Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To study the role of the vasodilatory, antiaggregatory prostacyclin (PGI2) and its endogenous antagonist thromboxane A2 (TxA2) in acute pancreatitis, we measured serum thromboxane B2 (TxB2, which indicates platelet TxA2 production) and plasma 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha, which indicates systemic PGI2 production) from sequential blood samples in trypsin and taurocholate induced acute canine hemorrhagic pancreatitis (AHP). In addition the effect of a prostaglandin synthesis inhibitor, ibuprofen, was studied and systemic (MAP) and pulmonary artery pressure (MPAP) were recorded for 4.5 hr. The animals were divided into a sham-operated group, an AHP group, an ibuprofen prophylaxis group, and an ibuprofen therapy group. In the sham group the parameters remained stable throughout the experiment. In the AHP group MAP decreased steadily and 6-keto-PGF1 alpha rose significantly from 80.0 +/- 7.8 to 956.0 +/- 287.0 pg/ml (P less than 0.001), whereas serum TxB2 and MPAP remained unchanged. Ibuprofen prophylaxis eliminated the initial fall in MAP and the rise of 6-keto-PGF1 alpha. Ibuprofen therapy normalized the initially decreased MAP and depressed the level of 6-keto-PGF1 alpha. We conclude that PGI2 may at least partly mediate the initial hypotension in canine AHP, whereas platelet TxA2 production obviously has a negligible role in the development of hemodynamic changes in AHP.
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PMID:Prostacyclin and thromboxane in acute hemorrhagic pancreatitis in dogs. 354 38

Acute pancreatitis can be induced experimentally in rats by the retrograde pancreatic duct injection of deoxycholic acid. In order to evaluate if prostaglandins have a protective or therapeutic role, pancreatitis was induced with 0.03, 0.1, or 0.2 ml of 3% deoxycholic acid. Then, 16,16 dimethyl prostaglandin E2 or prostaglandin I2 were infused i.v. for 30 min before the deoxycholic acid injection or for 1 or 24 h beginning 30 min or 1 h after the injection. Deoxycholic acid, 0.1 and 0.2 ml, produced an 80-100% mortality at 24 h after the induction of pancreatitis, and prostaglandin administration had no appreciable effect. Induction of pancreatitis with 0.03 ml deoxycholic acid was associated with a 15% mortality at 24 h, and both prostaglandins significantly increased the mortality. In the experimental model of pancreatitis tested, the administration of exogenous PGI2 and 16,16 dimethyl PGE2 significantly worsened the outcome.
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PMID:Prostaglandin E2 and I2 treatment of acute experimental pancreatitis in rats. 355 Jul 89

The ultrastructure of the liver was studied in 3 groups of dogs (5 in each) with acute experimental pancreatitis (AEP) induced by injection of bile-trypsin mixture into the pancreatic duct. Experiments were terminated after 12 h. In the group of untreated animals, severe degeneration of mitochondria, extensive autophagocytosis, hyperactivity of Kupffer cells, depletion of glycogen granules, dilatation of endoplasmic spaces and vacuolisation of cytoplasm were found. In the group treated with prostacyclin PGI2 (20 ng/kg/min) in continuous i.v. infusion for 12 h, ultrastructural alterations were less advanced. Even better results were obtained in the group additionally pretreated for 1 h with the same rate of prostacyclin infusion. The results indicate a protective effect of prostacyclin against damage to the liver in the course of AEP.
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PMID:Ultrastructure of liver in acute experimental pancreatitis in dogs treated with prostacyclin. 355 15

The inflammatory process in pancreas affects the function and structure of kidneys both by enzymatic toxemia and impairment of the renal circulation. In this study the stability of renal lysosomes in AEP in dogs treated with cytoprotective agent PGI2 was investigated. AEP was induced by injection of the bile and trypsin into the pancreatic duct; experiments were terminated after 12 hours. In lysosomal enriched subfraction of the kidney cortex (sedimenting in 15 000 x g) in untreated group (N = 5) relative free activity (r.f.a.) of cathepsins (Cs), acid phosphatase (APh) and beta-glucuronidase (BG) increased to 51,67 and 62% respectively, whereas in healthy dogs (N = 6) these activities were 20,38 and 25%. In dogs (N = 6) treated with PGI2 at the dose of 20 ng/kg/min. during 12 hrs, the r.f.a. of Cs, APh and BG was 18,40 and 49%, whereas in dogs (N = 5) additionally pretreated during 1 hr before induction of AEP with the same dose of PGI2, its values achieved 19,40 and 47% respectively. Our results suggest the stabilizing effect of PGI2 on kidney lysosomes damaged in acute experimental pancreatitis in dog. As possible mechanisms of prostacyclin action are discussed: limitation of necrotic process in the pancreas; improvement of renal haemodynamics; direct cytoprotective effect on the kidney.
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PMID:The renal lysosomes in acute experimental pancreatitis in dogs treated with prostacyclin (PGI2). 637 45

In 15 mongrel dogs acute experimental pancreatitis (AEP) was induced by injection of bile and trypsin into the pancreatic duct. After 12 hrs in lysosomal enriched subfraction of the liver in untreated group (N = 5) relative free activity of cathepsins (Cs), acid phosphatase (AP) and beta-glucuronidase (beta G) increased to 50,62, and 53% respectively in comparison to the healthy dogs (N = 6) : 19,43 and 20%. In dogs with AEP treated with prostacyclin (PGI2) in the dose of 20 ng/kg X min for 12 hrs these activities of Cs, AP and beta G were lowered to 30,55 and 41% in comparison with the untreated group. In dogs with AEP (N = 5) additionally pretreated during 1 hr before the induction of AEP with the same rate of PGI2 i.v. infusion, the relative free activity of enzymes was similar to the treated group. After two hrs incubation of lysosomal enriched subfraction in acidic medium (pH = 5,0), the highest values of relative free activity were observed in untreated group, the difference being more pronounced in comparison with control group than before incubation. In those animals treated and pretreated with PGI2, postincubation activities were much lower than in untreated dogs. These results suggest the stabilising effect of PGI2 on hepatic lysosomes, damaged during the course of AEP in dogs.
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PMID:Prostacyclin (PGI2) stabilises hepatic lysosomes during acute experimental pancreatitis in dogs. 675 74

In a rat model with acute necrotizing pancreatitis (ANP), the administration of exogenous prostacyclin (PGI2) significantly increased the pancreatic and renal blood flow, brought the level of 6-keto-PGF1 alpha to TXB2 in renal vein blood back to normal, reduced the severity of pancreatic and renal histolcagic damage, decreased the mortality, and prolonged survival time. The study showed that exogenous PGI2 can increase pancreatic blood flow in rats with ANP, help to prevent ANP, and protect from renal damage following ANP.
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PMID:[Protective effects of prostacyclin on acute necrotizing pancreatitis and its renal damage in rats]. 758 68

The effect of bradykinin on nitric oxide generation and eicosanoid production in the early stage of an experimental model of acute necrotizing pancreatitis induced by sodium taurocholate has been evaluated. We have compared the effect of administering a long-acting bradykinin antagonist, HOE 140, and an inhibitor of nitric oxide synthase, NG-nitro-L-arginine methyl esther L-NAME) on pancreatic prostanoid synthesis. Plasma lipase levels were increased after acute pancreatitis induction, and reduced after HOE 140 or L-NAME administration. Nitric oxide production and thromboxane B2 levels were increased after pancreatitis induction and the increases were reduced by L-NAME or HOE 140 administration. In contrast, increased prostacyclin production, reflected as 6-keto-PGF1 alpha levels, was not modified by L-NAME or HOE 140. Bradykinin seems to be involved in nitric oxide and thromboxane synthesis during the initial phases of acute necrohemorrhagic pancreatitis.
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PMID:A bradykinin antagonist inhibited nitric oxide generation and thromboxane biosynthesis in acute pancreatitis. 765 83

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

The role of liver in the respiratory dysfunction associated with acute pancreatitis has been evaluated. For this purpose, an experimental necrohemorrhagic pancreatitis was induced in rats by intraductal administration of 3.5% sodium taurocholate. Additionally, a portocaval shunt was performed before induction of acute pancreatitis to prevent the initial passage through the liver of substances released by the pancreas. Twelve hours after the induction of pancreatitis, increases in lung prostacyclin and thromboxane B2 synthesis, decreased lung superoxide dismutase activity, and increases in plasma phospholipase A2 activity were found. In addition, inflammatory injury was evidenced in lung by histopathological analysis. The portocaval shunt was able to prevent the metabolic changes and ameliorate the inflammatory process in the lung, suggesting that the liver plays an active role in the systemic inflammatory response to acute pancreatitis.
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PMID:Hepatic involvement in pancreatitis-induced lung damage. 877 95

The damage to the liver appears to be an important aspect of multisystem organ failure in acute pancreatitis with poor prognosis. The objective of this study was to evaluate the protective effect of stable prostacyclin analogue--tilsuprost on the liver energy metabolism in taurocholate pancreatitis in rats preceded by acute ethanol intake. The respiratory control ratio (RCR) and ADP/O ratio of liver mitochondria with glutamate+malate as substrates and mitochondrial DNP (uncoupler)-dependent ATPase activity were significantly depressed after 12 h of taurocholate pancreatitis-the effects that were not significantly aggravated by antecedent acute ethanol intake. Tilsuprost (0.3 mg/kg i.g.) given just before induction of pancreatitis partly prevented the impairment of mitochondrial oxidative and phosphorylative functions, however these positive effects were limited in acute pancreatitis preceded by acute ethanol intake. These results suggest that prostacyclin analogues could be effective in the treatment of hepatic complications in acute pancreatitis, however their effectiveness could be limited in the case of acute ethanol antecedent abuse.
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PMID:The effect of tilsuprost on the liver mitochondria in taurocholate pancreatitis in rats with antecedent acute ethanol abuse. 887 59


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