Glossopharyngeal nerve makes greater contribution than hypoglossal nerve to respiratory phasic changes in Pcrit

Abstract

Neuromechanical control of pharyngeal airway (PA) patency involves many muscles. The relative contributions of these PA muscles and nerves are unclear although dilators (especially genioglossus, GG) and hypoglossal nerve (XII) received most attention. Our recent study showed a markedly lower Pcrit (PA critical pressure, an index of PA collapsibility) during inspiration (I) vs. expiration (E), inversely correlated with GG activity. The phasic change in Pcrit (PCP) was unaltered by superior laryngeal nerve cut but eliminated by paralysis. This study tested the relative role in PCP of GG innervated by the medial branch of XII (mXII) and other PA muscles innervated by XII and/or glossopharyngeal nerve (IX). Adult male Sprague-Dawley rats were anesthetized, vagotomized and ventilated. PA collapse was achieved by quickly delivering a negative pressure to a tracheal cannula. Pcrit was measured in E and peak I, before and after transecting mXII, XII and/or IX. Baseline Pcrit was lower in I (−25±3 cmH2O) vs. E (−19±2). PCP (7±3) was unaltered (99±3% remained) by mXII cut, but was reduced (77±8% remained) by XII cut and eliminated (−1±5%) by additional IX cut, In another group, PCP was greatly reduced by IX cut (30±2% remained) and abolished by additional XII cut (−4±0.4%). E-Pcrit was barely altered by mXII cut but somewhat decreased by XII and/or IX cut. These data suggest that in anesthetized rats: GG (also geniohyoid) plays little role in PCP, the IX-mediated PA muscles’ activity accounts for ~70% of PCP, while the XII-mediated portion only accounts for ~30%, and the bulk of, if not all, neuromuscular mechanisms underlying PCP are mediated via IX plus XII. (Supported by NIH HL64912)