Ottlecz A, Gecse A, Faragó M, Forster T, Telegdy G
Endokrinologie. 1979 Apr;74(1):57-62.
The effect of adrenal and gonadal hormones on vascular permeability induced by intradermal injection of prostaglandins (PGs) E1, F2alfa, arachidonic acid and compound 48/80 have been examined in the rate. PGE1, arachidonic acid and compound 48/80 produced an increase in local vascular permeability. PGF2alfa decreased the action of these vasoactive agents, when it was injected in a mixture intradermally with PGE1, arachidonic acid and compound 48/80. Vasoactive response induced by PGE1, arachidonic acid and compound 48/80 was inhibited by the removal of adrenals and testes, and it was restored to normal by injection either of cortisol, deoxycorticosterone (DOC) or testosterone. In adrenalectomized rats, no change was observed in the inhibition of vascular permeability elicited by PGF2alfa response to compound 48/80. The blocking effect of PGF2alfa on vascular permeability evoked by PGE1 and arachidonic acid showed a considerable decrease. After orchidectomy the inhibitory effect of PGF2alfa on the vascular permeability induced by arachidonic acid and compound 48/80 was completely blocked, while in the case of PGE1 the inhibition was partial. Testosterone treatment restored the anti-inflammatory effect of PGF2alfa against compound 48/80. Ovariectomy was without any effect on vascular response.
已在大鼠中研究了肾上腺和性腺激素对皮内注射前列腺素(PGs)E1、F2α、花生四烯酸和化合物48/80所诱导的血管通透性的影响。PGE1、花生四烯酸和化合物48/80可使局部血管通透性增加。当F2α与PGE1、花生四烯酸和化合物48/80混合皮内注射时,它可降低这些血管活性药物的作用。切除肾上腺和睾丸可抑制PGE1、花生四烯酸和化合物48/80所诱导的血管活性反应,而注射皮质醇、脱氧皮质酮(DOC)或睾酮可使其恢复正常。在肾上腺切除的大鼠中,未观察到PGF2α对化合物48/80反应所引起的血管通透性抑制作用有变化。PGF2α对PGE1和花生四烯酸所诱发的血管通透性的阻断作用明显降低。睾丸切除后,PGF2α对花生四烯酸和化合物48/80所诱导的血管通透性的抑制作用被完全阻断,而对于PGE1,抑制作用只是部分性的。睾酮治疗可恢复PGF2α对化合物48/80的抗炎作用。卵巢切除对血管反应无任何影响。