glycine max trypsin inhibitor/bjúgur

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The role of bradykinin in mediating ischemic brain edema in rats.

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OBJECTIVE We investigated the hypothesis that bradykinin generation may induce ischemic brain edema in spontaneously hypertensive rats. METHODS Cerebral ischemia lasting 3 hours was produced by bilateral common carotid artery occlusion in 67 rats. After the ischemic period, the rats were reperfused.

[Studies on the involvement of bradykinin in the formation of ischemic brain edema].

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Bradykinin (BK) is known to be involved in the inflammatory process causing various tissue reactions such as peripheral vasodilation and increased vascular permeability. The aims of this study was to investigate the involvement of the kallikrein-kinin system (K-K system) in the generation and

Role in kinin in rat epinephrine pulmonary edema (REPE).

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High doses (10-40 micrograms/Kg, i.v.), of epinephrine evoke conspicuous consumption of circulatory rat kininogen (Kg), an effect not observed in animals pre-treated with either soybean trypsin inhibitor (SBTI, 10 mg/Kg, i.v.), Trasylol (1000 KIU/Kg, i.v.) or Aspirin (10 mg/Kg). Kg consumption by

Rat paw edema induced by trimucase II, a kinin-releasing enzyme from Trimeresurus mucrosquamatus venom.

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Trimucase II, a proteolytic enzyme isolated from Trimeresurus mucrosquamatus venom, caused rat hind-paw edema dose dependently. Captopril potentiated significantly, while pretreatment with cellulose sulfate suppressed the trimucase II-induced edematous response. Pretreatment with diphenhydramine and

Effect of C'1 esterase on vascular permeability in man: studies in normal and complement-deficient individuals and in patients with hereditary angioneurotic edema.

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When purified human C'1 esterase is injected intradermally in man, increased vascular permeability results. This effect is not blocked by soybean trypsin inhibitor and is not abolished by pretreatment with the antihistamine, pyribenzamine, or by compound 48/80. Thus, the effect is not due to the

The kallikrein-kinin system as mediator in vasogenic brain edema. Part 3: Inhibition of the kallikrein-kinin system in traumatic brain swelling.

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Evidence has previously been provided that administration of kinins to the cerebrum causes edema and opening of the blood-brain barrier. It has further been shown that these highly active compounds are formed in the brain under pathophysiological conditions. Their formation was enhanced when

The modulation of inflammation by the acute phase reaction in adjuvant arthritis in rats.

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In adjuvant-arthritic rats the carrageenin edema of the non-arthritic hind paw was significantly inhibited 24 hours and 3 days after adjuvant injection, but the edema was not influenced at day 14 when the acute phase reaction was still evident and increased anew. Inhibition of the edema in the

Vascular permeability enhancement by Vibrio mimicus protease and the mechanisms of action.

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Vibrio mimicus, a causative agent of gastroenteritis, has also been reported to attribute to extraintestinal infections. Recently we have purified a metalloprotease produced by the pathogen: however, the role of the protease in V. mimicus infection has not been documented. The V. mimicus protease

Tongue angioedema in vivo: antagonist response of anti-inflammatory drugs.

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BACKGROUND The toxicity of Dieffenbachia picta, an ornamental plant, arises from its ability to cause painful edema of oral mucous membranes, buccal ulcerations, and tongue hypertrophy after chewing on the stem or contact with the sap. OBJECTIVE We compared the anti-inflammatory effect of eugenol

Endothelial functional responses and increased vascular permeability induced by polycations.

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Polycations such as poly-L-lysine powerfully stimulated cultured endothelial cells from pig aorta to release prostacyclin and cytoplasmic purines in a dose (charge)-dependent and molecular weight (size) dependent manner. Neutral or anionic polymers were inactive. Qualitatively similar findings were

Enhancement of vascular permeability upon serratial infection: activation of Hageman factor--kallikrein--kinin cascade.

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A zinc dependent serratial 56K protease caused enhancement of vascular permeability followed by edema formation when injected into the guinea pig peripheral cornea, the subconjunctival space, or the skin. Because this enhancement was not affected by antihistamine, involvement of the kinin-generating

Penetrating the conjunctival barrier. The role of molecular weight.

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Dinitrophenyl (DNP) derivatives of various molecular weights were tested for their ability to elicit ocular anaphylaxis after topical application to the eye of immunized animals. Adult male Sprague-Dawley rats were immunized by intraperitoneal injection of DNP-Ascaris suum extracts and alum and were

Activation of the plasma kallikrein-kinin system by Vibrio vulnificus protease.

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Vibrio vulnificus protease enhanced hypodermic vascular permeability when injected into the dorsal skin of a guinea pig. Enhancement of permeability was observed within 2 min, and the permeability-enhancing reaction terminated at about 10 min postinjection. The permeability-enhancing reaction was

Human plasma alpha 2-macroglobulin. An inhibitor of plasma kallikrein.

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Activation of plasma kallikrein arginine esterase activity by kaolin resulted in peak activity at 1 min of incubation and a 50% reduction in activity at 5 min in normal plasma, and 30% reduction in the plasma of patients with hereditary angioneurotic edema who lacked the C1 inactivator. The peak

Role of the protease in the permeability enhancement by Vibrio vulnificus.

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The protease produced by Vibrio vulnificus enhances vascular permeability through histamine release from mast cells and activation of the plasma kallikrein-kinin system which generates bradykinin when injected into the dorsal skin. V. vulnificus living cells also enhanced vascular permeability

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