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 levels of the proenzymes trypsinogen and chymotrypsinogen were studied in guinea pigs with pancreatitis induced by injection of sodium taurocholate containing the antibiotic cephalothin. This treatment inhibited the enzyme activities and prolonged the activation times of the proenzymes. Both trypsinogen and chymotrypsinogen content decreased after induction of pancreatitis, but there were no significant changes in the proenzyme contents in relation to injection-to-excision times. Sodium taurocholate and cephalothin were cleared from the pancreas in 2 h. Administration of chlorophyll-a together with the inducer caused a slight increase in proenzyme levels.
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PMID:Proteolytic proenzymes in the pancreas in the course of experimental bile-induced pancreatitis in the guinea pig. 75 Feb 63

The role of infectious factors in the pathogenesis of acute pancreatitis and the protective effect of combined therapy with a new potent synthetic protease inhibitor, E3123, and a new potent synthetic cephalosporin, Shiomarin (SM) were examined in rat acute pancreatitis. Sodium taurocholate injection into the pancreatico-biliary duct of rats caused severe pancreatitis with a high mortality rate, characterized by hyperamylasemia, high amylase activity in ascitic fluid, and hyperendotoxemia and a high serum level of fibrin degradation products (FDP), redistribution of cathepsin B from the lysosomal fraction to the zymogen fraction. In rats with E3123 infusion almost all parameters were improved, including mortality rate, serum and ascitic fluid amylase levels, plasma endotoxin and serum FDP levels, and distribution of lysosomal enzyme. But combination therapy with E3123 and SM was significantly more protective than E3123 therapy alone. These results indicate that infection plays an important role in the development of severe pancreatitis and that combination therapy with a new synthetic protease inhibitor and a new potent antibiotic may be useful in the treatment of severe pancreatitis.
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PMID:Combined therapy of a cephalosporin, Shiomarin and a new potent protease inhibitor, E3123 in rat taurocholate-induced pancreatitis. 130 80

Using an in vivo microscopy technique, we studied the microcirculatory changes in sodium taurocholate-induced pancreatitis in rats. With a computerized image analyzer system, blood flow, vascular permeability changes, and capillary densities were measured. Intraductal infusion of 0.4 ml saline had only minor effects on the microcirculation. Various concentrations and volumes of sodium taurocholate solutions were infused into the pancreatic duct. Sodium taurocholate (0.4 ml, 4%) led to increased vascular permeability preceding stasis within 232 +/- 47 s, followed by hemorrhagic necrosis in the head of the pancreas. In the corpus close to the tail of the pancreas capillary blood flow was maintained. In conclusion, this study shows that the microcirculation of the pancreas can be excellently investigated with in vivo microscopy. With this method, tremendous distribution disturbances of the microcirculation in the pancreas can be seen in the course of acute pancreatitis. Vascular permeability changes and stasis of the microcirculation represent the primary microcirculatory events in acute pancreatitis induced by sodium taurocholate in the areas where hemorrhagic necrosis occurs.
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PMID:Microcirculatory changes in sodium taurocholate-induced pancreatitis in rats. 199 52

Sodium taurocholate pancreatitis in the rat is a frequently used experimental model for evaluating therapeutical regimes in this disease. It is, however, uncertain when treatment should be started, as the early phase of this experimental model and thus the time when the pancreatitis really develops is unknown. Serum and pancreatic enzymes, as well as pancreatic morphology, were therefore studied 5, 30, and 60 min after induction of sodium taurocholate pancreatitis. It was found that increase in serum enzymes and decrease in pancreatic enzymes and morphological changes characteristic for acute pancreatitis develop as early as 5 and 30 min after induction of pancreatitis. Thus, therapy in this model may be started shortly after induction of acute pancreatitis.
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PMID:When should treatment of acute experimental pancreatitis be started? The early phase of bile-induced acute pancreatitis. 245 4

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

Sodium taurocholate injected into the pancreatic duct system of the rat caused acute haemorrhagic pancreatitis. The pancreatic lesions were immediate and characterized by interstitial oedema, extensive necrotic changes of the acinar cells, and haemorrhages during the first 24 h after the injection. In animals surviving 72 h there were marked acinar atrophy and pancreatic fibrosis. The mortality increased according to the amount of sodium taurocholate injected. Except for necrosis of occasional liver cells, other organs examined were histologically normal. This investigation created an experimental model for studying the pathogenesis of acute pancreatitis. The results support the hypothesis that bile can initiate acute haemorrhagic pancreatitis.
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PMID:Experimental pancreatitis in the rat. Sodium taurocholate-induced acute haemorrhagic pancreatitis. 743 3

We investigated the concentration of immunoreactive pancreatic phospholipase A2 (pan-PLA2) and the catalytic activity of phospholipase A2 (CA-PLA2) in plasma, peritoneal fluid, and pancreas of rats in which acute hemorrhagic pancreatitis was induced by an intraductal injection of sodium taurocholate. The contribution of pancreas to the CA-PLA2 in plasma was studied by removing pancreatic PLA2 by absorbing plasma samples with a polyclonal antibody raised in a rabbit against rat pancreatic PLA2. Sodium taurocholate injected into the pancreatic duct produced hemorrhagic pancreatitis with necrosis and inflammatory cell invasion within 8 hr. Saline injection caused edematous pancreatitis, but sham operation did not alter pancreatic morphology from normal. The concentration of pan-PLA2 increased rapidly in plasma in all animals, but significantly more in sodium taurocholate-injected animals than in saline-injected or sham-operated animals. The level of CA-PLA2 in plasma increased in sodium taurocholate-injected animals only. There was no correlation between pan-PLA2 and CA-PLA2 values in plasma in sodium taurocholate-injected animals. The CA-PLA2 was marginally increased in pancreatic tissue of sodium taurocholate-injected animals compared to that of saline-injected and sham-operated animals at 8 hr. Treatment by the anti-pan-PLA2 antibody effectively removed pan-PLA2 from plasma and peritoneal fluid samples in sodium taurocholate-injected animals. The level of CA-PLA2 in plasma was similar before and after antibody treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Phospholipase A2 in sodium taurocholate-induced experimental hemorrhagic pancreatitis in the rat. 763 43

The role of infectious factors in the pathogenesis of acute pancreatitis and the protective effect of combined therapy with a new potent synthetic protease inhibitor, E3123, and a new potent synthetic cephalosporin, Shiomarin were examined in rat acute pancreatitis. Sodium taurocholate injection into the pancreatico-biliary duct of rats caused severe pancreatitis with a high mortality rate, characterized by hyperamylasaemia, high amylase activity in ascitic fluid, hyperendotoxaemia and a high serum level of fibrin degradation products (FDP) and redistribution of cathepsin B from the lysosomal fraction to the zymogen fraction. Sodium taurocholate injection into the pancreatico-biliary duct also caused the bacterial growth in the pancreas. In rats with E3123 infusion almost all parameters were improved, including mortality rate, serum and ascitic fluid amylase levels, plasma endotoxin and serum FDP levels, and distribution of lysosomal enzyme. But combination therapy with E3123 and Shiomarin was significantly more protective than E3123 therapy alone. These results indicate that infection plays an important role in the development of severe pancreatitis and that combination therapy with a new synthetic protease inhibitor and a new potent antibiotic may be useful in the treatment of severe pancreatitis.
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PMID:Protective effect of a cephalosporin, Shiomarin, plus a new potent protease inhibitor, E3123, on rat taurocholate-induced pancreatitis. 843 63

With use of in vivo microscopy, pancreatic duct permeability, red blood cell (RBC) velocities, functional capillary density (FCD), and overall changes in capillary blood flow (perfusion index) were estimated after intraductal infusion of sodium taurocholate (0.8 ml, 4%) alone or in combination with systemic administration of cholecystokinin (CCK, 0.3 microg/100 g body wt) or secretin (Sec, 10 microg/100 g body wt). Sodium taurocholate mediated a significant increase in pancreatic duct and capillary permeability within 105 +/- 26 s followed by a transient decrease in RBC velocities and a sustained decrease in FCD, which were paralleled by dramatic flow heterogeneity. Therefore, a significant reduction in overall capillary blood flow was calculated. CCK stimulation aggravated the microcirculatory failure due to a decrease in RBC velocities, which was accompanied by an increase in acinar cellular necrosis. Sec stimulation attenuated microcirculatory failure due to a more moderate reduction of FCD. The enhanced pancreatic duct and capillary permeability, which enables free diffusion of pancreatic digestive enzymes into the parenchyma, is the initiating event in acute biliary pancreatitis, causing microcirculatory failure and tissue damage. The microcirculatory changes are secondary and a propagating factor for the development of acini necrosis. Stimulation with CCK worsened the course of acute biliary pancreatitis.
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PMID:Acute pancreatitis in rats: effects of sodium taurocholate, CCK-8, and Sec on pancreatic microcirculation. 912 55

Using in vivo microscopy, red blood cell (RBC) velocities, functional capillary density (FCD), and overall changes in capillary blood flow (PI) were estimated following intraductal infusion of sodium taurocholate (0.8 ml; 4%) alone or in combination with systemic administration of somstostatin (single bolus SMS 100 microg/100 g body wt). Sodium taurocholate mediated a significant transient decrease in RBC velocities and a sustained decrease in FCD, which were paralleled by dramatic flow heterogeneity. Therefore, a significant reduction in overall capillary blood flow was calculated. Additional SMS treatment reduced microcirculatory impairment as expressed by reduction of blood flow heterogeneity, a less rarified functional capillary density, and a recovery of RBC velocities and acinar capillary overall perfusion to control values. As a result of this microcirculatory improvement, pancreas histology revealed slightly less severe tissue damage compared to the non-SMS-treated pancreatitis group. These findings demonstrate that exogenous SMS infusion can improve microcirculatory failure in acute biliary pancreatitis, which should have a beneficial effect on the course of the disease.
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PMID:Somatostatin attenuates microcirculatory impairment in acute sodium taurocholate-induced pancreatitis. 953 54


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