Influence of α-tocopherol on prostacyclin synthesis by rat's arterial and myometrial tissues

Abstract

Influence of α-tocopherol on PGI 2 synthesis by rat arterial and myometrial tissues was investigated using a rat platelet antiaggregatory bioassay. Chronic administration of α-tocopherol to female rats (10 mg kg −1 day −1 s.c. for 14 days) significantly increased ex-vivo PGI 2 synthesis by the arterial tissue from 12.7 ± 0.3 (control, mean ± s.e.m) to 17.2 ± 0.4 ng PGI 2 mg −1 wet tissue and by the myometrial tissue (in proestrus) from 1.1 ± 0.07 (control) to 1.85 ± 0.1 ng PGI 2 mg −1 wet tissue (P < 0.05, n = 6). α-tocopherol (5 mg kg −1day −1 for 14 days) did not stimulate PGI 2 to any significant level. Pretreatment of male rat arterial tissue with α-tocopherol (0.02, 0.1 or 0.2 mM) in vitro increased PGI 2 synthesis in a dose-dependent manner. At a dose of 0.2 mM it increased PGI 2 synthesis from 13.70 ± 0.70 (control) to 22.6 ± 1.4 ng PGI 2 mg −1 wet tissue (P < 0.1, n = 6). Pre-treatment of 14-day pregnant rat myometrium with α-tocopherol 0.2 and 0.4 mM significantly increased PGI 2 synthesis from 1.2 ± 0.06 (control) to 1.90 ± 0.12 and 2.1 ± 0.1 ng PGI 2 mg −1 wet tissue, respectively (P < 0.05, n = 6). The results indicate that the ability of α-tocopherol to stimulate PGI 2 synthesis may partly contribute towards better understanding of the mechanisms that underly the protective effect of α-tocopherol against experimentally induced decreases in coronary flow and intravascular coagulations in some mammals. Furthermore adequate intake of α-tocopherol during pregnancy may enhance uterine blood flow and ensure adequate foetal nutrition.