Hypoxia changes the regional distribution of cerebral blood flow and stimulates the ventilatory chemoreflex, thereby reducing CO2 tension. We examined the effects of both hypoxia and isocapnic hypoxia on acute changes in internal carotid (ICA) and vertebral artery (VA) blood flow. Ten healthy male subjects underwent the following two randomly assigned respiratory interventions after a resting baseline period with room air: (i) hypoxia; and (ii) isocapnic hypoxia with a controlled gas mixture (12% O2; inspiratory mmHg). In the isocapnic hypoxia intervention, subjects were instructed to maintain the rate and depth of breathing to maintain the level of end-tidal partial pressure of CO2 ( ) during the resting baseline period. The ICA and VA blood flow (velocity × cross-sectional area) were measured using Doppler ultrasonography. The was decreased (-6.3 ± 0.9%, P < 0.001) during hypoxia by hyperventilation (minute ventilation +12.9 ± 2.2%, P < 0.001), while was unchanged during isocapnic hypoxia. The ICA blood flow was unchanged (P = 0.429), while VA blood flow increased (+10.3 ± 3.1%, P = 0.010) during hypoxia. In contrast, isocapnic hypoxia increased both ICA (+14.5 ± 1.4%, P < 0.001) and VA blood flows (+10.9 ± 2.4%, P < 0.001). Thus, hypoxic vasodilatation outweighed hypocapnic vasoconstriction in the VA, but not in the ICA. These findings suggest that acute hypoxia elicits an increase in posterior cerebral blood flow, possibly to maintain essential homeostatic functions of the brainstem.

译文

:低氧改变了脑血流的区域分布并刺激了通气的化学反射,从而降低了二氧化碳的张力。我们检查了缺氧和等容量低氧对颈内动脉(ICA)和椎动脉(VA)血流急性变化的影响。在基线空气静息期结束后,对十名健康的男性受试者进行以下两次随机分配的呼吸干预:(i)缺氧; (ii)受控混合气体(12%O2;吸气mmHg)的等碳酸血症性低氧。在低碳酸血症的低氧干预中,受试者被要求保持呼吸速率和呼吸深度,以在基线休息期间保持呼气末的CO2()潮气分压水平。使用多普勒超声测量ICA和VA血流(速度×横截面积)。在低氧状态下通气过度(分钟通气量12.9±2.2%,P <0.001)降低了(-6.3±0.9%,P <0.001),而在等碳酸血症性低氧状态下,则保持不变。在缺氧期间,ICA血流保持不变(P = 0.429),而VA血流增加(10.3±3.1%,P = 0.010)。相反,等碳酸血症性低氧会增加ICA(14.5±1.4%,P <0.001)和VA血流(10.9±2.4%,P <0.001)。因此,在VA中,低氧血管舒张超过了低碳酸血症性血管收缩,而在ICA中则不然。这些发现表明,急性缺氧引起后脑血流量增加,可能维持脑干的基本稳态功能。

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