CEREBRAL OXYGEN AVAILABILITY BY NIR SPECTROSCOPY DURING TRANSIENT HYPOXIA IN HUMANS
CEREBRAL OXYGEN AVAILABILITY BY NIR SPECTROSCOPY DURING TRANSIENT HYPOXIA IN HUMANS
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DOI：
10.1152/jappl.1990.69.3.907
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发表时间：
1990-09-01
影响因子：
3.3
通讯作者：
PIANTADOSI, CA
中科院分区：
文献类型：
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作者：
HAMPSON, NB;CAMPORESI, EM;PIANTADOSI, CA
应用近红外光谱技术研究了轻度缺氧对8名健康志愿者脑氧合血红蛋白、细胞色素a、a3氧化还原状态和脑血容量的影响。在正常碳酸血症[潮气末PCO 2（PETCO 2）36.9 ±. 2.6至34.9 .+-。3.4 Torr]或低碳酸血症（PETCO 2，32.8 ±. 0.6至23.7 .+-。0.6 Torr）通过8分钟再呼吸技术和调节吸入的CO2。正常碳酸性缺氧的特征是动脉PO 2的进行性降低（PaO 2，89.1 . ±. 3.5至34.1 .+-。0.1 TOrr），PETCO 2、动脉PCO 2（PaCO 2）和动脉pH稳定，并导致心率（35%）、收缩压（14%）和每分钟通气量（5倍）增加。低碳酸血症缺氧导致动脉血氧分压（PaO 2）降低（100.2 ± 0.01）。3.6至28.9 .+-。1.9 Torr），PaCO 2逐渐降低（39.0 ±. 1.6至27.3 .+-。1.9 Torr），以及动脉pH值的增加（7.41 ± 0.01）。0.02至7.53 ±。0.03）、心率（61%）和通气量（3倍）。在脑中，缺氧导致脑氧合血红蛋白含量的稳定下降和氧化细胞色素a，a3的减少。相对于正常碳酸性缺氧，在低碳酸性缺氧期间，对于氧合血红蛋白的给定降低，氧化细胞色素a，a3发生显著更大的损失。低氧时的总血容量反应也被低碳酸血症显著减弱，因为血容量的增加只有正常碳酸血症受试者的一半。我们的结论是，细胞色素a，a3氧化水平在体内降低在轻度缺氧PaCO 2是一个重要的决定因素，脑氧合，因为它调节呼吸，心血管和脑氧传递反应缺氧。
The effects of mild hypoxia on brain oxyhemoglobin, cytochrome a,a3 redox status, and cerebral blood volume were studied using near-infrared spectroscopy in eight healthy volunteers. Incremental hypoxia reaching 70% arterial O2 saturation was produced in normocapnia [end-tidal PCO2 (PETCO2) 36.9 .+-. 2.6 to 34.9 .+-. 3.4 Torr] or hypocapnia (PETCO2, 32.8 .+-. 0.6 to 23.7 .+-. 0.6 Torr) by an 8-min rebreathing technique technique and regulation of inspired CO2. Normocapnic hypoxia was characterized by progressive reductions in arterial PO2 (PaO2, 89.1 .+-. 3.5 to 34.1 .+-. 0.1 TOrr) with stable PETCO2, arterial PCO2(PaCO2), and arterial pH and resulted in increases in heart rate (35%) systolic blood pressure (14%), and minute ventilation (5-fold). Hypocapnic hypoxia resulted in progessively decreasing PaO2 (100.2 .+-. 3.6 to 28.9 .+-. 1.9 Torr), with progressive reduction in PaCO2 (39.0 .+-. 1.6 to 27.3 .+-. 1.9 Torr), and an increase in arterial pH (7.41 .+-. 0.02 to 7.53 .+-. 0.03), heart rate (61%), and ventilation (3-fold). In the brain, hypoxia resulted in a steady decline of cerebral oxyhemoglobin content and a decrease in oxidized cytochrome a,a3. Significantly greater loss of oxidized cytochrome a,a3 occurred for a given decrease in oxyhemoglobin during hypocapnic hypoxia relative to normocapnic hypoxia. Total blood volume response during hypoxia also was significantly attenuated by hypocapnia, because the increase in volume was only half that of normocapnic subjects. We conclude that cytochrome a,a3 oxidation level in vivo decreases at mild levels of hypoxia PaCO2 is an important determinant of brain oxygenation, because it modulates ventilatory, cardiovascular, and cerebral O2 delivery responses to hypoxia.