Peebles Karen, Celi Leo, McGrattan Ken, Murrell Carissa, Thomas Kate, Ainslie Philip N
Department of Physiology, University of Otago, Dunedin, New Zealand.
J Physiol. 2007 Oct 1;584(Pt 1):347-57. doi: 10.1113/jphysiol.2007.137075. Epub 2007 Aug 9.
This study examined cerebrovascular reactivity and ventilation during step changes in CO(2) in humans. We hypothesized that: (1) end-tidal P(CO(2)) (P(ET,CO(2))) would overestimate arterial P(CO(2)) (P(a,CO(2))) during step variations in P(ET,CO(2)) and thus underestimate cerebrovascular CO(2) reactivity; and (2) since P(CO(2)) from the internal jugular vein (P(jv,CO(2))) better represents brain tissue P(CO(2)), cerebrovascular CO(2) reactivity would be higher when expressed against P(jv,CO(2)) than with P(a,CO(2)), and would be related to the degree of ventilatory change during hypercapnia. Incremental hypercapnia was achieved through 4 min administrations of 4% and 8% CO(2). Incremental hypocapnia involved two 4 min steps of hyperventilation to change P(ET,CO(2)), in an equal and opposite direction, to that incurred during hypercapnia. Arterial and internal jugular venous blood was sampled simultaneously at baseline and during each CO(2) step. Cerebrovascular reactivity to CO(2) was expressed as the percentage change in blood flow velocity in the middle cerebral artery (MCAv) per mmHg change in P(a,CO(2)) and P(jv,CO(2)). During hypercapnia, but not hypocapnia, P(ET,CO(2)) overestimated P(a,CO(2)) by +2.4 +/- 3.4 mmHg and underestimated MCAv-CO(2) reactivity (P < 0.05). The hypercapnic and hypocapnic MCAv-CO(2) reactivity was higher ( approximately 97% and approximately 24%, respectively) when expressed with P(jv,CO(2)) than P(a,CO(2)) (P < 0.05). The hypercapnic MCAv-P(jv,CO(2)) reactivity was inversely related to the increase in ventilatory change (R(2) = 0.43; P < 0.05), indicating that a reduced reactivity results in less central CO(2) washout and greater ventilatory stimulus. Differences in the P(ET,CO(2)), P(a,CO(2)) and P(jv,CO(2))-MCAv relationships have implications for the true representation and physiological interpretation of cerebrovascular CO(2) reactivity.
本研究检测了人体在二氧化碳（CO₂）阶跃变化过程中的脑血管反应性和通气情况。我们假设：（1）在呼气末二氧化碳分压（P(ET,CO₂)）发生阶跃变化时，呼气末P(CO₂)（P(ET,CO₂)）会高估动脉血P(CO₂)（P(a,CO₂)），从而低估脑血管对CO₂的反应性；（2）由于颈内静脉血P(CO₂)（P(jv,CO₂)）能更好地反映脑组织P(CO₂)，因此以P(jv,CO₂)为参照时脑血管对CO₂的反应性会高于以P(a,CO₂)为参照时，且与高碳酸血症期间通气变化的程度相关。通过给予4%和8%的CO₂ 4分钟来实现递增性高碳酸血症。递增性低碳酸血症包括两个4分钟的过度通气步骤，以使P(ET,CO₂)朝与高碳酸血症期间相反的方向等量变化。在基线期以及每个CO₂ 阶跃变化期间同时采集动脉血和颈内静脉血样本。脑血管对CO₂ 的反应性以大脑中动脉血流速度（MCAv）每毫米汞柱P(a,CO₂)和P(jv,CO₂)变化的百分比来表示。在高碳酸血症期间（而非低碳酸血症期间），P(ET,CO₂)高估P(a,CO₂) 2.4±3.4 mmHg，并低估MCAv-CO₂ 反应性（P<0.05）。以P(jv,CO₂)为参照时，高碳酸血症和低碳酸血症时的MCAv-CO₂ 反应性更高（分别约为97%和约24%），高于以P(a,CO₂)为参照时（P<0.05）。高碳酸血症时MCAv-P(jv,CO₂)反应性与通气变化的增加呈负相关（R² = 0.43；P<0.05），这表明反应性降低会导致中枢CO₂ 清除减少和通气刺激增强。P(ET,CO₂)、P(a,CO₂)和P(jv,CO₂)与MCAv关系的差异对脑血管CO₂ 反应性的真实呈现和生理学解释具有重要意义。
