PLATELET-ACTIVATING FACTOR ACETHER(PAF-ACETHER)INVOLVEMENT IN ACUTE INFLAMMATORY AND PAIN PROCESSES
PLATELET-ACTIVATING FACTOR ACETHER(PAF-ACETHER)INVOLVEMENT IN ACUTE INFLAMMATORY AND PAIN PROCESSES
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DOI：
10.1007/bf01978740
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发表时间：
1981-01-01
期刊：
影响因子：
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通讯作者：
BESSIN, P
中科院分区：
文献类型：
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作者：
BONNET, J;LOISEAU, AM;BESSIN, P
PAF-乙酸酯是由参与急性炎症过程的各种细胞释放的强效聚集剂。在本文中，外源性PAF-乙酸酯已被调查的能力，产生的迹象，炎症（水肿测量体积）和痛觉过敏（Randall-Sellito测试）的标准足底注射在大鼠爪。从0.005 μg开始，PAF-乙酸酯诱导爪显著水肿，最大值在注射后1小时;从0.1至5 μg呈剂量依赖性。从1.25 μg开始出现显著的剂量依赖性痛觉过敏;注射后2 - 4小时达到平台期。这两种现象持续时间长（>6小时）。PAF-乙酸酯在引起水肿、疼痛和增加血管通透性方面比PGI_2和PGE_2强1.5 ~ 10倍。本文研究了2.5 μg PAF-醋酸酯引起的水肿和痛觉过敏与其他药物的相互作用。非甾体抗炎药（NSAI）对水肿仅产生中度影响，而不影响痛觉过敏。各种药物可显著减轻水肿：泼尼松龙、L-半胱氨酸、抗钙药物、茶碱、PGI 2、沙丁胺醇、可乐定。除可乐定外，所有这些药物与NSAI药物相比，对PAF-醋酸酯水肿比对高岭土水肿更有效;这些药物之间的可能联系是它们能够增加细胞中的环AMP水平，从而减少溶酶体酶释放。PAF-醋酸酯本身，腹腔注射，抑制PAF-醋酸酯水肿，而不防止疼痛，在动脉压和红细胞压积无活性的剂量，但诱导显着的胃粘膜损伤。在测试的药物中，包括镇痛药，只有PGI 2和咪唑改善PAF诱导的痛觉过敏，显示水肿和痛觉过敏之间的分离，不仅在其诱导（所需的PAF剂量，时间过程的现象），但在药物能够拮抗其发展了。
PAF-acether is a potent aggregating agent released by various cells involved in acute inflammatory process. In this paper, exogenous PAF-acether has been investigated for its ability to generate signs of inflammation (edema measured by plethysmometry) and hyperalgesia (Randall-Sellito test) by standard subplantar injection in the rat paw. From 0.005 μg, PAF-acether induced significant edema of the paw, maximal 1 hour after injection; it was dose-dependent from 0.1 to 5 μg. Significant dose-dependent hyperalgesia occurred from 1.25 μg; it reached a plateau from 2 to 4 hours after injection. Both phenomena were long-lasting (>6 h). PAF-acether was 1.5 to 10 times stronger than PGI2and PGE2in inducing edema, pain, and in increasing vascular permeability. We investigated the interaction of miscellaneous drugs with the edema and the hyperalgesia caused by 2.5 μg of PAF-acether. Non-steroidal anti-inflammatory (NSAI) drugs exerted only moderate effects on the edema without affecting hyperalgesia. Edema was highly reduced by various agents: prednisolone,l-cysteine, anti-calcic drugs, theophylline, PGI2, salbutamol, clonidine. All of them, except clonidine, and in contrast to NSAI drugs, were more potent on PAF-acether edema than on kaolin edema; a possible link between these agents is their ability to increase cyclic AMP levels in the cells and consequently to reduce lysosomal enzyme release. PAF-acether itself, injected intra-peritoneally, inhibited PAF-acether edema without preventing pain, at doses inactive on arterial pressure and hematocrit, but inducing marked gastric mucosal damage. Among the drugs tested, including analgesics, only PGI2and imidazole improved PAF-induced hyperalgesia, showing a dissociation between edema and hyperalgesia not only in their induction (doses of PAF required, time course of the phenomena), but in the drugs able to antagonize their development too.