title: Effects of intralaryngeal carbon dioxide and acetazolamide on the laryngeal chemoreflex.
abstract: 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.
authors.affiliation: Department of Otolaryngology-Head and Neck Surgery, University of Minnesota, Hennepin County Medical Center, Minneapolis 55455, USA.
authors.forename: Y D
authors.initials: YD
authors.lastname: Heman-Ackah
authors.forename: G S
authors.initials: GS
authors.lastname: Goding
mesh_terms: D000086:Acetazolamide / Q000494:pharmacology*; D000328:Adult; D000818:Animals; D000831:Animals, Newborn; D002245:Carbon Dioxide / Q000097:blood / Q000494:pharmacology*; D002257:Carbonic Anhydrase Inhibitors / Q000494:pharmacology*; D002628:Chemoreceptor Cells / Q000187:drug effects* / Q000502:physiology; D006801:Humans; D007223:Infant; D007823:Laryngeal Nerves / Q000187:drug effects* / Q000503:physiopathology; D010100:Oxygen / Q000097:blood; D012123:Pulmonary Ventilation / Q000187:drug effects / Q000502:physiology; D012018:Reflex / Q000187:drug effects* / Q000502:physiology; D013398:Sudden Infant Death / Q000097:blood / Q000209:etiology; D013552:Swine
chemical_list: D002257:Carbonic Anhydrase Inhibitors; D002245:Carbon Dioxide; D000086:Acetazolamide; D010100:Oxygen