Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.21.4 (trypsin)
42,187 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Granulocyte elastase (GE, EC 3.4.21.37) is a key enzyme in tissue injury. To elucidate the role of GE in tissue injury, a new method of measuring GE activity in various inflammatory tissue fluids was developed using diazotization and the chromogenic synthetic substrate, L-pyroglutamyl-L-prolyl-L-valine-p-nitroanilide (S-2482). GE activity demonstrated first order kinetics in the range from 1.9 to 30 U/l. Other proteases, such as pancreatic elastase, trypsin, and chymotrypsin did not hydrolyze S-2484. This assay permits the determination of GE activity with a coefficient of variance less than 7.8% and 95.6 to 105.4% recovery. With this method, hydrolytic GE activity was found to be increased in bronchoalveolar lavage fluid from patients with ARDS or pneumonia, synovial fluid from patients with rheumatoid arthritis, and blister fluid from burn patients.
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PMID:A sensitive and specific assay for granulocyte elastase in inflammatory tissue fluid using L-pyroglutamyl-L-prolyl-L-valine-p-nitroanilide. 231 34

Thoracic duct drainage (TDD) may be of value for removing toxic substances released by the inflamed pancreas and which are responsible for lung damage. We have prospectively assessed the efficacy of TDD in improving pulmonary gas exchange in 12 patients with severe acute pancreatitis (SAP) complicated by persistent respiratory failure despite standard conservative treatment including peritoneal dialysis in 8 patients. In group A were 6 patients (mean Ranson score = 7.3) with adult respiratory distress syndrome (ARDS) and in group B were 6 hypoxemic patients (mean Ranson score = 6.6) judged to be at risk of developing ARDS. The duration of TDD ranged from 3 to 10 days and the total amount of drained lymph (L) varied from 770 to 15,600 ml. Immunoreactive trypsin levels were significantly higher in L when compared to blood in both groups. Leukocyte myeloperoxidases in L (normal value less than than 332 +/- 82 ng/ml in plasma) were increased in 5 of 5 group A patients (830 +/- 317 ng/ml) and in 3 of 6 patients in group B (671 +/- 467 ng/ml). After TDD pulmonary gas exchange as measured by median PaO2/FiO2 (mmHg) improved from 148 +/- 60 to 285 +/- 42 in group A and from 192 +/- 37 to 330 +/- 42 in group B (p less than 0.05). All patients were weaned after ventilation for a mean of 8 days in group A and 4 days in group B. All patients survived apart from 1 group B patient who died of sepsis on day 34.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prospective evaluation of thoracic-duct drainage in the treatment of respiratory failure complicating severe acute pancreatitis. 255 89

To know the pathogenesis of the lung fibrosis after ARDS, we investigated the role of PMN-elastase after endotoxin-induced pulmonary edema in awake sheep with chronic lung lymph fistulas. The permeability of the pulmonary circulation increased 2 hours after endotoxin injection. Four hours after endotoxin injection, WBC migrated to the lung interstitium and the number of WBC in BALF increased. Endotoxin increased PMN-elastase in plasma and lymph whereas the level of alpha-1-protease inhibitor (alpha-1-PI) did not change. The activity of alpha-1-PI measured by trypsin inhibitory capacity was zero in the exudative phase. The level of PMN-elastase in lymph was significantly higher 1 week after endotoxin injection than baseline levels. Histologically, pulmonary fibrosis developed 1 week after endotoxin injection. These results suggest that inflammatory mediators released from PMN play an important part in progress to the fibrotic phase after ARDS.
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PMID:[Pulmonary fibrosis after endotoxin-induced permeability edema]. 279 51

The purpose of this study was to investigate the relation between serum lipase (LP), serum immunoreactive trypsin (IRT), and its inhibitors in patients with adult respiratory distress syndrome (ARDS) of diverse origin and to compare their time course with other acute conditions. The IRT and LP levels were determined at regular intervals in 41 patients hospitalized in the intensive respiratory unit with ARDS (n = 9), acute pancreatitis (n = 5), shock (n = 9), bronchopneumonia (n = 10), or acute cardiogenic pulmonary edema (n = 8). Several trypsin inhibitors were measured simultaneously: serum trypsin inhibitory capacity (TIC), alpha 1-antitrypsin, alpha 2-macroglobulin, and antithrombin III. Concomitantly, angiotensin-converting enzyme (ACE) activity was determined as a potential marker of the endothelial injury. A respective 19- and 13-fold increase in IRT and LP values were observed in patients with ARDS after a mean evolution of 6 days; similar increases were seen in patients with pancreatitis. These values were significantly higher than those observed in the other conditions studied. In patients with ARDS and acute pancreatitis, the evolution of IRT and LP values were associated with a sixfold rise in TIC. A low TIC/IRT ratio in patients with ARDS appeared to be an index of poor prognosis. Conversely, ACE activity evolution was characterized by an early decrease in all the conditions studied. These observations indicate that there is an acute delayed pancreas injury in ARDS. Thus, the release of pancreatic enzymes are not reliable markers of the early evolution of the disease but they may represent secondary mediators for enhancement of the increased endothelial permeability.
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PMID:Evidence for pancreas injury in adult respiratory distress syndrome. 298 86

The multisystem involvement in acute pancreatitis (AP) is a reflection of the pancreatic gland's capacity to produce a number of potent vasoactive peptides, hormones, and enzymes. The various prognostic criteria are early evaluations of these metabolic derangements. The pathogenesis of hypocalcemia, long recognized as an indicator of severity of AP, is multifactorial. Imbalances of parathyroid hormone (PTH)-calcitonin, the interactions of glucagon, gastrin and other pancreatic hormones with PTH-calcitonin, the role of free fatty acids in binding serum calcium with albumin, and the translocation of calcium ion in muscles and liver, have been recently described but remain conflicting theories. Yet, the time-honored theory of calcium-soap formation enjoys wide acceptance. Hyperglycemia, hypoglycemia, and occasional ketoacidosis in acute pancreatitis have been studied thoroughly. The complex cause-and-effect relationship between hyperlipidemia with acute pancreatitis needs further study. The coagulation abnormalities seem to be initiated by activated trypsin, and their role in microvascular coagulation appears to form a unifying hypothesis for major organ dysfunction, but this requires further investigation. Adult respiratory distress syndrome may be the result of active enzymes that digest pulmonary surfactant and/or microvascular thrombosis. The depression of cardiac function and shock are suspected to be secondary to vasoactive peptides such as bradykinin, or myocardial depressant factor, whose structure has yet to be elucidated. The renin-angiotensin alterations and renal complications in acute pancreatitis have received scant attention in the literature. The onset of moderate visual disturbances, or even blindness, in a patient with acute pancreatitis as a result of retinal vessel thrombosis is fortunately uncommon. Rare but interesting are the manifestations such as subcutaneous fat necrosis, arthralgia, and pancreatic encephalopathy. Despite the extensive literature on the complexities of the pathogenesis of complications of acute pancreatitis, there have been very few advances in the prevention and management of specific complications. It is hoped that further work on modification of enzymatic disturbances induced in acute pancreatitis will result in its effective treatment and prevention of serious complications.
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PMID:Systemic complications of acute pancreatitis. 328

Plasmatic immunoreactive trypsin (IRT), thromboxane and trypsin-like enzymatic activity were measured in 117 patients at risk of developing adult respiratory distress syndrome (ARDS) (53 multiple injury, 30 abdominal surgery, 17 acute pancreatitis, 12 burnt and 5 disseminated intravascular coagulation patients). 69 of these patients developed ARDS. Immunoreactive trypsin and thromboxane were measured by radio-immuno-assay and trypsin-like enzymatic activity by spectrophotometry, using a specific chromogenic substrate. Mean IRT value was 675 ng/ml in ARDS and 265 ng/ml in non ARDS patients (p less than 0.05). Mean IRT value was 685 ng/ml in septic and 170 ng/ml in non septic patients (p less than 0.01). An abnormal trypsin-like enzymatic activity was measured in 26 ARDS patients. In 60 patients (37 ARDS and 23 non ARDS), thromboxane appeared in plasma simultaneously or about 24 hours after the beginning of IRT release. The importance of thromboxane release parallels the intensity of IRT. Originating from pancreas, trypsin can appear in plasma either by absorption from gastrointestinal tract or after pancreatic ischemia.
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PMID:Trypsin-like activity and thromboxane release in adult respiratory distress syndrome. 353 5

Complement fragments (C3, C3d, C5a), thromboxane B2 (TxB2), 6-keto-PGF1 alpha and immunoreactive trypsin (IRT) were measured in 98 patients at risk of developing the adult respiratory distress syndrome (ARDS): 53 multiple trauma, 28 abdominal surgery and 17 acute pancreatitis. Sixty-five of these patients developed ARDS: 30 multiple trauma, 19 abdominal surgery and 16 acute pancreatitis patients. Forty of the 65 ARDS patients and 9 out of the 33 non-ARDS patients died. Mean value of the C3d to C3 ratio was abnormal in both ARDS and non-ARDS patients. C5a-like activity was detected in 70 out of the 98 patients (49 ARDS and 22 non-ARDS patients). TxB2 abnormal values (greater than 100 pg . ml-1) were found in 70% of the patients, especially when sepsis occurred. No correlation could be made between abnormal 6-keto PGF1 alpha values and ARDS or sepsis. The mean peak IRT value was 675 micrograms . 1(-1) for ARDS patients and 274 micrograms . 1(-1) for non-ARDS patients (p less than 0.05). A firm correlation was also measured between IRT and sepsis (p less than 0.01). C5a-like activity was regularly detected soon after injury, while TxB2 and IRT tend to appear later in patients developing ARDS. Neither C3d/C3, nor C5a-like activity, nor TxB2, nor IRT are specific markers of ARDS, since they also appeared in severely ill patients who did not develop ARDS.
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PMID:Biochemical pathways of acute lung injury. 387 73

With the purpose of studying the role of proteinases in the development of ARDS, plasma levels of immunoreactive trypsin (IRT) and amylase were measured in 43 intensive care patients at risk of developing ARDS (22 polytrauma, seven abdominal surgery, four burns, two DIC and eight pancreatitis). Twenty four of these 43 patients developed ARDS and 31 presented abnormal IRT values (above 70 micrograms/L). Twenty-one of these 31 patients had ARDS; a significant correlation thus appeared between ARDS and abnormal IRT values. In nine patients, IRT values were higher than 800 micrograms/L and remained high for 3 to 4 days. A statistically significant correlation also appeared between abnormal IRT and septic phenomena: 20 patients with high IRT values presented septic problems. When IRT values were high, amylase values were often also abnormal: 12 of 23 patients with high IRT had abnormal amylase levels (the eight patients with documented pancreatitis were excluded); no other clinical signs or symptoms of pancreatitis were present in these patients. IRT could be one of the mediators of ARDS in septic patients. It is not clear that the pancreas is the origin of IRT in all cases.
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PMID:Immunoreactive trypsin in the adult respiratory distress syndrome. 619 96

Bronchoalveolar lavage (BAL) fluid was obtained from 24 sequentially studied patients with adult respiratory distress syndrome (ARDS) for assessment of potential activating and mediating factors. Proteolytic activity of the fluids was observed by measuring cleavage of radiolabeled proteins of the contact (Hageman factor) and complement systems. Proteolytic activity was observed in 17 of 24 (71%) patients with ARDS, and BAL fluid of the 7 ARDS patients without demonstrable, active, enzyme exhibited inhibitory activity for the proteolytic activity. The enzymes cleaved Hageman factor, prekallikrein, plasminogen, high molecular weight kininogen, C4, C3, C5, and Factor B of the complement system. Cleavage of the contact system proteins producted fragments similar or identical in size to the fragments observed during activation of these molecules, although continued incubation invariably reduced the protein to small peptide fragments. None of 7 normal individuals, and 29 of 99 patients (29%) with other forms of pulmonary disease contained measurable enzymes. The proteolytic activity in BAL fluid of ARDS patients was blocked by diisopropylphosphofluoridate (0.1 mM), Trasylol, soybean trypsin inhibitor, and normal plasma, or plasma deficient in inhibition of the first component of complement. Alpha(1)-proteinase inhibitor (alpha1-PI)-deficient plasma failed to inhibit the proteolytic activity and addition of alpha1-PI to the deficient plasma reconstituted the inhibition. MUCH OF THE PROTEOLYTIC ACTIVITY OF THE BAL FLUID FROM ARDS PATIENTS WAS IDENTIFIED AS NEUTROPHIL ELASTASE: the fluids cleaved elastin and synthetic peptide substrate of neutrophil elastase, neutrophil elastase antigen was present in the BAL fluids as determined immunologically using antineutrophil elastase, alpha1-PI was the major inhibitor in plasma, and the enzyme was inhibited by diisopropylphosphofluoridate but not chelation. In addition, purified neutrophil elastase produced cleavage fragments of proteins of the contact system similar to those of the BAL fluids. In each of the seven BAL fluids of ARDS patients that did not reveal active elastase, alpha1-PI was present in active form (as determined by (125)I-trypsin binding). In 9 of the 17 patients with active elastase in the BAL fluid, alpha1-PI antigen was present in the fluid, but was inactive (no binding of (125)I-trypsin). Immunoelectrophoretic analysis of elastase and alpha1-PI throughout proteins in these BAL fluids revealed the presence of both elastase and alpha1-PI that migrated with the same R(f), suggesting the presence of an enzyme-inhibitor complex. Free, inactive alpha1-PI was also observed in these fluids. The data reveal that in BAL fluids from all 24 patients with ARDS, leukocytic elastase and/or alpha1-PI exist. A complex of elastase and alpha1-PI was observed in BAL fluids, and in some cases where active enzyme and alpha1-PI coexisted, free, but inactive alpha1-PI was present.
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PMID:Studies on the pathogenesis of the adult respiratory distress syndrome. 703 51

The osmolality of contrast injected retrograde into the rat pancreatic duct did not affect the severity of the pancreatitis (Urografin, 1,300 mOsm/kg, and Hexabrix, 580 mOsm/kg). The severity of the pancreatitis induced in rats was assessed by survival rate, histologic grading, wet lung ratio, and serum levels of amylase, lipase, and trypsin-like activity. Rats with pancreatitis induced by retrograde injected Urografin, lipopolysaccharide, taurocholic acid plus enterokinase were treated with either intravenous (i.v.) FUT-175 (Nafamstat Mesilate), FUT-175 administered by retrograde pancreatic injection, i.v. terbutaline, i.v. piperacillin sodium, piperacillin sodium by retrograde pancreatic duct injection, or a combination of FUT-175 plus terbutaline and piperacillin. Survival among the rats was increased and the incidence of pancreatic infection reduced in rats treated with i.v. piperacillin or with a combination of FUT-175 plus i.v. terbutaline, plus i.v. piperacillin compared to controls.
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PMID:Therapeutic regimens in acute experimental pancreatitis in rats: effects of a protease inhibitor, a beta-agonist, and antibiotics. 747 69


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