著者
小田 隆治 鹿取 信
出版者
日本炎症・再生医学会
雑誌
炎症 (ISSN:03894290)
巻号頁・発行日
vol.11, no.1, pp.9-17, 1991-01-10 (Released:2010-04-12)
参考文献数
30

A series of the process of neutrophil extravasation induced by topical application of leukotriene B4 (LTB4) or formyl-methionyl-leucyl-phenylalanine (fMLP) on microvasculature of the hamster cheek pouch can be divided into five steps; I) rolling on the venular endothelium, II) adhesion on the endothelium, III) passage between the endothelial cells, IV) staying in the venular wall, V) migration from the venular wall to the interstitial space. In step II, topical application of chemoattractants on the microvasculature caused an increase in the number of neutrophils adhered to the venules. In step III, the size of the adhered neutrophils became gradually smaller and finallly disappear from the vascular lumen, as they were observed on the monitor screen. Over 80-90% of the adhered neutrophils passed through the endothelial cells. The whole process from step II to III took about 7 minutes. In step IV, the neutrophils which passed through the endothelial cells stay for about 30 minutes in the venular wall. In step V, neutrophils penetrated the basement membrane and migrated into the interstitial space.Step II and III were suppressed by a cyclic AMP phosphodiesterase inhibitor, fibronectin inhibitor and cytochalasin B. From these results, it was suggested that chemoattractant may cause the contraction of microfilament of neutrophil, and the contraction may induce the expression of adhesive glycoprotein on the neutrophil membrane. The increase of cyclic AMP in the neutrophil may inhibit the contraction of microfilament and/or the expression of adhesive glycoprotein of neutrophil. Dexamethasone did not affect the step I to IV, but suppressed the step V. Dexamethasone may inhibit synthesis and/or release of protease (s) in the neutrophil granules which degrade the basement membrane. In fact, the collagenase inhibitor suppressed the step V, although it did not the step I to IV. Thus, neutophil-derived collagenase may act on the passage of neutrophil through the basement membrane. The process of neutrophil extravasation is the chain of reaction.
著者
的場 愛子 川村 道子 原田 芳照 鹿取 信 田中 邦男
出版者
北里大学
雑誌
北里医学 (ISSN:03855449)
巻号頁・発行日
vol.22, no.1, pp.169-179, 1992-02-29

アラキドン酸(AA)及びコラーゲン(Col)により血小板はTXA_2生成を介して凝集・放出反応を起こす。インドメタシンは高濃度のAA又はColによるウサギ血小板凝集を抑制するが,TXA合成酵素阻害薬OKY-046はこれを抑制しなかった。しかし,OKY-046により凝集は抑制されなくてもTXB_2生成は抑制された。大動脈片を添加すると,6-keto-PGF_<1α>の生成が増加した。OKT-046にTXA_2/PGエンドペルオキシド受容体括抗薬ONO-3708を添加すると,凝集はほぼ完全に抑制された。OKY存在下でコラーゲンによる凝集濾液を第二セットのPRPに加えると凝集はやや減じたが,これに大動脈片を加えると著明な抑制が認められた。以上より,TXA合成酵素阻害薬によりTXA_2生成が抑制され,PGエンドペルオキシドが蓄積して血小板凝集をおこすと結論された。