Journal of applied physiology
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Hyperbaric oxygen and chemical oxidants stimulate CO2/H+-sensitive neurons in rat brain stem slices.
Hyperoxia, a model of oxidative stress, can disrupt brain stem function, presumably by an increase in O2 free radicals. Breathing hyperbaric oxygen (HBO2) initially causes hyperoxic hyperventilation, whereas extended exposure to HBO2 disrupts cardiorespiratory control. Presently, it is unknown how hyperoxia affects brain stem neurons. ⋯ Conversely, only 19% of HBO2-insensitive neurons were CO2/H+ chemosensitive. We conclude that hyperoxia decreases membrane conductance and stimulates firing of putative central CO2/H+-chemoreceptor neurons by an O2 free radical mechanism. These findings may explain why hyperoxia, paradoxically, stimulates ventilation.
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Prolonged mechanical ventilation (MV) results in oxidative damage in the diaphragm; however, it is unclear whether this MV-induced oxidative injury occurs rapidly or develops slowly over time. Furthermore, it is unknown whether both soluble (cytosolic) and insoluble (myofibrillar) proteins are equally susceptible to oxidation during MV. These experiments tested two hypotheses: 1). ⋯ In contrast, both 6 and 18 h of MV promoted oxidative injury in the diaphragm, as indicated by increases in both protein RCD and lipid hydroperoxides. Electrophoretic separation of soluble and insoluble proteins indicated that the MV-induced accumulation of RCD was limited to insoluble proteins with molecular masses of approximately 200, 120, 80, and 40 kDa. We conclude that MV results in a rapid onset of oxidative injury in the diaphragm and that insoluble proteins are primary targets of MV-induced protein oxidation.
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The effects of intravenous norepinephrine (NE, group 1) and vasopressin (AVP, group 2) infusions on systemic, splanchnic, and renal circulations were studied in anesthetized dogs under basal conditions and during endotoxic shock. Under basal conditions, AVP infusion induced a 12 +/- 7% drop in left ventricular stroke work, a 45 +/- 5% fall in portal venous blood flow, and a 31 +/- 13% decrease in intestinal mucosal blood flow (P < 0.05). ⋯ AVP infusion restored renal blood flow and Do2 in endotoxic shock compared with animals resuscitated with NE, which had persistently low renal blood flow and Do2. Our data demonstrate that, in contrast to NE, administration of AVP effectively restores renal blood flow and Do2 with comparable systemic and splanchnic hemodynamic and metabolic effects in endotoxin-induced circulatory shock.
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We tested the hypotheses that active upper airway closure during induced central apneas in nonsedated lambs 1). is complete and occurs at the laryngeal level and 2). is not due to stimulation of the superior laryngeal nerves (SLN). Five newborn lambs were surgically instrumented to record thyroarytenoid (TA) muscle (glottal constrictor) electromyographic (EMG) activity with supra- and subglottal pressures. Hypocapnic and nonhypocapnic central apneas were induced before and after SLN sectioning in the five lambs. ⋯ We conclude that upper airway closure during induced central apneas in lambs is active, complete, and occurs at the glottal level only. Consequently, a positive subglottal pressure is maintained throughout the apnea. Finally, this complete active glottal closure is independent from laryngeal afferent innervation.
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Clinical Trial
Effects of gravity on lung diffusing capacity and cardiac output in prone and supine humans.
Both in normal subjects exposed to hypergravity and in patients with acute respiratory distress syndrome, there are increased hydrostatic pressure gradients down the lung. Also, both conditions show an impaired arterial oxygenation, which is less severe in the prone than in the supine posture. The aim of this study was to use hypergravity to further investigate the mechanisms behind the differences in arterial oxygenation between the prone and the supine posture. ⋯ At the same time, functional residual capacity decreased by 33 and 23%, respectively (P < 0.001 for supine vs. prone), and cardiac output by 40 and 31% (P = 0.007 for supine vs. prone), despite an increase in heart rate of 16 and 28% (P < 0.001 for supine vs. prone), respectively. The finding of a more impaired diffusing capacity in the supine posture compared with the prone at 5 G supports our previous observations of more severe arterial hypoxemia in the supine posture during hypergravity. A reduced pulmonary-capillary blood flow and a reduced estimated alveolar volume can explain most of the reduction in diffusing capacity when supine.