Role of endogenous histamine in postanaphylactic phase of allergic inflammation in rats.
Role of endogenous histamine in postanaphylactic phase of allergic inflammation in rats.
复制标题
内源性组胺在大鼠过敏性炎症的过敏后阶段的作用。
DOI：
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发表时间：
1987
期刊：
影响因子：
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通讯作者：
S. Tsurufuji
中科院分区：
文献类型：
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作者：
N. Hirasawa;K. Ohuchi;M. Watanabe;S. Tsurufuji
用大鼠气囊型过敏性炎症模型，研究了内源性组胺在过敏性炎症过敏后阶段的作用。渗出液中的组胺呈双相增加。过敏性增加后迅速下降，然后在过敏后阶段逐渐上升，在抗原激发后24小时左右达到最大值。它又逐渐下降。过敏后阶段的组胺增加伴随着炎症组织中组氨酸脱羧酶活性的增加。局部给药的吡拉明，一种H1拮抗剂，无论是麦角新碱，一种5-羟色胺拮抗剂，或西咪替丁，H2拮抗剂，不能抑制血管通透性反应在过敏后阶段。当在过敏后阶段局部给予组胺酶以减少渗出液中的组胺时，渗出液中的中性粒细胞蓄积增强，而渗出液蓄积无任何变化。增强的中性粒细胞聚集也可诱导局部施用西咪替丁，但不是与吡拉明。局部给予组胺可剂量依赖性地抑制中性粒细胞聚集。这些结果表明，内源性组胺释放在过敏后阶段有助于下调中性粒细胞在炎症部位的积累，而不影响血管通透性。
Role of endogenous histamine in postanaphylactic phase of allergic inflammation was examined by using a rat model of allergic inflammation of air pouch type. Histamine in the exudate revealed a biphasic increase. The anaphylactic increase was followed by rapid decrease and then by a gradual rising in postanaphylactic phase with the maximum attained around 24 hr after the antigenic challenge. It again decreased gradually. The histamine increase in the postanaphylactic phase was accompanied by the increase of histidine decarboxylase activity in inflammatory tissues. Local administration of pyrilamine, an H1 antagonist, together with either methysergide, a serotonin antagonist, or cimetidine, an H2 antagonist, was unable to inhibit vascular permeability response in the postanaphylactic phase. When histaminase was administered locally in the postanaphylactic phase to reduce histamine in the exudate, neutrophil accumulation in the exudate was enhanced without any change in exudate accumulation. Enhancement of the neutrophil accumulation was also inducible with local administration of cimetidine but not with pyrilamine. Local administration of histamine inhibited the neutrophil accumulation dose-dependently. These results suggest that endogenous histamine released in the postanaphylactic phase contributes to downward regulation of neutrophil accumulation in the inflammatory site without affecting the vascular permeability.