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

During hospitalization for severe acute necrotizing pancreatitis, a connection between the onset of retinopathy of pancreatitis and multiple-organ failure was studied. Ophthalmoscopy was repeated every second day and continuous staging for multiple-organ failure was performed in 38 patients. Typical retinopathy of pancreatitis developed in 7 of 10 patients with multiple-organ failure and only in 4 of the 28 patients without multiple-organ failure. Retinopathy of pancreatitis was observed in 7 of the 18 cases leading to lethal outcome and only in 4 of the 20 surviving patients. No correlation was observed between the development of retinopathy of pancreatitis and hemodialysis, pre-existing diabetes mellitus, abnormal platelet count, result of hemoculture, c reactive protein value, fraction of inspired oxygen and adult respiratory distress syndrome. In the 21 control patients in grave general state but without acute pancreatitis, retinopathy of pancreatitis was never observed. In our prospective study the onset of retinopathy of pancreatitis had clinical prognostic value and indicated multiple-organ failure and poor prognosis in severe acute necrotizing pancreatitis.
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PMID:Retinopathy of pancreatitis indicates multiple-organ failure and poor prognosis in severe acute pancreatitis. 801 83

The aim of this work is to establish a relationship between prostanoids and oxygen free radicals in the early stages of acute pancreatitis induced by sodium taurocholate and to study the possible cytoprotective effects of exogenous prostaglandin administration. Tissue prostanoid production (6-keto-prostaglandin F1 alpha, thromboxane B2, and prostaglandin E2) was studied after induction of an acute pancreatitis by intraductal administration of 3.5% sodium taurocholate (0.1 ml/100 mg). The effect of previous administrations of 16,16-dimethyl prostaglandin E2 (0.5 microgram/kg), indomethacin (20 mg/kg), or superoxide dismutase (13 mg/kg) was evaluated. Early pancreatitis induced significant increases of the three prostanoid levels as soon as 5 min after taurocholate administration. The administration of 16,16-dimethyl prostaglandin E2 was able to maintain the tissue prostanoid production at basal levels while superoxide dismutase treatment only partially prevented the increase of 6-keto-prostaglandin F1 alpha. On the other hand, indomethacin pretreatment, as expected, prevented the taurocholate-induced early prostanoid biosynthesis but increased the mortality, suggesting that endogenous prostanoids play a role in cellular defense mechanisms. The effect of superoxide dismutase suggests that oxygen free radicals are responsible, in part, for prostanoid enhanced biosynthesis in the earlier stages of necrohemorrhagic pancreatitis.
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PMID:Prostanoids and oxygen free radicals in early stages of experimental acute pancreatitis. 802 67

The purpose of this study was to evaluate the effect of free radical ablation therapy in acute hemorrhagic pancreatitis. Acute pancreatitis was induced in 64 rats by retrograde injection of 5% sodium taurocholate. Thirty animals were pretreated with 100,000 units/kg/hr of superoxide dismutase (SOD) and 400,000 units/kg catalase within the first 3 hr. After 0.5, 3.5, and 12 hr of observation time, serum enzymes and the tissue content of conjugated dienes, malondialdehyde, reduced and oxidized glutathione, as well as ATP, ADP and AMP were measured. In addition, tissue samples were examined by light microscopy. Untreated rats (N = 34) developed within 12 hr an acute hemorrhagic necrotizing pancreatitis with a concomitant increase in serum enzyme levels and a decrease in reduced glutathione and ATP. Within the 12-hr observation period, 57% of the animals died. Scavenger treatment improved the tissue damage and attenuated the increase of the serum enzyme levels and the decrease in reduced glutathione and ATP. Moreover, the lethality rate was significantly lower. Oxygen radicals seem to be instrumental for the development of acute hemorrhagic pancreatitis. Thereby, antioxidant treatment reduces tissue damage, biochemical alterations and extrapancreatic complications, thus improving the final outcome.
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PMID:Effect of antioxidant treatment in rats with acute hemorrhagic pancreatitis. 817 16

This paper is concerned with a hypothesis that disturbance of free radical reactions may lead to abnormality of hemorheological properties in vivo, and so the free radicals generated in vivo may damage certain tissue cells indirectly by reducing the supply of oxygen and nutrients to these cells through slowing the circulation of blood. This hypothesis is based on the following evidence: A. We have found that the whole blood viscosity at low shear rate correlates to the lipid peroxidation in the patients suffering from certain cardio- or cerebrovascular diseases, and in dogs during liver ischemia reperfusion or hemorrhagic pancreatitis. B. Reports have shown that several alterations of hemorheological properties may take place as a result of free radical reactions, such as lipid peroxidation. For instance, lipid peroxidation may lead to decrease of deformability of red cells, increase of aggregation of red cells, formation of liquid thrombin, etc. C. We have demonstrated that some alterations of hemorheological properties involve the role of free radicals in rats suffering from intestinal ischemia/reperfusion. As evidence for this conclusion, superoxide dismutase (SOD) used as a specific scavenger of superoxide anion radical (O2-) can significantly prevent the intestinal ischemia/reperfusion induced changes of lipid peroxidation, red cell aggregation, Cassion's viscosity and whole blood viscosity at low shear rate in rats.
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PMID:A new hypothesis about the relationship between free radical reactions and hemorheological properties in vivo. 818 28

It is postulated the pulmonary injury in acute necrotizing pancreatitis could be due to oxygen-derived free radicals released during the attack of acute pancreatitis. To elucidate the relationship between oxygen-derived free-radicals and the degree of pulmonary injury in acute necrotizing pancreatitis, lipid peroxide (LPO) in lung tissues, bronchoalveolar lavage fluid and serum were measured in 10 adult Mongrel dogs with acute necrotizing pancreatitis induced by injection of 5% sodium taurocholate into the pancreatic duct. Compared with the controls (n = 10), the weight of lung was increased (241.2 +/- 33.7 g vs 121.2 +/- 51.4 g, P < 0.05). LPO of bronchoalveolar lavage fluid (BALF) was higher (3.56 +/- 1.64 mumol/L vs 0.75 +/- 0.31 mumol/L, P < 0.05), LPO in peripheral and portal vein 10 hours after induction of acute pancreatitis was also significantly increased. The LPO content of lung tissue was not higher than that of the control group, but hemorrhage within alveolar space and infiltration by polymorphonuclear and phagocytic cells was seen on histological examination. In conclusion, lipid peroxidation could be an important cause of pulmonary injury in acute necrotising pancreatitis.
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PMID:Experimental study on pulmonary injury related to oxygen-derived free radicals in acute necrotizing pancreatitis in dogs. 819 81

To evaluate the therapeutic effects and mechanisms of tetramethylpyrazine (TMP), a Chinese herbal medicine, on the lung injury in bile-induced acute haemorrhagic necrotizing pancreatitis (AHNP) in the SD rats, the rats were randomly divided into three groups: sham-operative, untreated and TMP treated. AHNP model were induced by ligation with 5% taurocholate. The changes of lung index, serum lipid peroxide (LPO), TXB2, 6-keto-PGF1 alpha, and lung pathology at light and electron microscope were all investigated at 1, 6, 12 hours after induction of AHNP model. Survival rate of AHNP in rats were recorded also. Results of the study showed that in untreated group, the time-related progressive pancreatic haemorrhage and necrosis, accompanied by pancreatitis-associated lung injury, such as pronounced pulmonary congestion, alveolar and interstitial edema, polymorphonuclear granulocytes infiltration, transparent membrane formation, the density of layer body in type II endothelial cells decreasing, with some vacuole formation, mitochondria, endoplasmic reticulum swollen, basal membrane of endothelial cells rupture were observed. The level of LPO elevated at 1 hour after induction of AHNP and peaked at 12 hours. TXB2 and 6-keto-PGF1 alpha was increased. Using TMP treatment, survival rate increased, and lung at light and electron microscope were much improved and lung index, value of LPO, TXB2 decreased significantly, 6-keto-PGF1 alpha increased slightly, the ratio of TXB2/6-keto-PGF1 alpha was stabilized. It was suggested that TMP has definite therapeutic effects on AHNP-related lung injury in rats, and exerted by scavenging oxygen free radical, inhibiting synthesis of TXA2, augmenting production of PGI2 and maintaining balance between TXA2 and PGI2.
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PMID:[Therapeutic effects and mechanisms of tetramethylpyrazine on lung injury in acute haemorrhagic necrotizing pancreatitis in rats]. 831 99

Four models of acute pancreatitis have been previously developed that use the ex vivo perfused isolated canine pancreas preparation. The four models include the intraarterial infusion of oleic acid (FFA) that mimics hyperlipemic pancreatitis, partial obstruction of the pancreatic duct with secretin stimulation (POSS) that mimics gallstone pancreatitis, a 2-hour period of ischemia before perfusion (ISCH 2) that mimics shock pancreatitis, and the infusion of cerulein at supramaximal stimulatory doses (CER), which lacks an obvious clinical counterpart. In the FFA, POSS, and ISCH 2 pancreatitis, but not in the CER pancreatitis, toxic oxygen metabolites, generated by the enzyme xanthine oxidase (XO), have been shown to be important mediators in the early pathogenesis. Ordinarily XO primarily occurs as xanthine dehydrogenase (XD) but can be converted to XO, which is the form that generates toxic oxygen metabolites. This conversion of XD to XO may take place either reversibly by way of sulfhydryl group oxidation or irreversibly by means of proteolytic cleavage of XD. This study was undertaken to investigate the mechanism of conversion of XD to XO in the FFA-, POSS-, and ISCH 2-induced pancreatitis models. CER pancreatitis was studied for comparison. After 4 hours of perfusion, pancreatitis was manifest by edema, weight gain, and hyperamylasemia in all four models. Dithiothreitol, a sulfhydryl group protector, ameliorated the weight gain in the FFA (40 +/- 14 gm to 18 +/- 13 gm; p < 0.05), POSS (28 +/- 10 gm to 9 +/- 3 gm; p < 0.05), and ISCH 2 pancreatitis (30 +/- 13 gm to 15 +/- 3 gm; p < 0.05), and ameliorated the hyperamylasemia in the POSS pancreatitis (12,062 +/- 4304 units/dl to 5877 +/- 2659 units/dl; p < 0.05). The CER pancreatitis was not ameliorated with dithiothreitol. A serine protease inhibitor of low molecular weight, phenylmethylsulfonyl fluoride, ameliorated only the CER pancreatitis (weight gain from 28 +/- 10 gm to 17 +/- 10 gm, p < 0.05; amylase activity from 38,116 +/- 6491 units/dl to 23,372 +/- 11,654 units/dl, p < 0.05), and not the FFA, POSS, or ISCH 2 pancreatitis. We conclude that in the three models of pancreatitis (FFA, POSS, and ISCH 2) that are mediated by toxic oxygen metabolites, XD is converted to XO reversibly by way of sulfhydryl group oxidation rather than irreversibly by way of proteolysis. In the CER pancreatitis, where XO does not play a role in the pathogenesis, proteolytic enzymes may be important mediators in the injury.
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PMID:The mechanism of conversion of xanthine dehydrogenase to xanthine oxidase in acute pancreatitis in the canine isolated pancreas preparation. 841 95

Recent studies suggest that enhanced release of free oxygen radicals plays an important role in the pathogenesis of acute pancreatitis. Therefore, we studied the activity of the oxygen radical generating xanthine oxidase (XOD) in pancreatic tissue from rats treated with either dibutyltin dichloride/ethanol (DBTC/EtOH: 6 mg kg-1/13.7 mg kg-1, i.v.), ethanol alone (EtOH: 13.7 mmol kg-1, i.v.), or isotonic saline (NaCl) as control. We also investigated activities of the oxygen radical scavengers superoxide dismutase (SOD) and glutathione peroxidase (GPX). In addition, levels of the lipid peroxidation marker malondialdehyde (MDA) were determined. Enhanced activity of XOD was not detected. While SOD activity 1 and 6 h after treatment was significantly more reduced by DBTC/EtOH than by EtOH alone, no difference was found thereafter. Correspondingly, both regimens diminished GPX activity. Moreover, DBTC/EtOH and EtOH rapidly increased MDA levels within 1 h, indicating release of oxygen radicals early on after administration. After 16 h the MDA concentration was still elevated only in the DBTC/EtOH group. Although similar metabolic alterations were observed in both groups, only DBTC/EtOH induced acute interstitial pancreatitis within 24 h. We conclude that (a) a tissue imbalance between oxidants and antioxidants might be of importance in the pathogenesis of DBTC/EtOH-induced acute interstitial pancreatitis; (b) although EtOH increases oxygen radical levels, additional damage is required for development of acute pancreatitis; (c) XOD does not seem to be responsible for significant oxygen radical generation; and (d) the DBTC/EtOH model is a useful tool to study acute interstitial pancreatitis in rats.
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PMID:Oxygen radical generation and acute pancreatitis: effects of dibutyltin dichloride/ethanol and ethanol on rat pancreas. 853 55

In order to assess the cumulative effects of antecedent acute ethanol intake and acute pancreatitis on the liver, the mitochondrial respiratory functions and lysosomal membrane integrity of the liver were evaluated in taurocholate pancreatitis (AP) in rats, induced 6 hr after intragastric ethanol 40% (5 g/kg body wt). The oxygen consumption rate, RCR (respiratory control ratio), and ADP/O ratio were measured according to Estabrook. Fractional free activity of lysosomal hydrolases was assayed. RCR with glutamate + malate was most decreased at 12 hr of AP with partial improvement after 18 hr. The ADP/O ratio dropped maximally after 18 hr of AP. The fragility of lysosomal membranes increased significantly at 18 hr of AP. The antecedent ethanol intake abolished the partial restoration of RCR after 18 hr; however, it did not affect the ADP/O ratio or the integrity of lysosomal membranes impaired in AP at this time. In conclusion, the antecedent acute ethanol abuse could aggravate the liver mitochondrial deterioration, but not the lysosomal membrane labilization seen in AP.
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PMID:Hepatic mitochondrial and lysosomal alterations in acute experimental pancreatitis with ethanolic coetiology in rats. 856 47

It has been suggested that the gut plays a role in the development of bacterial complications, which are important contributors to morbidity and mortality in patients with acute pancreatitis. The present study evaluated the enteric bacterial translocation, bacterial homeostasis, and reticuloendothelial system function in experimental acute pancreatitis induced by intraductal injection of 5% sodium taurodeoxycholate in the rat. The incidence of bacterial translocation from the gut to mesenteric lymph nodes (MLNs) and lungs significantly increased after 12 hours and to the systemic circulation, ascites, and pancreas at 24 hours. The number of anaerobic bacteria and lactobacilli decreased in the colon and distal ileum from 6 or 12 hours, whereas the number of Escherichia coli increased from 12 hours. The systemic uptake rate of radiolabeled bacteria decreased from 6 hours after induction of acute pancreatitis. The uptake of radiolabeled bacteria by Kupffer cells decreased from 6 hours, whereas the uptake by macrophages from blood, lungs, and the intestine increased. A decrease in macrophage killing capacity was noted, reflected by an increase in the number of cultured viable bacteria from isolated macrophages. The whole-body oxygen extraction rate increased 4 to 24 hours after induction of pancreatitis, whereas the gut oxygen extraction rate decreased at 2 and 4 hours, followed by an increase at 12 to 24 hours. These data show that translocation of enteric bacteria occurs during the early stage of acute pancreatitis and that the MLN-thoracic duct-circulation may be a major route of bacterial dissemination. Compromised gut oxygen metabolism, overexaggerated intestinal macrophages, and impaired host immune function may be involved in the development of infectious complications associated with acute pancreatitis.
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PMID:Gut origin sepsis, macrophage function, and oxygen extraction associated with acute pancreatitis in the rat. 866 35


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