Effect of Hypoxia, Sex of the Animal and 17β-Estradiol on the Manifestationsof the Hypoxic Pulmonary Hypertension
We studied the effect of chronic administration of female sex hormone –17β‑estradiol (E2) at a dose of 15 µg/kg/day on the development of pulmonary hypertension (PH) caused by intermittent hypoxia with O<sub>2</sub> content of 13, 10, and 8% for 2 weeks. The study was carried out on gonadoectomized Wistar rats of both sexes. The degree of PH development was assessed by the magnitude of right ventricular systolic pressure (RVSP) and right ventricular hypertrophy. It was shown that all animals exposed to hypoxia developed PH, the degree of which depended on the O<sub>2</sub> concentration in the inhaled air. In males, the hypoxia (10% O<sub>2</sub>) increased the RVSP 19% less than in females (p < 0.05). Chronic administration of E2 caused gender-dependent changes in PH only at 10% O<sub>2</sub>. Thus, in males, the administration of E2 increased RVSP by 31% (p < 0.05), and in females it reduced hypertrophy by 10%. Also, E2 increased the survival rate of females at 8% O<sub>2</sub> by 2.5 times, but not males. An increase in hematocrit during hypoxia (10% O<sub>2</sub>) in females occurred due to an increase in the number of erythrocytes, and in males – due to an increase in their volume. Thus, the degree of development of the hypoxic pulmonary hypertension depends on the O<sub>2</sub> concentration in the inhaled air and has gender differences. E2 affects the development of this disease.