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首页> 外文期刊>Brain research >Effects of binge alcohol exposure in the second trimester on intracerebral arteriolar function in third trimester fetal sheep.
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Effects of binge alcohol exposure in the second trimester on intracerebral arteriolar function in third trimester fetal sheep.

机译:泪液暴露在妊娠中三个三个月胎儿胎儿胎儿颈绵的影响。

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Fetal alcohol syndrome is a leading cause of mental retardation, but mechanisms of alcohol-associated brain damage remain elusive. Chronic alcohol exposure attenuates fetal and neonatal hypoxic cerebral vasodilation in sheep. We therefore hypothesized that alcohol could alter development of cerebrovascular responses to adenosine, a putative mediator of hypoxic cerebral vasodilation. The objective of this study was to examine the effect of earlier fetal alcohol exposure on later reactivity to adenosine in fetal sheep cerebral arterioles. Penetrating intracerebral arterioles were harvested from the brains of third trimester fetal sheep previously exposed in the second trimester to maternal alcohol "binges" (1.5 g/kg IV over 90 min, 5 days/week for 4 weeks) or same-volume saline infusions. Arterioles were cannulated with a micropipette system and luminally pressurized. Fetal alcohol exposure did not affect spontaneous myogenic tone, but enhanced the dilator response of penetrating arterioles to extraluminal acidosis (pH 6.8). Alcohol exposure also resulted in an increase in maximal vessel response to CGS-21680, an adenosine A(2A) receptor agonist, but did not alter the concentration-dependent response curves to adenosine. Our results suggest that earlier alcohol exposure does not impair the subsequent responsiveness of fetal cerebral arterioles to vasodilator agents. Thus, alteration in cerebral vascular response to hypoxia in fetal sheep may not be attributed to changes in vascular reactivity to adenosine.
机译:胎儿酒精综合征是精神发育迟滞的主要原因,但酒精相关的脑损伤机制仍然难以捉摸。慢性酒精曝光衰减绵羊中的胎儿和新生儿缺氧脑血管舒张。因此,我们假设酒精可以改变对腺苷的脑血管反应的发展,一种缺氧脑血管血管凝固的推定介质。本研究的目的是研究早期胎儿酒精暴露对胎儿绵羊脑动脉瘤中腺苷的后期反应性的影响。从前三个三个月胎儿的大脑中收获渗透骨干细胞,以在第二孕三个月暴露于母体醇“弯曲”(1.5g / kg IV超过90分钟,5天/周4周)或相同盐水输注。动脉源性用微移液管系统插管并透明地加压。胎儿酒精暴露不影响自发性肌原色调,而是增强了穿透动脉酸的扩张响应,以渗透细胞酸中毒(pH6.8)。酒精曝光也导致最大血管响应对CGS-21680的响应增加,腺苷A(2A)受体激动剂,但未改变依赖于腺苷的浓度依赖性响应曲线。我们的研究结果表明,早期的酒精暴露不会损害胎儿脑动脉杆菌对血管扩张剂的后续反应性。因此,胎儿绵羊缺氧的脑血管反应的变化可能不会归因于对腺苷的血管反应性的变化。

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