Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.21.4 (trypsin)
 42,187 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Endogenous opioid peptides may play a role in the genesis of pancreatic damage in acute pancreatitis. The effects of naloxone on the haemodynamic changes in acute pancreatitis were investigated by inducing it in dogs with pancreatic ductal injection of fresh trypsin-bile mixture. In the control group (n = 8), acute pancreatitis was characterized haemodynamically by falls in the maximum positive and negative dP/dt (+/- dP/dt), cardiac output (CO) and cardiac index (CI), and increases in the pulmonary vascular resistance (PVR) and systemic vascular resistance (SVR) as well as an early reduction of pancreatic blood flow (PBF). In another set of eight dogs (naloxone group), naloxone was given intravenously 10 min after the induction of acute pancreatitis (80 micrograms/kg as a bolus + 80 micrograms/kg/h for 3 h). Compared with untreated dogs, naloxone significantly increased PBF and the +/- dP/dtmax; prevented the significant decreases in CO and CI and increases in PVR and SVR, and reduced significantly the severity of pancreatitis, as assessed by both the histological staging and the mortality rate. These results suggest that naloxone limits the progression of acute pancreatitis from oedematous to haemorrhagic form. It is proposed that endogenous opioid peptides may play a role in the pathophysiology of acute pancreatitis.
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PMID:Effect of naloxone on the haemodynamics and the outcome of experimental acute pancreatitis in dogs. 139 31

The test of peptide of trypsinogen activation (PTA) in various biological media is a principal new diagnostic test for acute pancreatitis. PTA levels in the pancreatic tissue and the plasma of the blood in acute experimental pancreatic necrosis reflects the process of the pathological activation of trypsin in the diseases focus and confirms the source of higher levels of activation peptide in the blood flow. Together with the values of other enzymatic systems of the pancreatic gland the discussed value permits one to make a more precise assessment of the mechanism and stages of autodigestive processes which develop in acute experimental pancreatitis.
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PMID:[Possibilities of the use of trypsinogen activation peptide in the pancreatic tissue in the diagnosis of pancreatic necrosis]. 143 93

The ascites accumulating during acute pancreatitis contain proteases that play a role in the progression of this disease. The proteases of the fibrinolytic system in the ascites were therefore studied in experimental acute pancreatitis induced in rats. Synthetic substrate assay and the fibrin plate method revealed high activities of proteases, including plasminogen activator, in the ascites. The plasminogen activator had a mol wt of about 50,000 by zymography. The plasminogen activator adsorbed on Lys-sepharose from the ascites was observed at the 100,000 mol wt position and in the 50,000-100,000 mol wt range on zymography and appeared at the 50,000 mol wt position after treatment by concentration. Its activity was enhanced by trypsin treatment. In other experiments, when incubated homogenate of normal pancreas lacking in zymographic activity was injected intraperitoneally into healthy rats, the recovered fluid displayed lytic zones between the 100,00 and 50,000 mol wt positions. These findings suggest that the ascites contained plasminogen activator, part of which was released by intrapancreatic substances and was present in the precursor form.
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PMID:Fibrinolytic enzymes in ascites during experimental acute pancreatitis in rats. 146 Mar 27

Effects of prostaglandin E (PGE) on acute pancreatitis have been controversial. This study shows the effects of PGE1 oligomer, MR-356, on trypsin-taurocholate-induced acute pancreatitis in rats. Divided intraperitoneal doses of 0.6 mg/rat were administered, which increased 24 h survival rates when the oligomer was given both at 1 h before and after (group A) and immediately and 3 h after (group B) induction of pancreatitis. In group A MR-356 significantly improved the survival rates at 18 h (94 vs 61%, P < 0.05) and 24 h (68 vs 33%, P < 0.05) when compared with controls. MR-356 improved the survival rates dose-dependently up to 0.6 mg/rat when given by the same protocol of group A. In group B MR-356 also improved the survival rate (72 vs 39%, P < 0.05) only at 24 h, while other parameters failed to improve. The present results suggest that the PGE1 oligomer may play a beneficial role in bile-induced pancreatitis, probably through its proposed effects of stabilization of lysosomal membranes, maintenance of microcirculation and inhibition of protease in the pancreas.
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PMID:Protective effects of a prostaglandin E1 oligomer on taurocholate-induced rat pancreatitis. 148 88

Eight weeks after a single intravenous injection of trypsin, more than half of 26 treated rats showed pulmonary emphysema, as demonstrated by a significant increase of the mean linear intercept (MLI = 107 microns) in comparison with 11 controls (69 +/- 15 microns) (mean +/- SD). As observed 56 days after the injection, the intraperitoneal administration of trypsin (24 rats) also leads to lung emphysema (MLI = 101-106 microns), as does endotracheal instillation of elastase (13 rats), (MLI = 108 microns). The intraperitoneal administration of trypsin in animals constitutes a model close to human pathology with which lung alterations in acute pancreatitis may be studied. Having no elastolytic properties, trypsin cannot directly induce emphysema. The observation of a pulmonary leucostasis in eight rats sacrificed early after the trypsin injection suggested that leucocyte trapping and activation are important for the genesis of this trypsin-triggered emphysema.
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PMID:Parenteral administration of trypsin triggers lung emphysema. 149 4

Experimental studies have shown that verapamil inhibits pancreatic exocrine secretion. In order to determine whether verapamil has any effect on acute pancreatitis (AP), we undertook an experimental study in Wistar rats. We used 72 animals divided into two groups. In all animals of both experimental groups, AP was induced by ligation of the biliary duct at its entrance in the duodenum. Animals were given saline (NaCl 0.9%), or 0.30 mgrs/hour verapamil. Subgroups of 9 animals, were treated for 6, 12, 18 and 24 hours; 6 animals group were then sacrificed, for biochemical studies (serum amilase, lipase, and calcium; and trypsin and chemotrypsin in the homogenized pancreas); the other 3 animals were used for morphologic study of the pancreas. Verapamil treatment decreased significantly tissue activity of trypsin (p less than 0.001) and chemotrypsin (p less than 0.0001) and increased serum lipase (p less than 0.05), and calcium. There was no statistical difference in serum amylase. Morphological findings include oedema, acinar necrosis, hemorrhage and vasculitis in non treated animals. Only oedema was observed in animals treated with verapamil. These results suggest a beneficial effect of verapamil on experimental AP induced by ligation of the bile duct in the rat.
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PMID:[The effects of verapamil in experimental acute pancreatitis in the rat]. 152 May 48

The pathogenesis of acute pancreatitis is based on the following principles: 1. Biliary. In biliary pancreatitis there is a causal relationship between the induction of acute pancreatitis and the migration of gallstones. The basic pathomechanism seems to be a combination of an increase in permeability and pressure in the ductal system. 2. Intraacinar. Caerulein-pancreatitis is a well established experimental model which reflects the intracellular/interstitial type of activation. Basolateral secretion of pancreatic enzymes into the interstitial space represents the initial event. Intracellular activation of trypsin by the fusion of zymogen-granules and lysosomes has been advocated as an alternative mechanism. 3. Alcohol. The acute alcohol pancreatitis comprises a combined pathogenesis. Obstruction and reflux as well as the cytotoxic effect of alcohol seem to be the main principles. 4. Disturbance of pancreatic microcirculation. Ischemia of the pancreas seems to play a key role in the transition from pancreatic edema to necrosis. Improvement of capillary perfusion by isovolemic hemodilution with dextran 60 has been shown to be an efficient therapeutic tool.
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PMID:[Etiology and pathogenesis of acute pancreatitis]. 152 49

The role of ethanol in precipitating acute pancreatitis has been studied in model experiments. The influence of ethanol on the survival of isolated pancreatic acinar cells (PAC) and a possible coaction with noxious agents (such as trypsin, chymotrypsin, temporary anoxia, and partial uncoupling of the oxidative phosphorylation by 2,4-dinitrophenol [DNP]) has been investigated. Isolated PACs withstood ethanol levels up to 180 mM without significant decrease of viability within 4 h incubation at 37 degrees C. A 90-min deprivation of oxygen was widely tolerated also. However, with a combination of both ethanol application and oxygen deprivation, a clearly forced cell damage was observed as was true with a combination of ethanol and chymotrypsin. The action of DNP or of extracellular trypsin on cell survival was not amplified by the addition of ethanol (180 mM). This study reveals two possible sites of action at which ethanol may contribute to the pathogenesis of acute pancreatitis.
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PMID:Influence of ethanol on survival of acinar cells isolated from rat pancreas. 157 Apr 15

To study the development of acute pancreatitis after intraductal trypsin instillation, at 4 hours, 1, 2, 4 and 6 days after this treatment and after instillation of physiologic saline viable acinar cells were isolated from rat pancreas. Gross anatomic and histologic findings were used to evaluate the time course of pathomorphologic changes. The isolated cells were incubated at 37 degrees C in Eagle's medium in a shaking water bath and the time course of their damage was studied. Additionally, by means of the active accumulation of the fluorophore rhodamine 6 G alterations of the mitochondrial membrane potential, an important parameter of the cellular energy metabolism was evaluated. The most severe histological damage was seen 1 and 2 days after trypsin instillation. At the same time yield and survivability of cells isolated, and their mitochondrial membrane potential reached a minimum. In the controls the time course of these parameters was very similar, but their decrease was less pronounced. Since a direct action of trypsin on acinar cells cannot be responsible for the findings presented a possible involvement of inflammatory cells and their products in the alteration of the cells and of their energy metabolism must be considered.
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PMID:Influence of trypsin-induced acute pancreatitis on survival and energy state of isolated acinar cells from rat pancreas. 159 92

Blood samples of 300 consecutive subjects suspected for drunken driving were prospectively analyzed for concentrations of pancreatic and hepatic enzymes. Mean alcohol concentration was 1.5 +/- 0.8 0/00 (+/- SD; range 0-3.7 0/00). Increased enzyme concentrations were found in 25/300 subjects for amylase, in 43/300 for trypsin, in 49/300 for gamma-glutamyl transferase and in 82/300 for glutamic oxaloacetic transaminase. Subjects with alcohol concentrations greater than 1 0/00 had abnormal pancreatic and hepatic enzymes more frequently than subjects with alcohol concentrations smaller than 1 0/00. However, pancreatic enzyme levels were higher than twice the upper normal limit only in 3/300 subjects, whereas hepatic enzyme levels exceeded twice the upper normal limit in 31/300 subjects. Therefore, other factors in addition to alcohol are necessary to initiate acute pancreatitis. The liver is more susceptible to acute injury by alcohol than the pancreas.
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PMID:Does acute consumption of large alcohol amounts lead to pancreatic injury? A prospective study of serum pancreatic enzymes in 300 drunken drivers. 169 81


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