Brain research
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Previously, we reported that paradoxical sleep (PS) is sexually dimorphic in mice and rats. Since some early studies indicate that PS is suppressed during proestrus night, it is important to know whether the estrus cycle and accompanying circulating ovarian hormones could explain the sexual dimorphism of PS. To examine this, sleep patterns of male rats were compared with those of normal cycling female rats and ovariectomized females in a 12:12 h light/dark cycle. ⋯ In sum, normal cycling females show no change in daytime sleep patterns across the estrus cycle, but have significantly less PS during proestrus nights than during metestrus and diestrus nights. The results indicate that the sex difference in nighttime PS is due to the suppression of PS by ovarian hormones during proestrus and, to a less extent, estrus nights. The sex difference in daytime PS, on the other hand, appears to be independent of circulating ovarian hormones.
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Endothelin-1 (ET-1) has been implicated in hematoma-induced cerebral vasoconstriction and modification of cerebral microvascular reactivity, particularly attenuation of vasodilation to cAMP-dependent dilators and enhanced vasoconstriction to ET-1. We examined effects of the ET-1 antagonist, BQ-123, on hematoma-induced modification of pial arteriolar responses to ET-1 and iloprost, a cAMP-dependent dilator, in vivo, plus the effects of such treatment on the cortical CSF cAMP. Closed cranial windows were implanted in alpha-chloralose anesthetized piglets 4 days following cortical subarachnoid injection of: (1) artificial cerebrospinal fluid (aCSF); (2) autologous blood; (3) BQ-123 alone; or (4) BQ-123 in combination with blood. ⋯ Thus, cerebral hematoma appears to attenuate iloprost-induced dilation and reduce basal cAMP level 4 days following hematoma via release that involves ET-1 of substance(s) on day 1 of hematoma. This substance(s) may act by inhibiting adenylyl cyclase. These results suggest that ET-1 plays an important role in the blood-induced prolonged cerebral vasoconstriction and altered vasoreactivity that follows cerebral hemorrhage via stimulation of ETA receptor.