Abstract:
Preeclampsia is a major cause of premature birth, intrauterine growth retardation and perinatal mortality. In developed countries, it is the cause of about 16-18% of maternal deaths and up to 40% of fetal and neonatal deaths [1]. Endothelial dysfunction can lead to the development of preeclampsia. The administration of the nonselective NOS inhibitor L-NAME to female rats during placenta caused morphological abnormalities in the frontal cortex neurons of rat offspring on day 1 of postnatal development, which were manifested by an increase in cell size and an increased proportion of hypochromic neurons.