Anatomical vertebral artery hypoplasia and insufficiency impairs dynamic blood flow regulation
Anatomical vertebral artery hypoplasia and insufficiency impairs dynamic blood flow regulation
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DOI：
10.1111/cpf.12179
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发表时间：
2015-11-01
影响因子：
1.8
通讯作者：
Ogoh, Shigehiko
中科院分区：
文献类型：
--
作者：
Sato, Kohei;Yoneya, Marina;Ogoh, Shigehiko
近年来的研究表明椎动脉发育不良是后脑卒中的一个易感因素。我们检查了解剖性椎基底动脉缺血，即，单侧VA发育不全和功能不全，损害动态血流调节。根据规定的标准将28名女性受试者分为三组：（i）单侧VA发育不全（n = 8），（ii）VA功能不全（n = 6）和（iii）对照组（n = 14）。发育不良VA标准为VA血流量40 ml min（-1），而VA不足标准为VA净（左+右）血流量100 ml min（-1）或更少。我们通过超声检查在高碳酸血症、正常碳酸血症和低碳酸血症期间评估左、右和净VA血缺陷，以评估VA CO2反应性。单侧VA发育不良组在发育不良VA处的CO反应性低于非发育不良VA处（2.65 +/- 0.58 vs 3.00 +/- 0.48%/mmHg，P = 0.027）和净VA CO2反应性得以保留（单侧VA发育不全，2.95 +/- 0.48与对照组，2.93 +/- 0.42%/mmHg，P = 0.992）。然而，VA功能不全组的净VA CO2反应性低于对照组（2.29 +/- 0.55 vs 2.93 +/- 0.42%/mmHg，P = 0.032）和单侧VA发育不全组（P = 0.046）。VA发育不全降低了CO2反应性，尽管非发育不全VA可以补偿这种监管限制。在VA功能不全的受试者中，两个VA的CO2反应性降低不能保持正常的净VA CO2反应性。这些发现为VA发育不良和功能不全受试者后脑卒中风险增加提供了可能的生理机制。
Recent studies have suggested that vertebral artery (VA) hypoplasia is a predisposing factor for posterior cerebral stroke. We examined whether anatomical vertebrobasilar ischemia, i.e., unilateral VA hypoplasia and insufficiency, impairs dynamic blood flow regulation. Twenty eight female subjects were divided into three groups by defined criteria: (i) unilateral VA hypoplasia (n = 8), (ii) VA insufficiency (n = 6), and (iii) control (n = 14). Hypoplastic VA criterion was VA blood flow of 40 ml min(-1), whereas VA insufficiency criterion was net (left + right) VA blood flow of 100 ml min(-1) or less. We evaluated left, right, and net VA blood flaws by ultrasonography during hypercapnia, normocapnia, and hypocapnia to evaluate VA CO2 reactivity. The unilateral VA hypoplasia group showed lower CO) reactivity at hypoplastic VA than at non-hypoplastic VA (2.65 +/- 0.58 versus 3.00 +/- 0.48% per mmHg, P = 0.027) and net VA CO2 reactivity was preserved (Unilateral VA hypoplasia, 2.95 +/- 0.48 versus Control, 2.93 +/- 0.42% per mmHg, P = 0.992). However, the VA insufficiency group showed a lower net VA CO2 reactivity compared to the control (2.29 +/- 0.55 versus 2.93 +/- 0.42% per mmHg, P = 0.032) and the unilateral VA hypoplasia (P = 0.046). VA hypoplasia reduced CO2 reactivity, although non-hypoplastic VA may compensate this regulatory limitation. In subjects with VA insufficiency, lowered CO2 reactivity at the both VA could not preserve normal net VA CO2 reactivity. These findings provide a possible physiological mechanism for the increased risk of posterior cerebral stroke in subjects with VA hypoplasia and insufficiency.