Eriksson L I, Sato M, Severinghaus J W
Department of Anesthesiology, University Hospital, Linköping, Sweden.
Anesthesiology. 1993 Apr;78(4):693-9. doi: 10.1097/00000542-199304000-00012.
A previous study has demonstrated a decrease in the hypoxic ventilatory response in volunteers partially paralyzed with vecuronium. However, in this study, hypocapnia was allowed to occur. Because hypocapnia counteracts the ventilatory response to hypoxia during partial vecuronium-induced neuromuscular block and isocapnia, the hypoxic ventilatory response (HVR) was tested in 10 awake volunteers.
To avoid hypocapnia, the resting hyperoxic control end-tidal PCO2 was increased to 43.3 +/- 2.4 mmHg, raising inspiratory minute ventilation (VI) to 140 ml.kg-1.min-1. Hypoxic ventilatory response (delta VI/delta SpO2, L.min-1.%-1) was measured during a 5-min isocapnic step reduction to a mean arterial hemoglobin oxygen saturation (SpO2) of 84.8 +/- 1.4%. Immediately thereafter, hypercapnic ventilatory response (HCVR; delta VI/delta PETCO2, L.min-1.mmHg-1) was determined at the end of a 6-min step increase of PETCO2 to 50.5 +/- 2.7 mmHg. During a subsequent 30-40-min pause, an intravenous infusion of vecuronium was adjusted to reduce the adductor pollicis train-of-four ratio to 0.70, as monitored using mechanomyography. Ventilatory parameters, HVR and HCVR, were then redetermined.
Resting VI, PETCO2, and SpO2 were unchanged by drug infusion. Hypoxic ventilatory response decreased from control (a) of 0.97 +/- 0.43 to 0.74 +/- 0.41 L.min-1.%-1 (P < 0.02) during drug infusion (b), while HCVR was unchanged (a = 1.91 +/- 0.82, b = 1.62 +/- 0.46 L.min-1.mmHg-1; NS). To correct HVR for possible vecuronium-induced respiratory muscle weakness or otherwise altered central nervous system reactivity, the drug/control ratio (HVRb/a) was divided by the associated HCVRb/a ratio. This HVR index, FHVR, was 0.84 +/- 0.12 (P < 0.01).
We conclude that a vecuronium-induced partial neuromuscular block impairs HVR more than it does HCVR in humans, suggesting an effect of vecuronium on carotid body hypoxic chemosensitivity.
先前的一项研究表明,在使用维库溴铵导致部分麻痹的志愿者中,低氧通气反应有所降低。然而,在该研究中,出现了低碳酸血症。由于在维库溴铵诱导的部分神经肌肉阻滞和等碳酸血症期间,低碳酸血症会抵消对低氧的通气反应,因此对10名清醒志愿者的低氧通气反应(HVR)进行了测试。
为避免低碳酸血症,将静息高氧对照呼气末PCO2提高至43.3±2.4 mmHg,使吸气分钟通气量(VI)增加至140 ml·kg-1·min-1。在等碳酸血症状态下5分钟内逐步将平均动脉血红蛋白氧饱和度(SpO2)降至84.8±1.4%的过程中,测量低氧通气反应(δVI/δSpO2,L·min-1·%-1)。此后立即在PETCO2逐步增加6分钟至50.5±2.7 mmHg结束时,测定高碳酸通气反应(HCVR;δVI/δPETCO2,L·min-1·mmHg-1)。在随后30 - 40分钟的暂停期间,调整维库溴铵静脉输注量,以使拇内收肌四个成串刺激比值降至0.70,采用肌机械图进行监测。然后重新测定通气参数、HVR和HCVR。
药物输注后静息VI、PETCO2和SpO2未发生变化。药物输注期间,低氧通气反应从对照值(a)的0.97±0.43降至0.74±0.41 L·min-1·%-1(P<0.02),而HCVR未改变(a = 1.91±0.82,b = 1.62±0.46 L·min-1·mmHg-1;无显著差异)。为校正维库溴铵可能引起的呼吸肌无力或其他中枢神经系统反应性改变对HVR的影响,将药物/对照比值(HVRb/a)除以相关的HCVRb/a比值。该HVR指数,即FHVR,为0.84±0.12(P<0.01)。
我们得出结论,在人类中,维库溴铵诱导的部分神经肌肉阻滞对HVR的损害大于对HCVR的损害,提示维库溴铵对颈动脉体低氧化学敏感性有影响。