Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0001339 (acute pancreatitis)
 10,593 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A rat model of taurocholate-induced acute pancreatitis has been employed to investigate the effect of heparin on the protease-antiprotease balance. Heparin was applied intraperitoneally at a dose of 6 mg/kg body weight during 24 hrs. At 24 and 48 hours of acute pancreatitis, heparin evidently diminished the consumption of trypsinogen in pancreatic tissue and decreased trypsin generation. The use of heparin prevented the consumption of alpha 1 anti-chymotrypsin, alpha 1-anti-trypsin and AT-III in pancreatic tissue, whereas in plasma the concentration of the mentioned inhibitors was restored or even increased. Heparin does not affect evidently lowered alpha 2-macroglobulin concentration, either in pancreatic tissue or in plasma. We conclude that heparin applied in acute pancreatitis markedly moderates the dysfunction of protease-antiprotease balance both in plasma and in pancreatic tissue.
 ...
PMID:Does heparin modify protease-antiprotease balance in acute experimental pancreatitis in rats. 242 15

The pulmonary complications are severe sequeles of acute pancreatitis. The pathogenesis of these complications is unsolved. The purpose of this work was to evaluate the status of lung lysosomes and phospholipase A activity in acute experimental pancreatitis (AEP) and the effect of heparin as a potentially protective agent. Taurocholate-induced AEP in rats lasting 24 and 48 hours was treated with heparin intraperitoneally (2 mg/kg every 8 hours). The total activity of cathepsins and B-glucuronidase in lysosomal enriched subfraction increased markedly during 48 hours of AEP in untreated animals, but the relative free activity was maximal after 24 hours. Free activity of cathepsins and acid phosphatase in supernatant was maximal after 24 hours. The phospholipase A activity was maximally elevated (more than twofold) after 48 hours. Heparin prevented the increase of activity of B-glucuronidase, depressed the relative free activity of all investigated lysosomal hydrolases and inhibited the phospholipase A activity in the lung homogenate. Our results indicate the significance of labilization of lung lysosomes and increment of phospholipase A activity in the lungs in the damage of this organ during AEP in the rats, and suggest the beneficial effect of heparin on these factors.
 ...
PMID:The lung lysosomal hydrolases and phospholipase A in acute experimental pancreatitis with reference to heparin treatment. 243

Eleven of 43 nonimmune patients with falciparum malaria had one or several organ complications: cerebral malaria, acute respiratory failure, acute renal failure, secondary infection, autoimmune haemolysis, spontaneous spleen rupture, and acute pancreatitis. Parasitaemia was 0.1 to 60%. Initial antiparasitic therapy with quinine given parenterally resulted in rapid regression of parasitaemia. An additional schizonticide agent was given depending on parasitic resistance. Supportive therapy comprised intensive-care monitoring including fluid and electrolyte balance and, if necessary, early haemodialysis and (or) endotracheal intubation with PEEP breathing. In one patient with excessive parasitaemia exchange transfusion was performed. Heparin was given only in proven disseminated intravascular coagulation, corticosteroids only in persistent autoimmune haemolysis. All patients survived without suffering permanent defects. Retrospective analysis shows that, apart from rapid specific therapy, supportive treatment of the individual organ complications determines course and prognosis of complicated falciparum malaria.
 ...
PMID:[Complicated malaria tropica: specific and supportive therapy in the imported diseases]. 351 46

Hypertriglyceridemia has been noted in patients with acute pancreatitis and respiratory failure. Utilizing an isolated, perfused, canine pulmonary lobe, the effect of triglyceride infusion on pulmonary function was evaluated. When heparin was used to anticoagulate the perfusion circuit, the addition of triglyceride to the autologous blood perfusate resulted in massive weight gain (226 gm), intrapulmonary shunting (36%), and a marked drop in pulmonary compliance (congruent to 50%). Heparin activates lipoprotein lipase, and therefore some triglyceride in the perfusate was lipolyzed with a resultant increase in serum free fatty acids (FFAs) to 253 mumole/dl. When anticoagulation of the perfusion circuit was accomplished by defibrinogenation with Arvin, the addition of triglyceride to the autologous blood perfusate caused minimal weight gain (28 gm), no intrapulmonary shunting, and only a slight decrease in pulmonary compliance (22%). Arvin has no effect on lipoprotein lipase, and the FFA level in the perfusate remained normal (less than 70 mumole/dl). Thus it appears that FFA release secondary to the action of pulmonary lipoprotein lipase on blood triglyceride is the important pathogenic step in the induction of respiratory failure in this model.
 ...
PMID:Respiratory failure in acute pancreatitis: the role of free fatty acids. 736 1

Redistribution of vitamin E in the rat body was studied during acute pancreatitis induced by two intraperitoneal doses of cerulein 40 micrograms/kg of body weight at 1-hr intervals. Hyperamylasemia (2064 +/- 521 vs 6419 +/- 129 U/dL) and pancreatic edema (pancreatic water content, 71 +/- 1.2% vs 78 +/- 2%) were observed. In this model the increased level of lipid soluble fluorophore was also observed (274 +/- 18 vs 120 +/- 9.0 relative fluorescence per g dry wt). Parallel with these changes was a decrease in the level of vitamin E in the serum and an increase in the pancreas. The concentration of vitamin E in the pancreas after 6 h was 162 +/- 8.5 ng/mg dry mass vs 128.1 +/- 6.1 ng/mg dry mass in control animals. The effect of heparin on vitamin E redistribution induced by acute pancreatitis was also investigated. It was found that heparin at a dose of 100 U/kg body mass prevents the drop of the vitamin E level in the serum as well as the increases in the concentration in the pancreas tissue. It was concluded that acute pancreatitis induced redistribution of vitamin E in the rat body. Moreover, we studied the effects of heparin treatment on oxidative stress in the pancreas tissue. Acute pancreatitis caused an increase in lipofuscin accumulation, and a decrease in protein sulfhydryl groups in citrate synthetase (CS) and in malate dehydrogenase (MDH) activity. Heparin treatment that protected vitamin E accumulation in the pancreas tissue did not influence the changes in the level of lipofuscin and proteins sulfhydryl.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Cerulein-induced acute pancreatitis diminished vitamin E concentration in plasma and increased in the pancreas. 764 70

Local microcirculatory dysfunction within the pancreatic gland might be an important factor in the conversion of oedematous to necrotizing pancreatitis. Therapeutic agents, improving the pancreatic blood flow, might be valuable in acute pancreatitis treatment. An influence of nitric oxide, heparin and procaine treatment on microcirculatory values in acute pancreatitis (AP) in rats was investigated. Acute pancreatitis was induced by i.p. injection of cerulein in four doses of 15 microg kg-1 each at 1-h intervals. The rats with pancreatitis were divided into five groups, 12 animals each. One group remained without treatment, four groups were treated i.p. either with NO synthase inhibitor L-NNA (2x25 mg kg-1 or heparin 2x2.5 mg kg-1 or L-arginine 2x100 mg kg-1 or procaine 2x25 mg kg-1. Five control groups, ten animals each, received saline, L-NNA, heparin, L-arginine or procaine only. Five hours after the first ceruleine injection microcirculatory values within the pancreas were measured by means of laser Doppler flowmetry. Acute pancreatitis caused a significant drop of microcirculatory value to 37% of the basal value. The L-NNA administration resulted in a further insignificant reduction of the pancreatic blood flow to 34%. An improvement of microcirculation was observed in rats with pancreatitis receiving heparin (76%) and L-arginine (72%). Procaine had no effect on microcirculatory disturbances within the pancreas in rats with pancreatitis. Cn-induced acute pancreatitis (AP) causes microcirculatory deterioration within the pancreas. Heparin and nitric oxide donor, L-arginine, might be considered as therapeutic agents, improving the diminished pancreatic tissue perfusion observed in acute pancreatitis. Procaine does not improve the pancreatic blood flow in acute pancreatitis.
 ...
PMID:Microcirculatory disturbances of the pancreas in cerulein-induced acute pancreatitis in rats with reference to L-arginine, heparin, and procaine treatment. 934 40

The aim of this study was to investigate the impact of L-arginine (nitric oxide synthase substrate), L-NG-nitro-L-arginine (nitric oxide synthase inhibitor), and heparin on the pancreas microcirculation, serum IL-6 level and microscopic alterations of the pancreas in acute pancreatitis in rats. Acute pancreatitis was induced by 4 i.p. injections of cerulein (15mg/kg). Microcirculatory values were measured by means of laser Doppler flowmetry 5 h after the first cerulein injection. Remarkable histopathological changes in the pancreas, including parenchymal necrosis, an elevation of serum IL-6 level, and a significant drop of pancreatic capillary perfusion was observed in rats with nitric oxide synthase inhibition. L-arginine improved the pancreatic microcirculation but worsened the microscopic alterations within the pancreas. Heparin had a beneficial effect on the microcirculatory values, serum IL-6 concentration, and morphologic changes. Authors conclude that inhibition of nitric oxide synthase aggravates acute pancreatitis. L-arginine treatment improves pancreatic perfusion but potentiates morphological alterations. Heparin, improving the microcirculation and inflammatory changes within the pancreatic gland, may be considered as a promising therapeutic agent in acute pancreatitis.
 ...
PMID:Heparin and nitric oxide treatment in experimental acute pancreatitis in rats. 975 94

The aim of the study was to investigate the impact of L-arginine (nitric oxide donor), L-NNA (NO synthase inhibitor), heparin and procaine on the pancreas' microcirculation, serum interleukin 6 (IL-6) level, and microscopic alterations of the pancreatic gland in acute pancreatitis (AP) in rats. AP was induced by 4 i.p. injections of cerulein (15 micrograms/kg/h). Microcirculatory values of the pancreas were measured by means of laser Doppler flowmetry 5 h after the first cerulein injection. Remarkable morphologic changes in the pancreas, including parenchymal necrosis, an elevation of serum IL-6 activity, and significant drop of pancreatic capillary perfusion was observed in rats with NO synthase inhibition. L-arginine improved the pancreatic microcirculation but worsened the microscopic alterations within the pancreas. Heparin had a beneficial effect on the microcirculatory values, serum IL-6 activity, and morphologic changes. Procaine had no effect on the course of AP. Authors conclude that heparin, improving the pancreatic capillary blood perfusion, may be considered as a promising therapeutic agent in acute pancreatitis.
 ...
PMID:Nitric oxide, heparin and procaine treatment in experimental ceruleine-induced acute pancreatitis in rats. 1047 Apr 42

Hypertriglyceridaemia is thought to be the aetiology in 3% of patients with acute pancreatitis, often associated with poorly controlled diabetes mellitus or chronic alcohol abuse. However, in patients with non-biliary pancreatitis, chylomicronaemia is an underrated cause of acute pancreatitis. The activity of lipoprotein lipase (LPL) is crucial in removing triglycerides from the plasma; LPL gene mutations combined with secondary alterations in plasma lipoproteins, such as occur in pregnancy, diabetes mellitus, and alcohol abuse can cause severe hypertriglyceridaemia and pancreatitis. Heparin and insulin stimulate LPL activity. During a 12 months' period we consecutively screened all patients with the diagnosis of acute non-biliary pancreatitis for hypertriglyceridaemia, to evaluate the prevalence of hypertriglyceridaemia-induced pancreatitis and to assess the outcome under standardised treatment with intravenous heparin and insulin. Hypertriglyceridaemia-induced pancreatitis was diagnosed in 5 out of 46 patients (11%) with acute pancreatitis. In 2 patients hypertriglyceridaemia was associated with diabetes mellitus, in one patient with pregnancy and in another with chronic alcohol abuse. Four patients had to be referred to the intensive care unit. Plasma concentrations of triglycerides were (median +/- range) 43 mmol/l (14.7 to 80.4); pancreas amylase was 574 U/l (155 to 1606), and lipase was 1003 U/l (330 to 3010). All patients had oedematous pancreatitis demonstrated by CT scan. Treatment with i.v. heparin and i.v. insulin decreased trigylceride levels to less than 10 mmol/l within 2.8 days (1 to 6), the amylase and lipase levels returned to normal after 3 and 4 days respectively, and the abdominal pain was resolved. Hypertriglyceridaemia is a common and under-diagnosed etiology of acute non-biliary pancreatitis. Intravenous heparin and insulin is safe and effective in the treatment of hypertriglyceridaemia-induced pancreatitis. Low fat diet, supplements of (n-3) fatty acids ("fish oil") and fibrates are recommended for long-term maintenance therapy.
 ...
PMID:[Heparin and insulin in the treatment of acute hypertriglyceridemia-induced pancreatitis]. 1049 50

Heparin and insulin stimulate lipoprotein lipase and are known to decrease serum triglyceride levels. However, their efficacy in hypertriglyceridemia-induced acute pancreatitis is not well documented. We report a 51-year-old man in whom treatment with heparin and insulin was accompanied by reduction in serum triglyceride levels and resolution of pancreatitis.
 ...
PMID:Hypertriglyceridemia-induced acute pancreatitis--treatment with heparin and insulin. 1283 85


1 2 Next >>