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)

The effects of indomethacin administration on hemodynamics were investigated in canine acute hemorrhagic pancreatitis (AHP). Thirteen mongrel dogs were randomly divided into a fluid treatment group, an indomethacin prophylaxis group (IMP), and an indomethacin therapy (IM) group. Indomethacin (5 mg/kg) was administered as a bolus dosage 30 min before the induction of AHP in the IMP group. In the IM group, indomethacin was also given as a bolus (5 mg/kg) in 5 min starting 30 min after the induction of AHP. AHP was induced with a mixture of trypsin and sodium taurocholate infused into the pancreatic duct. Hemodynamics were monitored during the 4.5 h of surveillance time. Heart rate did not change significantly between the groups. Indomethacin prophylaxis maintained mean arterial pressure at a significantly higher level (P less than 0.05) and prevented the initial fall in blood pressure when compared to the fluid treatment or IM group. Indomethacin increased cardiac output (P less than 0.05) in the IM group, but did not differ significantly in the IMP group in comparison with the fluid treatment group. In conclusion, the inhibition of the initial fall in blood pressure by indomethacin in AHP suggests prostaglandins to play a role in hemodynamic changes and pancreatic shock to be "septic" as evaluated by hemodynamic changes.
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PMID:Indomethacin in canine acute hemorrhagic pancreatitis. 335 85

The effect of methylprednisolone on hemodynamics and oxygen transport was investigated in acute hemorrhagic pancreatitis in 13 dogs randomly allocated to a fluid treatment group, a methylprednisolone prophylaxis (MPP) group and a methylprednisolone therapy (MP) group. Methylprednisolone (30 mg/kg) was given as a bolus dose, starting 30 min before induction of pancreatitis in the MPP group and 30 min after induction in the MP group. Acute hemorrhagic pancreatitis was induced with a mixture of trypsin and sodium taurocholate, and hemodynamics and blood gases were monitored for 4.5 hours. MPP improved cardiac output significantly and prevented the initial increase in the arteriovenous oxygen content difference. In the MP group there were no significant differences from the control group in hemodynamics or oxygen transport. Prophylactically administered methylprednisolone thus partially attenuated the hemodynamic changes caused by acute hemorrhagic pancreatitis. It seemed especially to improve cardiac performance, assessed from changes in cardiac output.
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PMID:Methylprednisolone in acute canine hemorrhagic pancreatitis. 335 81

The possible role of thromboxane A2 (TXA2) in acute necrotizing pancreatitis (ANP) was investigated in rats. After ANP was induced by injecting sodium taurocholate (5% w/v) into the pancreatic duct, the thromboxane B2 (TXB2) levels in plasma increased significantly. The effects of indomethacin, a general blocker of prostaglandin synthesis, on survival time and on plasma TXB2 levels were compared with those of dazoxiben, a more specific blocker of TXA2 synthesis, and Flunarizine, a calcium entry blocker known to inhibit the effects of TXA2. In a test group without any treatment, all animals died within 30 h of ANP induction. Although TXB2 levels were lowered by the administration of indomethacin, dazoxiben, and Flunarizine, survival times were not significantly altered. Indomethacin pretreatment had no beneficial effect, whereas 30% and 40% of the animals survived for 36 h after treatment with Flunarizine and dazoxiben, respectively. The results of the present study indicate that inhibition of TXA2 synthesis alone does not dramatically alter survival time. However, a potential role for other arachidonate metabolites in ANP cannot be ruled out by this study.
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PMID:Raised plasma thromboxane B2 levels in experimental acute necrotizing pancreatitis in rats. The effects of flunarizine, dazoxiben, and indomethacin. 336 91

Controlled intraduct infusion and peri-acinar dispersal of 100 microliter buffer containing sodium glycodeoxycholate (GDOC) at concentrations of 8.5, 17 and 34 mmol/l in rats caused a progressively severe acute pancreatitis from which none of the animals died over the experimental period. Infusion of affinity-purified active human enterokinase in buffer did not cause pancreatitis, presumably because of the inability of the macromolecule to gain access to its specific intracellular substrate trypsinogens. The addition of enterokinase 200 ng to GDOC 34 mmol/l in the infusate resulted in a severe systemic disturbance and a form of acute necrotizing pancreatitis which was uniformly and rapidly lethal. This effect was not seen when equimolar trypsin was substituted for enterokinase. These findings show that enterokinase specifically increases the lethality of experimental bile salt pancreatitis and suggest that this bile-borne enzyme may in some cases pose a significant clinical threat.
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PMID:Intraduct enterokinase is lethal in rats with experimental bile-salt pancreatitis. 354 76

Both colectomy and intestinal lavage combined with kanamycin instillation proved effective in reducing mortality from sodium taurocholate-induced acute haemorrhagic pancreatitis (AHP) in the rat, supporting the concept that the intestinal flora must be considered a major factor influencing mortality in AHP in the rat. The results of this study are consistent with the clinical observation that abdominal sepsis is the most frequent cause of death in severe acute pancreatitis. The conclusions of the study advocate clinical trials in which besides established symptomatic treatment, intestinal decontamination is the main goal of therapy in severe acute pancreatitis.
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PMID:The protective effect of a reduction in intestinal flora on mortality of acute haemorrhagic pancreatitis in the rat. 357 Jan 40

Buprenorphine (15 micrograms/kg b.wt. per hour) distinctly reduced pain sensitivity in acute 3% sodium-taurocholate pancreatitis in male Wistar rats without interfering with the course of the disease. This was seen by assessment of enzyme elevation in serum and ascites and by histological evaluation of the pancreas. Buprenorphine is therefore recommended for animal experiments to study the effect of therapeutic principles in acute pancreatitis.
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PMID:Influence of buprenorphine on acute experimental pancreatitis. 361 38

High resolution 31P nuclear magnetic resonance (NMR) was used to evaluate the severity of acute pancreatitis in rats. Experimental pancreatitis was induced by intraparenchymal injection of 10% sodium taurocholate. pancreases were removed at various time periods and the NMR spectrum of the whole organ was recorded. Metabolic changes taking place during the progression of the disease were measured and correlated with the pathologic changes. Gradual depletion of the high energy compounds, adenosine triphosphate and phosphocreatine, was observed. The NMR spectral changes paralleled the extension of the pathologic lesions and were found to constitute a reliable indicator of the severity of acute pancreatitis. It is suggested that high resolution NMR may be used to evaluate the pathogenesis and therapy of various forms of experimental pancreatitis.
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PMID:Acute pancreatitis in rats: a 31P nuclear magnetic resonance study. 362 39

Sixty-four severe infections in hospitalized patients were treated with intravenous Timentin. Most patients (mean age: 50.5 years, range 18-85) had serious underlying conditions such as agranulocytosis, heart failure, cancer, diabetes mellitus, chronic alcoholism or other functional or anatomical abnormalities. Forty-three episodes were bacteriologically proved, and bacteraemia was diagnosed in 18. The sites of infection were: lower respiratory tract (10), upper respiratory tract (10), soft tissues (9), urinary tract (7), bones (6), peritoneal cavity (3), meninges (1) and pelvis (1). In addition, 13 episodes of fever and four of septicaemia in patients with agranulocytosis were treated with Timentin plus amikacin. Overall, 59% of the episodes were cured, 14% improved and 17% failed to respond. In 9% of cases the efficacy of the Timentin was unassessable mainly because of concurrent administration of other antimicrobials. Failure appeared to be more frequent in soft tissue and intra-abdominal infections, in patients infected with bacteria susceptible to Timentin but resistant to ticarcillin and in patients superinfected with Timentin-resistant strains. Major side effects were haemorrhagic diathesis with platelet dysfunction (1), severe water sodium overload (1), and possibly pancreatitis (1). Other side effects were mild: catheter-related phlebitis, and abnormal but clinically insignificant laboratory test results. Timentin appears to be an effective and safe broad-spectrum combination which compares favourably with third-generation cephalosporins in the treatment of severe hospital infections. More experience is needed to decide whether the somewhat lower response rate in patients infected with ticarcillin-resistant strains is significant.
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PMID:Clinical experience with Timentin in severe hospital infections. 363 28

A randomised, prospective, stratified, double blind study comparing two contrast media in endoscopic retrograde cholangio-pancreatography (ERCP) was undertaken. Forty-six patients received Meglumine/Sodium Ioxaglate (Hexabrix 320) and forty-eight received Meglumine/Sodium Diatrizoate (Urografin 310). The two groups were evenly matched for age, sex and diagnosis. Radiographs were examined independently by two radiologists. There were no differences in radiograph quality with either type of contrast medium. More patients developed pancreatitis following Urografin, suggesting that Hexabrix is a safer contrast medium for ERCP.
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PMID:A randomised, prospective study comparing two contrast media in ERCP. 367 61

The hemodynamic effect of pancreatic ascitic fluid was studied in a porcine model. Pancreatitis was induced by a low-pressure infusion of trypsin and taurocholate sodium into the pancreatic duct. The ascitic fluid that accumulated was then injected into the inferior vena cava of five pigs, with each pig receiving five infusions at 40-minute intervals. Mean arterial blood pressure and peripheral vascular resistance fell with each infusion, while pulmonary artery pressure increased. The magnitude of the drop in arterial blood pressure decreased with subsequent infusions, suggesting tachyphylaxis. The rise in pulmonary artery pressure increased with successive infusions. Anesthesia artifact and decay of the pancreatic ascitic fluid were ruled out as causes of the tachyphylaxis. Filtration separated the substances producing pulmonary effects and systemic blood pressure effects (0.2 to 11 microns vs 10,000 daltons to 0.2 micron). These data suggest that two mediators may produce the hemodynamic effects of pancreatic ascitic fluid.
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PMID:The vasoactive properties of ascitic fluid in acute pancreatitis in a porcine model. 370 41


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