Hunt C E, Hazinski T A, Gora P
Pediatr Res. 1982 Jan;16(1):79-81. doi: 10.1203/00006450-198201001-00016.
The effect of chloral hydrate (CH)-induced sleep on inspiratory drive has not been systematically assessed. To determine the effects of CH on the ventilatory responses to hypercarbia and to hypoxia, nine unanesthetized adult rabbit with chronic tracheostomy were studied. We compared awake ventilatory measurements before CH to non-REM sleep assessments at 30, 60, 90, and 120 min after administration of 250 mg/kg of CH. There were no significant differences between any of these assessment intervals for respiratory rate, PACO2, PAO2, tidal volume (VT), minute volume, Ti/Ttot, or VT/Ti. Hypercarbic ventilatory response to slopes were not diminished at any of the CH-sleep intervals compared to the awake mean slope. In addition, the ventilatory response to hypoxia at PAO2=70 mm Hg (V70) and the hypoxic response slope demonstrated no significant decrease at any of the CH-sleep intervals. In summary, absence of any significant decrease in either hypercarbic or hypoxic ventilatory response after CH administration indicates absence of any CH effect on chemical inspiratory drive.
水合氯醛(CH)诱导的睡眠对吸气驱动的影响尚未得到系统评估。为了确定CH对高碳酸血症和低氧通气反应的影响,我们对9只患有慢性气管造口术的未麻醉成年兔进行了研究。我们比较了给予250mg/kg CH之前的清醒通气测量值与给药后30、60、90和120分钟时的非快速眼动睡眠评估值。在这些评估间隔中的任何一个时间点,呼吸频率、动脉血二氧化碳分压(PACO2)、动脉血氧分压(PAO2)、潮气量(VT)、分钟通气量、吸气时间/总呼吸时间(Ti/Ttot)或潮气量/吸气时间(VT/Ti)均无显著差异。与清醒时的平均斜率相比,在任何CH睡眠间隔期间,对高碳酸血症的通气反应斜率均未降低。此外,在PAO2 = 70 mmHg时对低氧的通气反应(V70)以及低氧反应斜率在任何CH睡眠间隔期间均无显著下降。总之,给予CH后高碳酸血症或低氧通气反应均无显著下降,这表明CH对化学性吸气驱动没有任何影响。