Involvement of Histamine in Vascular Permeability Increase of the Rat Pleurisy Induced by Phorbol Myristate Acetate

Kikuchi, Motohiro; Oh‐ishi, Sachiko

doi:10.1254/jjp.39.467

Cited by 16 publications

(6 citation statements)

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“…Simul taneous treatment with mepyramine and CV 3988 suppressed the 1 nmol PMA-induced dye leakage, and this effect appeared to be additive effect as shown in Table 1, although the difference was statistically significant only between the control and each treated group, i.e., mepyramine, CV-3988, or mepyramine CV-3988, but not between mepyramine-CV 3988 and each single treatment. In a previous study, we found that PMA induced mast cell degradation and release of histamine when injected into the rat pleural cavity (5) and that PMA also released PAF from resident mono nuclear cells to cause plasma leakage into the pleural cavity (6). The above results with mouse paw are mostly consistent with the previous observations in rats.…”

supporting

confidence: 90%

Assessment of vascular permeability increase in the mouse by dye leakage during paw edema.

Hayashi

Yamaki

et al. 1990

Jpn.J.Pharmacol

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confidence: 90%

Assessment of vascular permeability increase in the mouse by dye leakage during paw edema.

Hayashi

Yamaki

et al. 1990

Jpn.J.Pharmacol

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“…The precise procedure for sample collection was described previously (Kikuchi & Oh-ishi, 1985). The rats were killed at selected times; and blood and pleural cavity washings, the latter obtained with two 1-ml volumes of sterile saline, were collected in polyethylene tubes containing 1/10 volume of 3.8% sodium citrate.…”

Section: Experimental Protocolmentioning

confidence: 99%

Infiltration of neutrophils by intrapleural injection of tumour necrosis factor, interleukin‐1, and interleukin‐8 in rats, and its modification by actinomycin D

Utsunomiya

Ito

Watanabe

et al. 1996

British J Pharmacology

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To assess in vivo chemotactic activity of tumour necrosis factor (TNF), interleukin‐1 (IL‐1), IL‐8, and cytokine‐induced neutrophil chemoattractant (CINC), we injected these cytokines into the pleural cavity of rats. CINC (0.1‐1 μg) and recombinant human IL‐8 (rhIL‐8, 0.2–5 μg) caused neutrophil infiltration into the rat pleural cavity in a dose‐dependent fashion, peaking at 3 h. The number of leukocytes in the peripheral blood did not change significantly. RhTNFα and rhIL‐1α also induced neutrophil accumulation. The dose response curves of rhTNFα (0.67 ng‐6.7 μg) and rhIL‐1α (0.45 ng‐4.5μg) at 3 h were bell shaped. On the other hand, unlike CINC and rhIL‐8, rhTNFα and rhIL‐1α caused transient marked leukopenia at 3 h in a simple dose‐dependent fashion. Concomitant injection of actinomycin D dose‐dependently and completely at 10 μg inhibited neutrophil infiltration induced by rhTNFα (0.67 μg) and rhIL‐1α (0.45 μg) at 3 h. However, that induced by CINC or rhIL‐8 was not affected by actinomycin D. Peaking at 1 h, CINC production in the pleural cavity was found after intrapleural injection of rhTNFα (0.67 μg) or rhIL‐1α (0.45 μg), but not after that of rhIL‐8 (5 μg). The CINC production induced by rhTNFα or rhIL‐1α and the neutrophil infiltration was suppressed by concomitant injection of actinomycin D (1 and 10 μg). These results indicate that CINC and IL‐8 themselves are direct chemoattractants for neutrophils, whereas TNF and IL‐1 induce neutrophil infiltration indirectly via newly synthesized mRNA for chemotactic protein including CINC, which may be involved in neutrophil emigration at local inflammatory sites in rats.

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“…Agonists (0.1 ml) were injected intradermally into shaved dorsal skin of rats, who had received an intravenous injection of pontamine sky blue 10 min before. Procedure and extraction of dye were described previously [6], Agents Used. Kinins (bradykinin and T-kinin) were purchased from Peptide Institute (Minoh).…”

Section: Methodsmentioning

confidence: 99%

Pharmacological Demonstration of Inflammatory Mediators Using Experimental Inflammatory Models: Rat Pleurisy Induced by Carrageenin and Phorbol Myristate Acetate

Oh‐ishi

Hayashi

et al. 1989

Dermatology

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Rat pleurisy induced by carrageenin or phorbol myristate acetate (PMA) was utilized for examination of the plasma exudation process of inflammation. Chemical mediators responsible for induction of vascular permeability increase were examined. In carrageenin-induced pleurisy, kinin and PGI₂ were demonstrated as the main mediators, and in PMA pleurisy histamine, PGI₂ and platelet-activating factor were the main mediators. These results indicate that different stimuli may activate different enzymatic processes to produce different mediators, but they may result in similar inflammatory reactions by action of these multiple mediators simultaneously released.

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Involvement of Histamine in Vascular Permeability Increase of the Rat Pleurisy Induced by Phorbol Myristate Acetate

Abstract: Abstract-Rat pleurisy was induced by an intrapleural injection of 1 nmol (0

Cited by 16 publications

References 10 publications

Assessment of vascular permeability increase in the mouse by dye leakage during paw edema.

Assessment of vascular permeability increase in the mouse by dye leakage during paw edema.

Infiltration of neutrophils by intrapleural injection of tumour necrosis factor, interleukin‐1, and interleukin‐8 in rats, and its modification by actinomycin D

Pharmacological Demonstration of Inflammatory Mediators Using Experimental Inflammatory Models: Rat Pleurisy Induced by Carrageenin and Phorbol Myristate Acetate

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