Effect of monoamine oxidase inhibitors on rat paw edema induced by various phlogistic agents

Kurti, Aishe

doi:10.1016/0014-2999(70)90282-7

Cited by 10 publications

(3 citation statements)

References 11 publications

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“…2 and Table 1), from which it was concluded that 5-HT contributed substantially to oedema formation in the first few hours. These findings are contrary to those reported by Winter (1965) who used cyproheptadine and methdilazine, both of which antagonize 5-HT, but are in agreement with the results of Fekete & Kurti (1970) who used methysergide, and the results of Bhalla & Tangri (1970) who used bromolysergic acid.…”

Section: Discussionsupporting

confidence: 56%

“…The kininogen concentrations of female Wistar rats were greatly reduced by intravenous injection of ellagic acid (Gautvik & Rugstad, 1967) or rat saliva and these procedures have been used in our investigation. The extent of the contribution to the oedema formation made by 5-hydroxytryptamine (5-HT) is indicated in the studies of Fekete & Kurti (1970) in which methysergide, an antagonist of 5-HT, was found to suppress the carrageenin reaction. In this study we have observed changes in the time course of oedema formation, in animals having low concentrations of plasma kininogen as well as in animals treated with antagonists of histamine and 5-HT in an attempt to determine the relative importance of kinins, histamine and 5-HT in the production of oedema by carrageenin.…”

Section: Introductionmentioning

confidence: 99%

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Mediators of the inflammation induced in the rat paw by carrageenin

Crunkhorn¹,

Meacock²

1971

British J Pharmacology

321

179

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Summary1. The time course of oedema formation in rats caused by injection of carrageenin into the paw was followed for 5-5 hours. Intact or adrenalectomized rats which had previously been injected with ellagic acid or saliva to reduce considerably the concentration of blood kininogens, or with methysergide to antagonize 5-hydroxytryptamine (5-HT) showed a reduced inflammatory response. It was concluded that kinins and 5-HT contributed significantly to oedema formation during this period. 2. Mepyramine alone had no effect on oedema formation, but in combination with ellagic acid treatment, with or without methysergide, it caused a reduction suggesting that histamine played a minor role in oedema formation during the first 3 hours. 3. Vascular permeability studies indicated that injection of ellagic acid did not interfere with the normal responses in skin to intradermal injections of histamine, 5-HT, bradykinin or compound 48/80. Mepyramine and methysergide, at the doses used in the carrageenin experiments, completely antagonized histamine and 5-HT, respectively, and did not affect the skin responses of bradykinin. 4. Treatment in vivo with ellagic acid or rat saliva was equally effective in reducing plasma kininogen concentrations by an amount equivalent to more than 10 times the quantity of substrate 1 measured by Gautvik & Rugstad (1967). 5. Rat saliva, but not ellagic acid, lowered complement levels by approximately 20%.

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Section: Discussionsupporting

confidence: 56%

Section: Introductionmentioning

confidence: 99%

Mediators of the inflammation induced in the rat paw by carrageenin

Crunkhorn¹,

Meacock²

1971

British J Pharmacology

321

179

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“…In experi-ments studying the inflammatory processes of a carrageenan-induced inflammation, 5-HT (together with histamine) is considered to be especially involved in the early phase of inflammation (Spector and Willoughby 1964;Fekete and Kürti 1970;Crunkhorn et al 1971;Di Rosa et al 1971;Garcia Lerne et aJ. 1973;Capasso et al 1975).…”

Section: Discussionmentioning

confidence: 99%

Activation of normal and inflamed fine articular afferent units by serotonin

Herbert

Schmidt

1992

Pain

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SummaryIn cats anesthetized with alpha-chloralose, extracellular recordings were made from fine afferent units belonging to the medial articular nerve (MAN) of the knee joint. The excitatory and sensitizing effects on articular afferents of serotonin (5-HT) applied intra-arterially close to the joint were examined. The joints were either normal or an experimental arthritis had been induced some hours before the recording session. Bolus injections of 1.35-135 p,g 5-HT excited about 43% of group 111 (CV: 2.5-20 mjsec) and 73% of group IV units (CV: < 2.5 mjsec) from normal joints. The latency was usually between 10 and 30 sec, and the duration and size of the responses were dose-dependent. Fast group 111 units (CV: > 16 mjsec) and group li units (CV: > 20 mjsec) were never excited by 5-HT. Repetitiveadministration led to pronounced tachyphylaxis of the 5-HT response. Inflammation induced an enhanced sensitivity of group III articular afferent units to close intra-arterial application of 5-HT. In particular the total duration of each response was considerably prolonged (4-10 min against 1-2 min under normal conditions). At the same time the tachyphylaxis seen under normal conditions was gteatly reduced. In contrast, group IV articular afferent units did not become sensitized to 5-HT in the course of inflammation. In normal joints 5-HT did not sensitize fineafferent units for movement-induced responses. However, after inflammation, a distinct sensitization to such movements by 5-HT application could be observed bothin group 111 and group IV fiber ranges. The sensitization had a short time course not exceeding 7 min. The tonic component of the movement-induced response was more enhanced than the phasic one. The bolus application of 5-HT led to temporary vasoconstriction of the knee joint vessels. This vasoconstriction was especially pronounced in inflamed joints and impeded the access of subsequently applied substances to the terminal regions of the afferent units under observation.lt is concluded that the present results support the notion that 5-HT may participate in the mediation of pain from inflamed tissue such as an arthritic joint by exciting and sensitizing fine afferent units. During inflammation group 111 units are particularly sensitive to 5-HT and, thus, may carry the bulk of the 5-HT-induced nociceptive messages.

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