Role of Bradykinin System in Acute Hemorrhagic Pancreatitis

Ryan, James W.; Moffat, John G.; Thompson, Amanda L.

doi:10.1001/archsurg.1965.01320130016003

Cited by 61 publications

(5 citation statements)

References 29 publications

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“…The activation of bradykinin through the action of kallikreins, which are present in several tissues including the small bowel, mediates acute inflammation with increases in microvascular permeability, vasodilation, and leukocyte migration and accumulation (25)(26)(27)(28). Furthermore, bradykinin is known to be a key enzyme in the activation of phospholipase A 2 , which generates prostaglandins and LTs (29).…”

Section: Discussionmentioning

confidence: 99%

Bradykinin B2 Receptor Antagonist FR173657 Ameliorates Small Bowel Ischemia?Reperfusion Injury in Dogs

et al. 2005

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Bradykinin mediates acute inflammation by increasing microvascular permeability, vasodilation, leukocyte migration and accumulation, and the production of arachidonic acid via phospholipase A2 activation. Arachidonic acid metabolites, or eicosanoids, are potent modulators of biological functions, particularly inflammation. Bradykinin exerts its inflammatory effects via the bradykinin B2 receptor. The aim of this study was to evaluate the effect of a bradykinin B2 receptor antagonist, FR173657 (FR), on intestinal ischemia-reperfusion (I/R) injury. Twenty-eight mongrel dogs were divided into four groups (n = 7 per group). Group I underwent I/R alone, Group II underwent I/R and received FR treatment, Group III was sham operated, and Group IV was sham operated and received FR treatment. The FR treatment consisted of FR continuously from 30 min prior to ischemia to 2 hr after reperfusion. In the I/R procedure, the superior mesenteric artery (SMA) and vein were clamped for 2 hr and then released to permit reperfusion for 12 hr. The intramucosal pH (pHi), SMA blood flow, and mucosal tissue blood flow were measured during the reperfusion period. The serum thromboxane B2 and 6-keto-prostaglandin F1alpha levels were determined, and tissue samples were examined histologically. Results showed that tissue blood flow, pHi, and SMA blood flow after reperfusion were maintained in Group II in comparison with Group I. Histopathological examination showed less severe mucosal damage after reperfusion in Group II than in Group I. The serum thromboxane B2 and 6-keto-prostagland in F1alpha levels were significantly lower in Group II than in Group I (P < 0.05). We conclude that FR treatment appears to have clear protective effects on small bowel I/R injury by inhibiting the release of eicosanoids.

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Section: Discussionmentioning

confidence: 99%

Bradykinin B2 Receptor Antagonist FR173657 Ameliorates Small Bowel Ischemia?Reperfusion Injury in Dogs

et al. 2005

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“…Necrotizing pancreatitis (NP), however, frequently is connected with lethal complications. The disintegrating tissue releases vasoactive and toxic substances into the abdominal cavity [2][3][4] and the blood [2][3][4][5][6][7][8], thus causing multiple complications. Hypovolemia, renal and pulmonary insufficiency, and cardiocirculatory complications as well as septic complications are the reason for the high morbidity and mortality of patients with NP [%14].…”

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confidence: 99%

Results of surgical treatment of necrotizing pancreatitis

et al. 1985

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In 205 patients with necrotizing pancreatitis, surgery was carried out following failure of medical treatment. Intraoperatively, according to the size of the necrotic area and the weight of the surgically removed necrotic tissue, 79 patients showed a limited panereatic necrosis, and 126 patients an extended necrotizing process. In 40.4% of 138 patients with bacteriological reports, a bacterial contamination of the pancreatic necrosis was found. The main objective of surgical management was the removal of the necrotic tissue. This was performed with 2-way drainage and postoperative continuous peritoneal and/or local lavage, in a smaller group of patients with inner drainage of the necrosis cavity, and in a few patients with drainage alone. The overall hospital mortality rate was 24.4%. The Iowest mortality was achieved in patients treated with necrosectomy and postoperative continuous local lavage (6.0%). In patients with necrosis of approximately 30% of the pancreas, mortality was lower (7.6%) than in patients with a 50% necrosis (24.0%) or in patients with a subtotal/total necrosis (51.0%) (p < 0.0001). Formation of extrapancreatic necrosis resulted in a significantly increased mortality rate (p < 0.02). In patients with bacterially contaminated necrosis, a mortality rate of 32.1% was found, whereas in patients with a steri|e neerosis, mortality was down to 9.8% (p < 0.01). Based on the results of this study, we eonclude that the clinical course of necrotizing pancreatitis depends essentially on the extent of the necrosis in the pancreas itself, the development of extrapancreatic necrosis, and the bacteriological status of the necrotic area. Adequate surgical management leads to a considerably increased survival rate of patients with necrotizing pancreatitis.

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“…With (9) Enzyme-digestion products were prepared by incubation of the pure enzyme solution, or equal parts of en¬ zyme solution and fresh autologous whole blood, for 24 hours at 37.5 C in a constant temperature water bath.…”

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confidence: 99%

Further Inquiry Into the Pathogenesis of Acute Pancreatitis

Anderson¹

1969

Arch Surg

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Role of Bradykinin System in Acute Hemorrhagic Pancreatitis

Cited by 61 publications

References 29 publications

Bradykinin B2 Receptor Antagonist FR173657 Ameliorates Small Bowel Ischemia?Reperfusion Injury in Dogs

Bradykinin B2 Receptor Antagonist FR173657 Ameliorates Small Bowel Ischemia?Reperfusion Injury in Dogs

Results of surgical treatment of necrotizing pancreatitis

Further Inquiry Into the Pathogenesis of Acute Pancreatitis

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