Heffernan Matthew J, Muller Matthew D
Pennsylvania State University College of Medicine, Penn State Hershey Heart and Vascular Institute, Hershey, Pennsylvania.
Physiol Rep. 2014 Oct 24;2(10). doi: 10.14814/phy2.12181. Print 2014 Oct 1.
Voluntary apnea activates the central and peripheral chemoreceptors, leading to a rise in sympathetic nerve activity and limb vasoconstriction (i.e., brachial blood flow velocity and forearm cutaneous vascular conductance decrease to a similar extent). Whether peripheral and/or central chemoreceptors contribute to the cutaneous vasoconstrictor response remains unknown. We performed three separate experiments in healthy young men to test the following three hypotheses. First, inhibition of peripheral chemoreceptors with brief hyperoxia inhalation (100% O2) would attenuate the cutaneous vasoconstrictor response to voluntary apnea. Second, activation of the peripheral chemoreceptors with 5 min of hypoxia (10% O2, 90% N2) would augment the cutaneous vasoconstrictor response to voluntary apnea. Third, activation of the central chemoreceptors with 5 min of hypercapnia (7% CO2, 30% O2, 63% N2) would have no influence on cutaneous responses to voluntary apnea. Studies were performed in the supine posture with skin temperature maintained at thermoneutral levels. Beat-by-beat blood pressure, heart rate, brachial blood flow velocity, and cutaneous vascular conductance were measured and changes from baseline were compared between treatments. Relative to room air, hyperoxia attenuated the vasoconstrictor response to voluntary apnea in both muscle (-16 ± 10 vs. -40 ± 12%, P = 0.023) and skin (-14 ± 6 vs. -24 ± 5%, P = 0.033). Neither hypoxia nor hypercapnia had significant effects on cutaneous responses to apnea. These data indicate that skin blood flow is controlled by the peripheral chemoreceptors but not the central chemoreceptors.
自主呼吸暂停会激活中枢和外周化学感受器，导致交感神经活动增强和肢体血管收缩（即肱血流速度和前臂皮肤血管传导率在相似程度上降低）。外周和/或中枢化学感受器是否参与皮肤血管收缩反应尚不清楚。我们在健康年轻男性中进行了三项独立实验，以检验以下三个假设。第一，通过短暂吸入高氧（100%氧气）抑制外周化学感受器，将减弱自主呼吸暂停引起的皮肤血管收缩反应。第二，通过5分钟的低氧（10%氧气，90%氮气）激活外周化学感受器，将增强自主呼吸暂停引起的皮肤血管收缩反应。第三，通过5分钟的高碳酸血症（7%二氧化碳，30%氧气，63%氮气）激活中枢化学感受器，对自主呼吸暂停引起的皮肤反应没有影响。实验在仰卧姿势下进行，皮肤温度维持在热中性水平。逐搏测量血压、心率、肱血流速度和皮肤血管传导率，并比较各处理组相对于基线的变化。与室内空气相比，高氧减弱了肌肉（-16±10%对-40±12%，P = 0.023）和皮肤（-14±6%对-24±5%，P = 0.033）对自主呼吸暂停的血管收缩反应。低氧和高碳酸血症对呼吸暂停引起的皮肤反应均无显著影响。这些数据表明，皮肤血流受外周化学感受器而非中枢化学感受器控制。
