The integrity of the microcirculation is essential for adequate tissue oxygenation, particularly after organ transplantation. Experimental evidence indicates that brain death determines microcirculatory alterations, including mesenteric hypoperfusion, endothelial activation and leukocyte migration associated with reduced serum concentrations of endogenous corticosterone. Hormonal changes secondary to pituitary failure cause hemodynamic and metabolic changes, which potentiate the degenerative process in the organs after brain death. Clinical and experimental evidence indicates that sex hormones influence the course of the inflammatory response, highlighting the beneficial effect of the female hormone oestrogen and the deleterious effect of the male hormone testosterone. Furthermore, gonadal steroid 17beta-oestradiol protects against ischemic cardiovascular, metabolic and inflammatory lesions. However, there are no data about the role of this hormone on microcirculatory changes due to brain death. This study aims to investigate the action of 17beta-oestradiol on the expression of nitric oxide synthase isoforms (iNOS and eNOS) and endothelin in the mesenteric microcirculation in male rats brain death model.
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