Swingle K F, Reiter M J
Agents Actions. 1986 Jun;18(3-4):359-65. doi: 10.1007/BF01964997.
Three classes of drugs were found, after their i.p. administration, to inhibit Paf-acether-induced edema of the rat's paw. These were beta-adrenergic agonists (isoproterenol, salbutamol), alpha-adrenergic antagonists (prazosin, ergotamine, yohimbine, phenoxybenzamine), and calcium entry blockers (nifedipine, verapamil, diltiazem). A number of other drugs including steroidal and nonsteroidal antiinflammatory agents, alpha-agonists, beta-antagonists, pyrilamine, atropine, methysergide, a lipoxygenase inhibitor, and a leukotriene antagonist did not inhibit the development of the edema. Propranolol, but not practolol, antagonized the inhibitory effect of isoproterenol which provided evidence for involvement of beta-2 receptors in the mechanism of action of the beta agonists. It is suggested that cellular calcium influx is involved in the edemagenic response observed after the injection of Paf-acether into the rat's paw.
经腹腔注射给药后,发现有三类药物可抑制血小板活化因子(Paf - 乙酰醚)诱导的大鼠爪部水肿。这些药物分别是β - 肾上腺素能激动剂(异丙肾上腺素、沙丁胺醇)、α - 肾上腺素能拮抗剂(哌唑嗪、麦角胺、育亨宾、酚苄明)以及钙通道阻滞剂(硝苯地平、维拉帕米、地尔硫䓬)。包括甾体和非甾体抗炎药、α - 激动剂、β - 拮抗剂、吡苄明、阿托品、甲基麦角新碱、一种脂氧合酶抑制剂以及一种白三烯拮抗剂在内的许多其他药物均未抑制水肿的发展。普萘洛尔而非醋氨心安可拮抗异丙肾上腺素的抑制作用,这为β - 2受体参与β - 激动剂的作用机制提供了证据。提示细胞钙内流参与了将Paf - 乙酰醚注射到大鼠爪部后所观察到的致水肿反应。