Heman-Ackah Y D, Goding G S
Department of Otolaryngology-Head and Neck Surgery, University of Minnesota, Hennepin County Medical Center, Minneapolis 55455, USA.
Ann Otol Rhinol Laryngol. 2000 Oct;109(10 Pt 1):921-8. doi: 10.1177/000348940010901005.
Sudden infant death syndrome is the leading cause of death in infants in the United States. The laryngeal chemoreflex (LCR) is thought to contribute to its pathogenesis. In adult animals, increasing levels of intralaryngeal CO2 result in a decrease in ventilatory activity. Intravenous acetazolamide (AZ) abolishes this response. The purpose of this study was to determine the effects of intralaryngeal CO2 and AZ on the LCR and respiratory physiology of piglets under normoxic and hypoxic conditions. We applied 0% or 10% CO2 in a randomized order to the larynx of 26 piglets. Intubation via tracheotomy prevented inhalation of the gas mixtures. Laryngeal stimulation was performed under normoxic conditions (PaO2 of >70 mm Hg) in 15 animals and under hypoxic conditions (PaO2 of 50 to 65 mm Hg) in 11 animals both with and without intravenous AZ (5 mg/kg). Respiratory and cardiovascular response data were recorded. Ten percent intralaryngeal CO2 has no significant effect on mean baseline respiratory rate, systemic PaCO2 or PaO2 levels, or apnea duration (p > .05). The use of AZ (versus no AZ) resulted in significantly higher baseline respiratory rates (64 versus 51 breaths per minute; p = .016), a decreased baseline systemic PaCO2 level (38.8 versus 45.9 mm Hg; p < .001), a higher baseline PaO2 level (97.9 versus 82.8 mm Hg; p < .001), shorter mean apnea durations (15.5 versus 24.8 seconds; p = .001), a higher lowest O2 saturation level after the stimulus (78.0% versus 68.4%; p = .003), and fewer profound apneas (10 of 90 versus 41 of 90 trials; p < .001). We conclude that 10% intralaryngeal CO2 does not decrease ventilatory activity in piglets and has no significant effect on the LCR. Acetazolamide, however, appears to have a protective effect against the LCR, resulting in shorter and less severe apneas. The protective effect of AZ against the LCR appears to be related to its ability to stimulate the respiratory drive and increase oxygenation at baseline.
婴儿猝死综合征是美国婴儿死亡的主要原因。喉化学反射（LCR）被认为与其发病机制有关。在成年动物中，喉内二氧化碳水平升高会导致通气活动减少。静脉注射乙酰唑胺（AZ）可消除这种反应。本研究的目的是确定在常氧和低氧条件下，喉内二氧化碳和AZ对仔猪LCR和呼吸生理学的影响。我们以随机顺序向26头仔猪的喉部施加0%或10%的二氧化碳。通过气管切开插管可防止吸入混合气体。在15只动物的常氧条件下（动脉血氧分压>70 mmHg）和11只动物的低氧条件下（动脉血氧分压50至65 mmHg）进行喉部刺激，两组均使用或不使用静脉注射AZ（5 mg/kg）。记录呼吸和心血管反应数据。10%的喉内二氧化碳对平均基线呼吸频率、全身动脉血二氧化碳分压或动脉血氧分压水平以及呼吸暂停持续时间均无显著影响（p>.05）。使用AZ（与未使用AZ相比）导致基线呼吸频率显著升高（每分钟64次与51次呼吸；p = .016），基线全身动脉血二氧化碳分压水平降低（38.8 mmHg与45.9 mmHg；p<.001），基线动脉血氧分压水平升高（97.9 mmHg与82.8 mmHg；p<.001），平均呼吸暂停持续时间缩短（15.5秒与24.8秒；p = .001），刺激后最低血氧饱和度水平升高（78.0%与68.4%；p = .003），深度呼吸暂停次数减少（90次试验中10次与90次试验中41次；p<.001）。我们得出结论，10%的喉内二氧化碳不会降低仔猪的通气活动，对LCR也无显著影响。然而，乙酰唑胺似乎对LCR有保护作用，可导致呼吸暂停时间缩短且严重程度减轻。AZ对LCR的保护作用似乎与其刺激呼吸驱动和在基线时增加氧合的能力有关。
