites are generated at an early stage of the disease. The source of the enhanced production of oxygen radicals, however, still remains unclear. Experimentally, the effectiveness of antioxidant treatment varies from one model to the other, the differences depending on the experimental model and not on the form of pancreatitis that was induced. In most studies, the experimental animals were pretreated before acute pancreatitis was induced. This does not mirror clinical reality because patients are admitted to the hospital after the onset of the disease. It was shown in cerulein-induced pancreatitis, however, that scavenger treatment also mitigated the pancreatic tissue damage after induction of acute pancreatitis. Moreover, antioxidant treatment also attenuated the extrapancreatic complications, thus improving the final outcome of the disease. Initial indirect observations also suggest that in human acute, acute recurrent, and chronic pancreatitis, oxygen free radicals are generated and add to the damage. Concomitantly, these patients suffer from a severe depletion of oxidative stress. Whether or not this disbalance is instrumental in the development and course of disease remains unanswered. Supplementation with antioxidants that are deficient in patients with acute pancreatitis might be a feasible option to the present therapy to avoid extrapancreatic complications. Well-defined, controlled clinical trials involving patients suffering from acute pancreatitis are therefore needed to validate the role of oxygen radicals in this disease.
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PMID:Oxidative stress in acute and chronic pancreatitis. 749 25

The role of oxygen-derived free radicals in the pathogenesis of acute pancreatitis was studied in a new model of acute hemorrhagic pancreatitis and cerulein-induced edematous pancreatitis in rats. Hemorrhagic pancreatitis was produced by administering two intraperitoneal doses of cerulein [40 micrograms/kg body weight (BW)] at 1-h intervals following water immersion stress applied for 5 h. Edematous pancreatitis was induced by injecting cerulein as described but without water immersion. Five hours after the first injection of cerulein, pancreatic edema and elevation of serum amylase level were more marked in the animals with hemorrhagic than with edematous pancreatitis. Five hours after the first injection of cerulein, marked hemorrhage and venous dilatation were observed only in those with hemorrhagic pancreatitis. Local pancreatic blood flow decreased to approximately 60% of control values in the animals with edematous pancreatitis, and to approximately 30% of control values in those with hemorrhagic pancreatitis. To evaluate the involvement of oxygen radicals, some rats received three intraperitoneal injections of superoxide dismutase (SOD 10,700 U/kg BW) and catalase (132,000 U/kg BW) beginning 15 min before the first injection of cerulein and repeated at 1-h intervals. No significant effect of free radical scavengers was observed on the edematous pancreatitis. However, in hemorrhagic pancreatitis, treatment with SOD and catalase completely suppressed the hemorrhage and venous dilatation of the pancreas, significantly reduced the pancreatic wet weight and the serum amylase level, and reduced the histologic alterations. However, after treatment with SOD and catalase, no differences were observed in local pancreatic blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of oxygen-derived free radicals in hemorrhagic pancreatitis induced by stress and cerulein in rats. 750 65

Oxygen free radicals (OFR) are postulated to play a role in the pathogenesis of acute pancreatitis. The aim of this work was to examine the role of xanthine oxidase in the generation of OFR and the activity of the endogenous defense mechanisms as reflected by pancreatic superoxide dismutase (SOD) activity in a model of edematous pancreatitis induced in rats by administration of cerulein at supramaximal doses, as well as in necrohemorrhagic model induced by intraductal administration of sodium taurocholate. Comparison between these two models of pancreatitis suggests important differences in origin and importance in the evolution of injury. In necrohemorrhagic pancreatitis OFR can be produced by xanthine oxidase activity probably associated to cell death. By contrast, in cerulein induced pancreatitis, other sources of oxygen free radicals, such as inflammatory cells, can be of more importance.
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PMID:Xanthine oxidase activation in cerulein- and taurocholate-induced acute pancreatitis in rats. 752 65


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