Comparison of two commercially available near-infrared spectroscopy instruments for cerebral oximetry - Technical note
Comparison of two commercially available near-infrared spectroscopy instruments for cerebral oximetry - Technical note
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DOI：
10.3171/jns.2000.93.2.0351
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发表时间：
2000-08-01
影响因子：
4.1
通讯作者：
Yonas, H
中科院分区：
文献类型：
--
作者：
Cho, H;Nemoto, EM;Yonas, H
比较了两个近红外光谱 (NIRS) 设备对五名健康志愿者因缺氧和高碳酸血症引起的脑血红蛋白氧合变化的反应。每个 NIRS 设备的传感器分别放置在志愿者前额的两侧。经美国食品和药物管理局批准的 INVOS3100A 设备可记录氧合血红蛋白 (HbO(2)) 饱和度的百分比，而研究中的 NIRO500 设备可记录参照任意基线的微摩尔浓度的 HbO(2)、脱氧血红蛋白和总血红蛋白的绝对变化。志愿者以随机顺序分别呼吸 7% CO2 的 O-2 和 10% O-2 的混合物 5 分钟。持续监测动脉血压、呼气末二氧化碳 (ETCO2)、动脉 O-2 饱和度和心电图数据。高碳酸血症使 ETCO2 从 42 +/- 2 增加到 56 +/- 3 mm Hg（平均值 +/- 标准差），导致检测到的脑 HbO(2) 饱和度增加 7.3 +/- 0.2% (p < 0.005) INVOS3100A 设备检测到 HbO(2) 增加 11.6 +/- 3 μM (p < 0.0008)，NIRO500 检测到 HbO(2) 增加 11.6 +/- 3 μM。缺氧使动脉 HbO(2) 饱和度从 98 +/- 1 降低到 87 +/- 3%，导致 INVOS3100A 设备检测到的 HbO(2) 饱和度百分比下降 5.1 +/- 1.2% (p < 0.01)，并且由 INVOS3100A 设备检测到的 HbO(2) 下降 9.7 +/- 6.3 μM NIRO500。NIRO500 和 INVOS3100A 仪器对高碳酸血症和缺氧引起的脑氧合变化的反应总体相似；然而，使用 NIRO500 设备记录时，反应往往更大，这可能是因为与 INVOS3100A 设备不同，NIRO500 无法纠正皮肤和骨骼污染。
Two near-infrared spectroscopy (NIRS) devices were compared with regard to their responses to changes in cerebral hemoglobin oxygenation induced by hypoxia and hypercapnia in five healthy volunteers.Sensors belonging to each NIRS device were placed on opposite sides of the volunteer's forehead. The INVOS3100A device, approved by the United States Food and Drug Administration, records the percentage of oxyhemoglobin (HbO(2)) saturation and the investigational NIRO500 device records absolute changes in HbO(2), deoxyhemoglobin, and total hemoglobin in micromolar concentrations referenced to an arbitrary baseline. The volunteers breathed separate mixtures of 7% CO2 in O-2 and 10% O-2 for 5 minutes in random order. Arterial blood pressure, end-tidal CO2 (ETCO2), arterial O-2 saturation, and electrocardiographic data were continuously monitored.Hypercapnia increased (p < 0.01) ETCO2 from 42 +/- 2 to 56 +/- 3 mm Hg (mean +/- standard deviation), resulting in a 7.3 +/- 0.2% increase (p < 0.005) in cerebral HbO(2) saturation detected by the INVOS3100A device and an 11.6 +/- 3 mu M increase (p < 0.0008) in HbO(2) detected by the NIRO500. Hypoxia decreased (p < 0.01) arterial HbO(2) saturation from 98 +/- 1 to 87 +/- 3%, causing a 5.1 +/- 1.2% decrease (p < 0.01) in the percentage of HbO(2) saturation detected by the INVOS3100A device and a 9.7 +/- 6.3 mu M decrease in HbO(2) detected by the NIRO500.The responses of the NIRO500 and the INVOS3100A instruments to changes in cerebral oxygenation resulting from hypercapnia and hypoxia were generally similar; however, responses tended to be greater when recorded by the NIRO500 device, perhaps because, unlike the INVOS3100A device, the NIRO500 does not correct for skin and bone contamination.