Significance of the kinin system in rat paw oedemas and drug effects on it

Bonta, I. L.; Vos, C. J. de

doi:10.1016/0014-2999(67)90007-6

Cited by 21 publications

(7 citation statements)

References 10 publications

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“…Effectiveness of non-steroidal antiinflammatory drugs expected to act by inhibiting prostaglandin generation [28] could be explained by the ability of kinins to trigger biosynthesis of prostaglandins [29]. The effectiveness of low doses of dexamethasone emphasizes a parallelism between the pro-inflammatory activity of collagenase and of standard agents such as carregeenin [30], kaolin [31] or phospholipase A2-containing animal venoms [32]. (c) Although activation of endogenous kininreleasing mechanisms could result from a dilution response to haemorrhage, another explanation may be based on the strongly chemotactic effect of collagenase for neutrophils [331.…”

Section: Discussionmentioning

confidence: 98%

Haemorrhagic and inflammatory properties of collagenase fromC. histolyticum

1976

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Collagenase from Clostridium histolyticum induced haemorrhages when applied to the surface of dog lung; it exerted a similar effect on mouse lung when injected intrathoracically. Injected into rat paws, bacterial collagenase induced haemorrhage and oedema. Effects of collagenase were prevented by several procedures that inhibit collagenolytic activity (heating at various temperatures and incubation with metal-complexing agents such as EDTA, penicillamine and dithiothreitol). Protein protease inhibitors, dexamethasone and standard acidic anti-inflammatory drugs had only a slight or no effect on collagenase-induced haemorrhages; dexamethasone and acidic anti-inflammatory drugs blocked collagenase-induced oedema. Inhibition of endogenous kinin-releasing mechanisms by administration of hexadimethrine, a recognized inhibitor of the activation of clotting Factor XII, and depletion of kininogen by administration of carrageenin blocked collagenase-induced oedema. Collagenase did not increase permeability of rat skin vessels, nor did it release potential inflammatory mediators, such as bradykinin or prostaglandins, from plasma or platelets. Bacterial collagenase-induced haemorrhage presumably resulted from enzymatic destruction of membranous structures; at least a portion of the inflammatory response may be due to activation of a kinin-like system.

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Section: Discussionmentioning

confidence: 98%

Haemorrhagic and inflammatory properties of collagenase fromC. histolyticum

1976

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“…It is worth noting that bradykinin is released in response to tissue injury in nanogram quantities, and that the composite kinin-forming ability of rabbit's blood is equivalent to 6-10 jug/ml bradykinin (Garcia Leme, 1978). Thus, very low bradykinin concentrations, near the threshold for intra-arterial excitation of polymodal nociceptors, probably approach in vivo release quantities in severe inflammatory conditions (Bonta & de Vox, 1967).…”

Section: Discussionmentioning

confidence: 99%

Selective responsiveness of polymodal nociceptors of the rabbit ear to capsaicin, bradykinin and ultra‐violet irradiation.

Szolcsányi

1987

The Journal of Physiology

172

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SUMMARY1. The activity of single C-and A-fibre cutaneous sensory units was recorded from the great auricular nerve of anaesthetized rabbits to compare the effects of chemical with other forms of stimulation under several experimental conditions. Chemical agents were delivered by close arterial injection.2. Small intra-arterial injections of bradykinin (0-2 ,ug) and a substantial range of capsaicin doses (2-200 ,sg) consistently activated C polymodal nociceptors without exciting other types of C-or A-fibre cutaneous sense organs.3. Topical application of xylene to the receptive field of polymodal nociceptors evoked a strong excitation which lasted several minutes.4. The responses of polymodal nociceptors to mechanical, chemical (bradykinin, xylene) and noxious thermal stimuli were suppressed or abolished after large intra-arterial doses of capsaicin. Capsaicin desensitization of polymodal nociceptors to one kind of stimulation often was not paralleled by similar changes in responsiveness to other stimuli. However, on the average, capsaicin desensitization altered responses to thermal, chemical and mechanical stimuli without afferent selectivity.5. Background discharge developed in C polymodal nociceptors of the rabbit ear following ultra-violet irradiation sufficient to produce evidence of delayed inflammation. Noxious heat and bradykinin injection (0-2 ,ug) evoked more activity from C polymodal nociceptors in the irradiated ears than from control units.

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“…La participation de facteurs tissulaires dans le mécanisme de libération de bradykinine a déjà été décrit [9] ; par ailleurs, des fac teurs vraisemblablement libérés lors de l'inflammation aiguë ou de l'attaque anaphylactique, et qui ne libèrent pas de kinines in vitro, peuvent en libérer in vivo [1,7]. Le venin de N. naja, qui ne con tient pas d'enzymes capables d'attaquer les esters synthétiques de l'arginine [15] et qui ne libère pas de kinines in vitro déclenche la libération endogène de kinines lorsque injecté dans la patte du rat (Bontn, commun, pers.).…”

Section: Discussionunclassified

“…Les analgésiques non-narcotiques s'opposent, sur certaines préparations, aux actions de la bradykinine ou de la kallidine [2,16] et antagonisent sur d'autres la libération endogène des kinines [1]. Par ailleurs, divers agents libèrent des kinines plasmatiques in vitro, comme les kallikréines, la trypsine ou certains venins de serpents.…”

Section: Introductionunclassified

Antagonisme par les analgésiques non-narcotiques de la libération de kinines plasmatiques due au venin de B. jararaca et la kallikréine pancréatique

Vargäftig¹

1967

Pharmacology

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Significance of the kinin system in rat paw oedemas and drug effects on it

Cited by 21 publications

References 10 publications

Haemorrhagic and inflammatory properties of collagenase fromC. histolyticum

Haemorrhagic and inflammatory properties of collagenase fromC. histolyticum

Selective responsiveness of polymodal nociceptors of the rabbit ear to capsaicin, bradykinin and ultra‐violet irradiation.

Antagonisme par les analgésiques non-narcotiques de la libération de kinines plasmatiques due au venin de B. jararaca et la kallikréine pancréatique

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