Endocrine Abstracts

Objective: The role of sex in pulmonary hypertension (PAH) is not fully known. The majority of animal studies have suggested a protective role of female sex hormone in PAH. But women of various ages are more subjected to PAH compared with male. The aim of current research was to test the hypothesis that the level of oxygen in the inspired air can influence on the effect of estradiol on the development of experimental PAH in female rats.

Methods and design: Female gonadectomized Wistar rats were divided into 6 groups, three from which were injected subcutaneously during 4 weeks with 1,2-propandion (vehicle, 200 mkl/rat/day, C.); and three groups with estradiol (15 mkg/kg/day E₂). The procedures followed the FELASA/ICLAS guide for use of laboratory animals. PAH was induced by exposure to hypobaric hypoxia in all 6 groups. 2 groups (C13, E13) had hypoxia with 13% O₂, 2 groups (C10, E10) – 10% O₂ and 2 groups (C6, E6) – 6% O₂. Rats were housed in a hypobaric chamber 10 h/day, 2wk. Right ventricular systolic pressure (RVSP) was measured as indices of PAH. Blood hematocrit (Hmt) were measured using a blood analyser Gemalait 1280.

Results: Chronic estradiol administration in groups with 13% O₂ caused a decrease of RVSP in group E13 on 14.6% compared with C13 (P<0.05). In groups 10% O₂ estradiol did not caused any change in the group of E10 vs. C10. E₂ increased degree of RVSP in group E6 vs C6; (54.8±1.4 vs 46.3±1.1 mm Hg; P<0.01). E2 decreased Hmt in all groups in the same extent.

Conclusions: Effect of estradiol on the development of hypoxic pulmonary hypertension in the female ovariectomized rats depends on the degree of hypoxia (O₂ 13%, 10%, 6%). Decreasing effect of estradiol on the levels of Hmt does not correlate with the effect estradiol on the development of hypertension.