Sex Differences in the Cerebral Collateral Circulation.
Sex Differences in the Cerebral Collateral Circulation.
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DOI：
10.1007/s12975-016-0508-0
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发表时间：
2017-06
影响因子：
6.9
通讯作者：
Zhang H
中科院分区：
文献类型：
--
作者：
Faber JE;Moore SM;Lucitti JL;Aghajanian A;Zhang H
绝经前的女性和完好无损的雌性啮齿动物的脑梗塞比雄性要小。一些与性别相关的差异已被确定为潜在的贡献者，但许多问题仍未得到回答。小鼠在自然侧支数量和直径(侧支范围)上表现出很大的差异，这取决于遗传背景、年龄和其他共病的差异，这也是导致它们在脑梗塞体积上也存在广泛差异的原因。同样，梗死体积的变化与急性缺血性卒中患者侧支循环依赖的血流的差异相关。我们研究了在年轻、老年、肥胖、高血压和遗传不同的小鼠中，软脑膜侧支动脉和后交通侧支动脉(PComA)的范围是否因性别而不同。我们将新数据与对之前发布的数据进行荟萃分析相结合。C57BL/6J(B6)和BALB/cByJ(BC)品系的雌性大鼠在永久性大脑中动脉闭塞后的心肌梗死范围比雄性小。在BC小鼠中，这种保护作用在导入dce1的B6等位基因后没有变化，dce1是导致小鼠软脑膜侧支变异的主要遗传决定因素。与此一致的是，这些品系和其他品系的侧枝程度没有性别差异。PComA和初级大脑动脉的范围也不随性别而变化。由于年龄、肥胖和高血压导致的软脑膜侧支数目和/或直径的丧失(侧支稀疏)，以及pMCAO后的侧支重构，没有明显的二型性。然而，长期患有高血压的女性的稀疏性更大。我们的结论是，雌性小鼠较小的脑梗塞体积并不是由于年龄、肥胖或高血压引起的侧支循环范围更大、重塑更大或稀疏程度更低。
Premenopausal women and intact female rodents sustain smaller cerebral infarctions than males. Several sex-dependent differences have been identified as potential contributors, but many questions remain unanswered. Mice exhibit wide variation in native collateral number and diameter (collateral extent) that is dependent on differences in genetic background, aging, and other comorbidities and that contributes to their also-wide differences in infarct volume. Likewise, variation in infarct volume correlates with differences in collateral-dependent blood flow in patients with acute ischemic stroke. We examined whether extent of pial collateral arterioles and posterior communicating collateral arteries (PComAs) differ depending on sex in young, aged, obese, hypertensive, and genetically different mice. We combined new data with meta-analysis of our previously published data. Females of C57BL/6J (B6) and BALB/cByJ (BC) strains sustained smaller infarctions than males after permanent MCA occlusion. This protection was unchanged in BC mice after introgression of the B6 allele of Dce1, the major genetic determinant of variation in pial collaterals among mouse strains. Consistent with this, collateral extent in these and other strains did not differ with sex. Extent of PComAs and primary cerebral arteries also did not vary with sex. No dimorphism was evident for loss of pial collateral number and/or diameter (collateral rarefaction) caused by aging, obesity, and hypertension, nor for collateral remodeling after pMCAO. However, rarefaction was greater in females with long-standing hypertension. We conclude that smaller infarct volume in female mice is not due to greater collateral extent, greater remodeling, or less rarefaction caused by aging, obesity, or hypertension.