The model of chronic intermittent stress by immobilization during pregnancy may produce alterations in the mechanisms that maintain adrenal gland homeostasis. In earlier investigations using this model, significant variations in plasma prolactin and corticosterone levels, and adrenal gland weights were observed. We hypothesized that chronic stress causes changes in apoptosis in the adrenal glands of pregnant rats. We identified and quantified apoptotic cells in the adrenal cortex and examined their ultrastructural characteristics using transmission electron microscopy. Adrenal glands of pregnant rats at gestation days 12, 17 and 21 were studied for control and experimental (stressed) rats. Immunolabelling techniques, stereological analysis and image quantification of adrenal gland sections were combined to determine differences in apoptosis in the different cell populations of the adrenal cortex. The apoptotic index of the experimental rats showed a significant reduction at gestation day 17, while at days 12 and 21 there were no differences from controls. Moreover, the apoptotic index of the reticular zones in control and experimental animals showed a significant increase compared to the glomerular and fascicular zones at the three gestation times studied. Chronic stress by immobilization reduced the caspase-dependent apoptotic index at gestation day 17, which may be related to variations in plasma concentrations of estrogens and prolactin.

The survival of developing embryos depends on the control and maintenance of homeostasis. Stress caused by chronic immobilization during pregnancy in rats may alter the normal development of the nervous system and increase susceptibility to psychiatric disorders. We investigated the effects of chronic stress on cell proliferation in the forebrains of embryos at 12 days of gestation, and in the hippocampus, dentate gyrus and cortex in embryos at 17 and 21 days of gestation. We examined serial sections of the embryonic brains of control and stressed rats at days 12, 17 and 21 of gestation. Brain sections were immunolabeled with anti-PCNA and stereological analysis was performed on 540 images. The results showed no statistical differences on days 12 and 17 of gestation in the proliferation area of the structures studied, whereas on day 21 of gestation, proliferation decreased in the cortex and dentate gyrus of embryos of the stressed group. These changes were related to decreased prolactin and increased corticosterone concentrations in the plasma.

Abstract:The increase intransplacental exchange depends primarily on the great development of the placental vascular bed. The aim of this study was to evaluate the pattern of placental vascular development at day 50 and 100 of pregnancy in goats and the relationship with the vascular endothelial growth factor (VEGF) immunolocalization. The placental morphometric variables: capillary area density, capillary perimeter density, capillary number density and average capillary perimeter of the caruncular (CAR) and cotyledonary (COT) tissues were measured at day 50 (n = 5) and 100 (n = 5) of gestation. Also, the immunolocalization of VEGF was performed. In the CAR and COT tissues a significant increase of capillary area density and capillary perimeter density at day 100 of the gestation was observed. In the COT tissue, this was due to the increase in the capillary number density; however in the CAR tissue this was due to the increase in the capillary size. We can conclude that in both tissues there were different strategies to increase the capillary area and, thereby, the nutrients exchange. The immunolocalization of VEGF in the COT tissue showed the endothelial cells of blood vessels and trophoblastcells surrounding the villi intensely inmunostained, which would indicate the involvement of VEGF in the placental vascular development.

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