Respiratory physiology & neurobiology · 2012
Effects of clonidine on breathing during sleep and susceptibility to central apnoea.
СтатьяРандомизированное исследованиеПоддержка NIH: внешняя программаПоддержка правительства СШАНазвание и аннотация: Перевод в очереди
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Sankri-Tarbichi Abdul Ghani, Grullon Kevin, Badr M Safwan
Аннотация
UNLABELLED: We hypothesized that administration of clonidine would decrease the hypocapnic apnoeic threshold (HAT) and widen the CO(2) reserve during non-REM sleep.
METHODS: Ten healthy subjects (4 females) (age 22.3 ± 3.0 years; BMI 25.5 ± 3.4 kg/m(2)) were randomized to receive placebo or 0.1 mg/45 kg of clonidine on 2 separate nights. Ventilation and upper airway resistance were monitored during wakefulness and sleep. Two separate experiments were performed: Protocol 1 (n=8), CO(2) reserve, HAT and HcVR were determined using non-invasive hyperventilation (NIV) to induce hypocapnia for at least 3 min; Protocol 2 (n=6), peripheral hypocapnic ventilatory response (HcVR) was determined by NIV using short (3 breaths) hyperventilation.
RESULTS: Clonidine decreased the systolic blood pressure by 12 ± 10 mmHg but did not affect baseline ventilation or upper airway resistance during wakefulness or sleep. Protocol (1), clonidine was associated with decreased HAT relative to placebo (37.3 ± 3.3 mmHg vs. 39.7 ± 3.4 mmHg, P<0.05), increased CO(2) reserve (-3.8 ± 1.3 mmHg vs. -2.8 ± 1.2 mmHg, P<0.05), and decreased HcVR (1.6 ± 0.6 L/min/mmHg vs. 2.5 ± 1.3 L/min/mmHg, P<0.05). Protocol (2), administration of clonidine did not decrease peripheral HcVR compared to placebo (0.5 ± 0.3 L/min/mmHg vs. 0.7 ± 0.3 L/min/mmHg, P=NS).
CONCLUSION: Clonidine is associated with diminished susceptibility to hypocapnic central apnoea without significant effect on ventilation or upper airway mechanics. Reduced susceptibility to hypocapnic central apnoea is not explained by the peripheral chemoreceptor pathway. This suggests a central rather than a peripheral effect of clonidine on the susceptibility to hypocapnic central apnoea.
METHODS: Ten healthy subjects (4 females) (age 22.3 ± 3.0 years; BMI 25.5 ± 3.4 kg/m(2)) were randomized to receive placebo or 0.1 mg/45 kg of clonidine on 2 separate nights. Ventilation and upper airway resistance were monitored during wakefulness and sleep. Two separate experiments were performed: Protocol 1 (n=8), CO(2) reserve, HAT and HcVR were determined using non-invasive hyperventilation (NIV) to induce hypocapnia for at least 3 min; Protocol 2 (n=6), peripheral hypocapnic ventilatory response (HcVR) was determined by NIV using short (3 breaths) hyperventilation.
RESULTS: Clonidine decreased the systolic blood pressure by 12 ± 10 mmHg but did not affect baseline ventilation or upper airway resistance during wakefulness or sleep. Protocol (1), clonidine was associated with decreased HAT relative to placebo (37.3 ± 3.3 mmHg vs. 39.7 ± 3.4 mmHg, P<0.05), increased CO(2) reserve (-3.8 ± 1.3 mmHg vs. -2.8 ± 1.2 mmHg, P<0.05), and decreased HcVR (1.6 ± 0.6 L/min/mmHg vs. 2.5 ± 1.3 L/min/mmHg, P<0.05). Protocol (2), administration of clonidine did not decrease peripheral HcVR compared to placebo (0.5 ± 0.3 L/min/mmHg vs. 0.7 ± 0.3 L/min/mmHg, P=NS).
CONCLUSION: Clonidine is associated with diminished susceptibility to hypocapnic central apnoea without significant effect on ventilation or upper airway mechanics. Reduced susceptibility to hypocapnic central apnoea is not explained by the peripheral chemoreceptor pathway. This suggests a central rather than a peripheral effect of clonidine on the susceptibility to hypocapnic central apnoea.