Chemical control of laryngeal vascular resistance in anesthetized dogs

The branch of the cranial superior thyroid artery that supplies the larynx was perfused unilaterally at a constant flow rate in dogs anesthetized with pentobarbitone sodium (30 mg.kg-1, i.v.). Laryngeal vascular resistance (RLv) was calculated. Intraluminal laryngeal pressure (PL) was determined. Asphyxia caused a diminution in PL (-27.7 +/- 4.2%) (p < 0.01) and an initial decrease followed by an increase in RLv (-10.9 +/- 2.3% and +12.8 + 2.8%) (p < 0.001). Following vagotomy, asphyxia decreased PL (-17.1 +/- 4.2%) and increased RLv (+45.5 +/- 11.0%). Systemic hypoxia induced by breathing 8% O2-N2 increased RLv (+8.4 +/- 1.3%) (p < 0.001) and decreased PL (-24.9 +/- 3.7%) (p < 0.001). In chemodenervated dogs, the response of PL to hypoxia was abolished while that of RLv was similar to that in intact animals. Breathing of 7% CO2 in air caused an increase in RLv (+6.1 +/- 1.6%) (p < 0.001) and a decrease in PL (-20.9 +/- 3.2%) (p < 0.001). Following chemodenervation, hypercapnia still increased RLv (+11.3 +/- 3.2%) (p < 0.01) and diminished PL (-29.9 +/- 2.5%). Bilateral vagotomy reduced the response of PL to hypercapnia (-13.3 +/- 6.9%) (p < 0.05). Local intra-arterial injection of KCN produced an increase in RLv and PL (+7.0 +/- 1.2%, +9.0 +/- 1.0%). After peripheral chemodenervation KCN injection slightly increased PL (+2.0 +/- 0.9%). The response of RLv was almost abolished. In conclusion, laryngeal vasoconstriction in response to systemic hypoxia after chemodenervation is probably mediated by increased sympathetic discharge to the larynx due to hypoxia of the CNS. Laryngeal responses to hypercapnia may be due to the action of central chemoreceptors.