Sedative Doses of Midazolam Depress Hypoxic Ventilatory Responses in Humans
Sedative Doses of Midazolam Depress Hypoxic Ventilatory Responses in Humans
复制标题
镇静剂量的咪达唑仑可抑制人类缺氧通气反应
DOI：
10.1213/00000539-198804000-00016
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发表时间：
1988
影响因子：
5.7
通讯作者：
J. Gross
中科院分区：
文献类型：
--
作者：
C. M. Alexander;J. Gross
在等二氧化碳再呼吸期间检查了咪达唑仑对八名健康志愿者的缺氧通气反应的影响。 IV 0.1 mg/kg 咪达唑仑后，缺氧通气反应斜率（&OV0312;E vs SaO2）从 1.48 ± 0.24 降至 0.70 ± 0.13 L·min−1 ± %SaO2−1 (&OV0398; ± SE, P < 0.005)。动脉饱和度为 90% 时计算的通气量也从 28.6 ± 4.4 下降至 19.9 ± 2.7 L/min (P < 0.05)。在使用咪达唑仑之前，缺氧至 SaO2 为 75 ± 2% 时，心率会增加 23 ± 3 次/分钟；服用咪达唑仑后，缺氧时心率增加仅为 4 ± 2 次/分钟（P < 0.003）。此外，一项双盲交叉研究评估了毒扁豆碱对咪达唑仑后意识和缺氧通气反应的影响。尽管毒扁豆碱显着提高了意识，但静脉注射毒扁豆碱 2.0 mg 后的缺氧反应斜率变化（增加 0.28 ± 0.34 L-min−1 ± %SaO2−1）与安慰剂后（增加 0.03 ± 0.22 L-min−1 ± %SaO2−1）没有显着差异。结论是镇静剂量的咪达唑仑可抑制缺氧通气反应并减轻与低氧血症相关的呼吸过度和心动过速。此外，毒扁豆碱-格隆溴铵逆转咪达唑仑诱导的镇静作用与恶心（五名受试者）、呕吐（三名受试者）和心动过速相关，但不会逆转抑制的缺氧通气反应。
The effect of midazolam on the hypoxic ventilatory response of eight healthy volunteers was examined during isocapnic rebreathing. The magnitude of the slope of the ventilatory response to hypoxia (&OV0312;E vs SaO2) decreased from 1.48 ± 0.24 to 0.70 ± 0.13 L·min−1 ± %SaO2−1 (&OV0398; ± SE, P < 0.005) after midazolam 0.1 mg/kg IV. The calculated ventilation at an arterial saturation of 90% also decreased from 28.6 ± 4.4 to 19.9 ± 2.7 L/min (P < 0.05). Before midazolam, hypoxia to an SaO2 of 75 ± 2% was associated with a 23 ± 3 beatslmin increase in heart rate; after midazolam, the increase in heart rate with hypoxia was only 4 ± 2 beatslmin (P < 0.003). Additionally, a double-blind crossover study evaluated the effect of phy-sostigmine on awareness and hypoxic ventilatory response after midazolam. The change in hypoxic response slope after physostigmine 2.0 mg IV (an increase of 0.28 ± 0.34 L-min−1 ± %SaO2−1) did not differ significantly from that after placebo (an increase of 0.03 ± 0.22 L-min−1 ± %SaO2−1), although physostigmine significantly increased awareness. It is concluded that a sedative dose of midazolam depresses hypoxic ventilatory response and attenuates the hyperpnea andtachycardia associated with hypoxemia. Furthermore, physostigmine-glycopyrrolate reversal of midazolam-induced sedation was associated with nausea (five subjects), vomiting (three subjects), and tachycardia without reversal of the depressed hypoxic ventilatory response.