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)

Aprotinin, a protease inhibitor, has been used in a wide variety of pathophysiological states thought to be associated with an increase in protease activity. Opinion differ with respect to the success of the therapy. This paper proposes a rationale for the therapeutic action of aprotinin based on biochemical and physiological evidence. In the kallikrein-kinin system, in addition to kallikrein, other serine-esterases such as trypsin, plasmin, etc. can generate kinin production. In certain disease states such as pancreatitis there is not only an increase in serine-protease activity but frequently these enzymes reach parts of the organism where they are not found in health. Thus in such circumstances increased production of kinins can result. The consequences of increased kinin generation are discussed in light of work indicating their role in metabolic and circulatory homeostasis. Aprotinin is specifically a serine-esterase inhibitor. It is suggested that perhaps the most important action of this compound is as an inhibitor of the kallikrein-kinin system. On this basis a therapeutic regime in various disease states for the use of aprotinin, which allows for control of kinin generation, is suggested.
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PMID:A rationale for the therapeutic action of aprotinin. 15 36

Plasma kallikrein releases bradykinin when activated by gram-negative septicemia or irreversible hemorrhagic shock. Pancreatitis releases glandular kallikrein causing hypotension and increased vascular permeability. Bradykinin in the brain produces hypertension. Renal kallikrein is released by high arterial pressure, vasodilators, low doses of noradrenaline, angiotensin II, mineralocorticoids and rapid volume expansion. It has a biphasic relation to sodium excretion. In essential hypertension, kallikrein release into the blood and urine is low and facilitates hypertension. High renin in Bartter's syndrome is balanced by high PGE and kallikrein without hypertension.
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PMID:Kallikrein, kininogen and kinins in control of blood pressure. 37 13

To study the degree of protease activation at reperfusion of a pancreatic allograft after cold storage for 24 hr, 18 porcine whole-organ pancreaticoduodenal allograft transplantations were performed. Twelve grafts were flushed with and stored in Perfadex. In six of these, a hyperosmotic salt solution was injected into the graft aorta at reperfusion. Six grafts were flushed and stored in UW solution. Eleven of twelve grafts in the Perfadex groups were functioning on the first postoperative day, compared with one of six in the UW solution group. There was a significantly more pronounced protease activation among grafts stored in UW solution than in the other groups, with a subsequent breakthrough of the local protease protection barrier made up of protease inhibitors. In surviving pigs (n = 14), biochemical signs of protease activation evolved in plasma, including formation of trypsin-protease inhibitor complexes, a decline in C3 and kininogen levels, and a decline in functionally active alpha 2-macroglobulin, functionally active antithrombin III, and plasma kallikrein inhibitory activity. These biochemical signs of pancreatitis correlated with a deteriorated graft function on the second postoperative day, indicating that graft tissue damage occurred due to protease activation.
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PMID:Protease activation following reperfusion of porcine pancreatic allografts. 127 75

A 44-year-old woman with C1q esterase inhibitor deficiency was seen in consultation for recurrent right upper quadrant abdominal discomfort, nausea, and vomiting. Each of these episodes was accompanied by concomitant peripheral edema. Initial diagnostic efforts were fruitless. In time, intermittent elevations in amylase and lipase developed, and a diagnosis of relapsing pancreatitis was made. We contend that the patient's recurrent acute pancreatitis is associated with her hereditary angioedema. Possible pathogenesis could involve intermittent intrapancreatic edema with partial ductal obstruction or loss of inhibition on the kallikrein-kinin system.
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PMID:Hereditary angioedema associated with pancreatitis. 143 59

Variations in urinary kallikrein in pancreatic diseases were ascertained, and possible influencing factors were investigated. Serum amylase and urinary excretion of glandular kallikrein, pancreatic ribonuclease (RNase), gamma-glutamyltransferase (GGT) and amylase were measured in 24 control subjects, 39 patients with pancreatic cancer, 49 with pancreatitis and 63 with extra-pancreatic diseases. Urinary kallikrein was found to be elevated in a substantial number of patients with pancreatitis. Higher levels were detected in patients with a relapse, which was diagnosed using clinical and biochemical examinations. RNase was also increased in a high number of patients with pancreatic diseases, but was not correlated with pancreatic damage. In patients with pancreatitis, a correlation was found between urinary kallikrein and RNase excretions. No correlations were found between kallikrein and serum or urinary amylase and GGT. We can conclude that urinary kallikrein excretion increases in pancreatitis, especially when a phlogistic involvement of the pancreas is present; this condition may lead to a release of this ultrafiltrable enzyme in the circulation. Renal tubular damage, which determines a reduced reabsorption of this enzyme, seems to play a concomitant but minor role in this process.
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PMID:Urinary kallikrein excretion in chronic pancreatic diseases. 172 73

With the aim of diagnosis of postoperative pancreatitis in 88 oncologic patients operated on for malignant tumors of the upper alimentary canal and pancreatoduodenal zone, including those with trauma or resection of the pancreas, the comparative analysis of significance of different biochemical indices was carried out. A high sensitivity and informative value of measuring a content of the middle molecular mass peptides and components of kallikrein-kinin system with calculation of a toxicity coefficient permit to recommend their use as the additional diagnostic criteria.
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PMID:[Biochemical criteria of early diagnosis of postoperative pancreatitis in oncologic patients]. 187 14

An experimental model of edematous pancreatitis in pigs was established and measurement of pancreatic macro- and microcirculatory parameters and determinations of pancreatic enzymes (lipase, phospholipase A) and vasoactive mediators (prostanoids, kallikrein, kininogen) were performed. During general anesthesia the pancreas was isolated in situ. Pancreatic microcirculatory parameters were measured using videofluorescence microscopy after iv administration of FITC-Dextran. In hourly collected samples lipase and phospholipase A activities were determined enzymatically, concentrations of kallikrein, kininogen, and selected prostanoids were measured by radioimmunoassay. Two experimental groups were studied: (1) control (n = 9); (2) edematous pancreatitis induced by injection of oleic acid into the pancreatic artery (free fatty acid, ffa; n = 10). The animals were followed up for 6 hr. Systemic hemodynamic parameters remained constant in both groups. In the pancreatitis group pancreatic blood flow and O2-consumption decreased significantly (-55 and -49%), while pancreatic vascular resistance increased significantly (+50%). During baseline conditions 41% of all capillaries were perfused. In the pancreatitis group there were both areas with persistent stasis as well as areas with continuous perfusion. However, in the latter areas the portion of perfused capillaries decreased significantly to 27%. In the control group the portion of perfused capillaries remained constant. Liberation of lipase and phospholipase A especially into lymph and ascites fluid was measured during pancreatitis. Furthermore, considerable releases of kallikrein into lymph (+50%) and ascites (+800%) and a marked consumption of kininogen in lymph (+90%) and in ascites fluid (+80%) were measured. Activation of the arachidonic acid cascade and a significant release of prostacyclin and thromboxane A2 into pancreatic venous blood and lymph was observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Oleic acid induced pancreatitis in pigs. 199 Feb 28

Biochemical signs of pancreatitis in plasma and pancreatic exudates were determined in 22 pigs subjected to pancreatic allograft transplantation after the graft had been in cold storage for 6 hr. Two perfusion and preservation media were used. We found signs of protease activation in the pancreatic exudate during the first hour after reperfusion. The local protease protection barrier was, however, not broken and no plasma changes indicating pancreatitis were seen during this period. On the first and second postoperative days, mild biochemical signs of pancreatitis were seen in the plasma, including a decrease in kininogen and C3 concentration as well as in plasma kallikrein inhibitory activity and the appearance of trypsin-protease inhibitor complexes. No correlation was seen between these biochemical signs of pancreatitis and graft appearance or function, indicating that the reperfusion pancreatitis seen after 6 hr of cold storage is of minor significance. No significant differences were seen between the two preservation media used (Perfadex and EuroCollins solution).
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PMID:Biochemical characterization of reperfusion pancreatitis in porcine pancreatic allografts after six hours of cold storage. 201 26

The kallikrein-kinin system (KKS) is activated in all forms of acute pancreatitis. The severity of toxemia in patients with pancreatitis correlates with KKS activity. 2-3 hemosorption procedures performed in patients with hemorrhagic pancreatitis in the first 1, 2 and 3, 4 days normalizes KKS activity by days 3-5, leads to a rapid improvement of the clinical manifestations of the disease, shortens the treatment period and improves the results.
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PMID:[The effect of hemosorption on the activity of the kallikrein-kinin system in patients with hemorrhagic pancreatitis]. 207 59

Acute pancreatitis was induced in pigs by retrograde injection of Na-taurocholate into the pancreatic duct. By means of chromogenic peptide substrate assays, increased plasma kallikrein activity, parallel with a reduction of plasma prekallikrein and functional kallikrein inhibition values, was found in peritoneal exudate. In plasma, however, no changes in the kallikrein-kinin system were found during the 6-h observation time. The study demonstrates the presence of components of the plasma kallikrein-kinin system in peritoneal fluid and suggests that the peritoneal cavity to a great extent is a functionally separate compartment from plasma. Activation of the plasma kallikrein-kinin system in peritoneal exudate during acute experimental pancreatitis appears to be of importance for the initial symptoms and the development of shock seen during this condition.
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PMID:Studies on the plasma kallikrein-kinin system in peritoneal exudate and plasma during experimental acute pancreatitis in pigs. 241 21


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