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暴露于产前酒精的雄性和雌性大鼠大脑阻力小动脉的收缩反应。

Constrictor responses of cerebral resistance arterioles in male and female rats exposed to prenatal alcohol.

机构信息

Division of Basic Biomedical Sciences, Sanford School of Medicine, University of South Dakota, Vermillion, South Dakota, USA.

出版信息

Physiol Rep. 2021 Nov;9(21):e15079. doi: 10.14814/phy2.15079.

DOI:10.14814/phy2.15079
PMID:34713985
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8554774/
Abstract

While it is known that dilation of cerebral arterioles to NOS-dependent agonists is impaired in rats exposed to prenatal alcohol, no studies have examined the influence of prenatal alcohol on constrictor response of cerebral arterioles. Our goal was to determine whether constrictor responses of cerebral resistance arterioles are altered by prenatal exposure to alcohol and if any changes differed as a function of age or sex. We fed Sprague-Dawley rat dams a liquid diet with or without alcohol (3% ethanol) for the duration of their pregnancy. We then examined reactivity of cerebral arterioles to thromboxane (U-46619; 0.01 and 0.1 µM), arginine vasopressin (0.1 and 1 nM), and angiotensin II (1 and 10 µM) in four groups of offspring: control male and female, and prenatal alcohol male and female at two different ages (adolescent: 4-6 weeks old and adult: 14-16 weeks old). Constriction of cerebral arterioles to U-46619 and AVP were similar in male and female rats regardless of exposure to prenatal alcohol and age. Similarly, adolescent male and female rats showed no difference to angiotensin II following prenatal exposure to alcohol. However, alcohol-exposed females exhibited an unexpected dilation to the high concentration of angiotensin II in adulthood, which was absent in males. We suggest that the findings from these studies may have implications regarding the susceptibility of the brain to cerebral ischemic damage. We speculate that impaired vasodilation, coupled with preserved vasoconstriction, can lead to a scenario favoring a decrease in cerebral blood flow during times of increased metabolic demand.

摘要

虽然已知暴露于产前酒精的大鼠大脑小动脉对 NOS 依赖性激动剂的扩张受损,但尚无研究检查产前酒精对大脑小动脉收缩反应的影响。我们的目标是确定产前酒精暴露是否改变大脑阻力小动脉的收缩反应,以及任何变化是否随年龄或性别而不同。我们用含有或不含有酒精(3%乙醇)的液体饮食喂养 Sprague-Dawley 孕鼠,持续整个孕期。然后,我们检查了 4 组后代的大脑小动脉对血栓素(U-46619;0.01 和 0.1 µM)、精氨酸加压素(0.1 和 1 nM)和血管紧张素 II(1 和 10 µM)的反应性:对照组雄性和雌性,以及产前酒精暴露的雄性和雌性,在两个不同年龄(青少年:4-6 周龄和成年:14-16 周龄)。无论是否暴露于产前酒精以及年龄如何,U-46619 和 AVP 引起的大脑小动脉收缩在雄性和雌性大鼠中相似。同样,在青少年时期,雄性和雌性大鼠在产前暴露于酒精后对血管紧张素 II 没有差异。然而,酒精暴露的雌性在成年时对高浓度血管紧张素 II 表现出意外的扩张,而雄性则没有。我们认为这些研究结果可能对大脑对脑缺血损伤的易感性有影响。我们推测,血管舒张受损,加上血管收缩保持不变,可能导致在代谢需求增加时,大脑血流减少的情况。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/57dc/8554774/9e3533c7d3d8/PHY2-9-e15079-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/57dc/8554774/409671c33e9d/PHY2-9-e15079-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/57dc/8554774/faf5f76a9284/PHY2-9-e15079-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/57dc/8554774/9e3533c7d3d8/PHY2-9-e15079-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/57dc/8554774/409671c33e9d/PHY2-9-e15079-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/57dc/8554774/faf5f76a9284/PHY2-9-e15079-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/57dc/8554774/9e3533c7d3d8/PHY2-9-e15079-g003.jpg

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