Journal of applied physiology
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Randomized Controlled Trial
The effect of increased genioglossus activity and end-expiratory lung volume on pharyngeal collapse.
Increasing either genioglossus muscle activity (GG) or end-expiratory lung volume (EELV) improves airway patency but not sufficiently for adequate treatment of obstructive sleep apnea (OSA) in most patients. The mechanisms by which these variables alter airway collapsibility likely differ, with increased GG causing airway dilation, whereas increased EELV may stiffen the airway walls through caudal traction. We sought to determine whether the airway stabilizing effect of GG activation is enhanced when EELV is increased. ⋯ The slope of the P(CRIT) curves remained unchanged in all conditions (P = 0.05). However, the CPAP level at which flow limitation developed was lower in both increased EELV conditions (P = 0.001). These findings indicate that while both increased GG and EELV improve airway collapsibility, the combination of both variables has little additional effect over increasing EELV alone.
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C(2) spinal hemisection (C2HS) interrupts ipsilateral bulbospinal pathways and induces compensatory increases in contralateral spinal and possibly supraspinal respiratory output. Our first purpose was to test the hypothesis that after C2HS contralateral respiratory motor outputs become resistant to vagal inhibitory inputs associated with lung inflation. Bilateral phrenic and contralateral hypoglossal (XII) neurograms were recorded in anesthetized and ventilated rats. ⋯ Bilateral vagotomy greatly enhanced ipsilateral phrenic bursting, which was either weak or absent in vagal-intact rats at both 2 and 8 wk post-C2HS. We conclude that 1) compensatory increases in contralateral phrenic and XII output after C2HS blunt the inhibitory influence of vagal afferents during lung inflation and 2) vagal afferents robustly inhibit ipsilateral phrenic bursting. These vagotomy data appear to explain the variability in the literature regarding the onset of the spontaneous crossed phrenic phenomenon in spontaneously breathing (vagal intact) vs. ventilated (vagotomized) preparations.
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Ventilatory long-term facilitation (vLTF) is a form of respiratory plasticity induced by acute intermittent hypoxia (AIH). Although vLTF has been reported in unanesthetized animals, little is known concerning the effects of vigilance state on vLTF expression. We hypothesized that AIH-induced vLTF is preferentially expressed in sleeping vs. awake male Lewis rats. ⋯ In association, Ve/Vco(2) (36 + or - 2%), tidal volume (14 + or - 2%), and frequency (7 + or - 2%) were increased 30-60 min post-AIH during d-NREM sleep. vLTF was significant but less robust during l-NREM sleep, was minimal during QW, and was not observed following acute sustained hypoxia or sham protocols in any vigilance state. Thus, vLTF is state-dependent and pattern-sensitive in unanesthetized Lewis rats, with the greatest effects during d-NREM sleep. Although the physiological significance of vLTF is not clear, its greatest significance to ventilatory control is most likely during sleep.
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Immersion pulmonary edema (IPE) can occur in otherwise healthy swimmers and divers, likely because of stress failure of pulmonary capillaries secondary to increased pulmonary vascular pressures. Prior studies have revealed progressive increase in ventilation [minute ventilation (Ve)] during prolonged immersed exercise. We hypothesized that this increase occurs because of development of metabolic acidosis with concomitant rise in mean pulmonary artery pressure (MPAP) and that hyperoxia attenuates this increase. ⋯ Alveolar-arterial Po(2) difference increased from E to L in normoxia, consistent with increased lung water. We conclude that increased Ve at 1 ATA is not due to acidosis and is more consistent with respiratory muscle fatigue and that progressive pulmonary vascular hypertension does not occur during prolonged immersed exercise. Wide variation in MPAP among healthy subjects is consistent with variable individual susceptibility to IPE.
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Wrapping low-birth-weight neonates in a plastic bag prevents body heat loss. A bonnet can also be used, since large amounts of heat can be lost from the head region, but may provide too much thermal insulation, thus increasing the risk of overheating. We assessed the time required to reach warning body temperature (t38 degrees C), heat stroke (t40 degrees C), or extreme value (t43 degrees C) in a mathematical model that involved calculating various local body heat losses. ⋯ When endogenous heat production rises, t38 degrees C ranged between 75 and 287, t40 degrees C between 185 and 549, and t43 degrees C between 287 and 702 min. When this increase was accompanied by a fall in skin temperature, overheating risk was accentuated (37