Effects of pulmonary stretch receptor blockade on laryngeal responses to hypercapnia and hypoxia.
Electromyographic patterns of the diaphragm and a posterior cricoarytenoid (PCA) muscle were evaluated in anesthetized rabbits with and without reversible blockade of pulmonary stretch receptors by inhalation of 200 ppm sulfur dioxide (SO2). Inspiratory activity of both muscles was increased by hypercapnia and by isocapnic hypoxia, with or without receptor blockade. Expiratory diaphragmatic activity was diminished by these stimuli and was likewise not qualitatively affected by SO2 exposure. Expiratory PCA activity was increased by hypercapnia and hypoxia prior to SO2 exposure, but decreased by these stimuli during stretch receptor blockade. These results are consistent with the previous finding that vagal afferents facilitate expiratory PCA activity, thus maintaining a patent laryngeal airway, even in the face of increased carotid chemoreceptor afferents, which inhibit expiratory activity of the PCA muscle. The results further indicate that some or all of the afferents responsible for this effect are from pulmonary stretch receptors.[1]References
- Effects of pulmonary stretch receptor blockade on laryngeal responses to hypercapnia and hypoxia. Bartlett, D., Knuth, S.L., Knuth, K.V. Respiration physiology. (1981) [Pubmed]
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