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Hydrogen Peroxide in the Lung Parenchyma Stimulates Vagally Mediated Phrenic Activity^*

Galia K. Soukhova, PhD; Muhammad Ahmed, MD; Eugene C. Fletcher, MD, FCCP and Jerry Yu, MD, PhD

^* From the Pulmonary Division, Department of Medicine, University of Louisville, Louisville, KY. Currently at the Pediatric Medical Academy of Russia, St. Petersburg, Russia.

Correspondence to: Jerry Yu, MD, PhD, Pulmonary Division, Department of Medicine, University of Louisville, ACB-3, 530 S Jackson St, Louisville, KY 40292; e-mail: j0yu0001{at}gwise.louisville.edu

Study objective: To elucidate the mechanism of hyperpnea and tachypnea, which are the common findings in cardiopulmonary patients.

Rational: Recently, it was found that activating pulmonary afferents by directly injecting hypertonic saline solution into the lung periphery causes a vagally mediated neural hyperpnea and tachypnea, ie, the excitatory lung reflex. Since reactive oxygen species are released during a variety of pulmonary diseases, we examined whether hydrogen peroxide (H₂O₂), a common mediator in cardiopulmonary diseases, can initiate the same excitatory lung reflex.

Measurements and results: We recorded phrenic efferent activity in anesthetized, open chest, artificially ventilated rabbits as an index of respiratory drive and examined the respiratory responses to injections of H₂O₂ (10 µmol in 0.1 mL). The responses were compared with those to hypertonic saline solution (8.1%, 0.1 mL). H₂O₂ and hypertonic saline solution increased both the rate (mean [± SEM], 43 ± 8% and 61 ± 10%, respectively; n = 30; p = 0.001) and the amplitude of phrenic bursts (12 ± 2% and 20 ± 4%, respectively; n = 30; p = 0.033). These responses were abolished by bilateral vagotomy.

Conclusion: H₂O₂ can initiate the excitatory lung reflex. Therefore, mediator(s) released in pulmonary diseases could be one of the mechanisms causing hyperpnea and tachypnea.

Key Words: breathing control • pulmonary receptors • reflex • vagus nerve

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