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  • Title: Activity of upper airway muscles during augmented breaths.
    Author: Van Lunteren E, Van de Graaff WB, Parker DM, Strohl KP, Mitra J, Salamone J, Cherniack NS.
    Journal: Respir Physiol; 1983 Jul; 53(1):87-98. PubMed ID: 6622866.
    Abstract:
    The effect of augmented breaths on the electrical activity of upper airway (UAW) muscles was studied in fourteen spontaneously breathing anesthetized dogs. Moving average traces of the electrical activity recorded from the genioglossus (GG), the posterior cricoarytenoid (PCA), and the alar portion of the nasalis muscle (AN) were compared to tracings of diaphragm electrical activity. During augmented breaths the electrical activity of the diaphragm showed the characteristic biphasic pattern previously described: an initial phase following the contour of a normal breath (phase I) and an augmented phase arising near the crest of the initial phase (phase II). During all augmented breaths, the GG, PCA and AN showed the same biphasic pattern as the diaphragm. The normally rounded shape of UAW muscle EMG activity during control breaths changed to a more sharply peaked form during the second phase of the augmented breath. Onset of activity of all UAW muscles studied preceded that of the diaphragm; during control breaths, the average interval was 0.29 sec for the PCA, 0.25 sec for the GG and 0.14 sec for the AN (P less than 0.05). The amount of pre-activation was decreased to less than 0.10 sec during the second phase of the augmented breath. The slopes and amplitudes of phase I were similar to that of control breaths. The peak EMG activity of the augmented breath was 214% of the control breaths for the diaphragm, 247% for the GG, 168% for the AN and 161% for the PCA (P less than 0.005 for GG, P less than 0.001 for the others). During hyperoxic hypercapnia the slopes and amplitudes of phase II remained nearly constant for all four muscles, whereas the slopes and amplitudes of phase I changed with the chemical drive just as in control breaths. UAW resistance, recorded in five additional spontaneously breathing anesthetized dogs, was 32% less during inspiration than expiration during control breaths, and 31% less during phase I of augmented breaths; there was a further 18% decrease during phase II of augmented breaths (P less than 0.001). The results suggest that mechanisms responsible for augmented breaths act similarly on upper airway muscles and the diaphragm.
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