Respiration physiology
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To examine the effect of changing tidal volume (VT) on ventilation distribution, we studied multiple breath nitrogen washouts in 4 normal subjects breathing with a VT of 0.6, 1.0 or 1.5 L. We used a recently developed technique of analysis (Crawford et al., 1985) that distinguishes inhomogeneity of gas concentrations due to the interaction of convection and diffusion in the lung periphery (DCDI) from ventilation maldistribution among larger units determined at more proximal branchpoints (CDI). The results indicate that increases in VT reduce the inhomogeneity due to DCDI but increase that due to CDI. In view of the VT dependence of physiological dead space, derived from arterial PCO2, we speculate that the increase in CDI has a dominant effect on gas exchange.
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Respiration physiology · Aug 1986
Respiratory resetting induced by activation of inspiratory bulbo-spinal neurons.
The respiratory effects elicited by spinal (C2-C3) stimulation at the level of descending inspiratory axons were studied in paralysed, non-vagotomized and artificially ventilated cats anaesthetized with urethane-chloralose. The activation of inspiratory bulbospinal axons in the ventrolateral quadrant was confirmed by recording the ipsilateral phrenic excitation following a single pulse. Brief stimulus trains delivered at the same locus during expiration elicited short- and long-term phrenic activations. ⋯ The long-term activation, of central origin, exhibited the same pattern as a spontaneous inspiration and consisted of an inspiratory resetting which necessitated weak anaesthesia and light hypocapnia. Control experiments (restricted lesions of the medulla and the cervical cord, recording of afferent activity in thalamic sensory nuclei, medullary stimulation) revealed that this inspiratory resetting could not be related to appreciable activation of either non-respiratory efferents or spinal afferent pathways studied but was likely to depend on the activation of the descending inspiratory axons. We conclude that the respiratory resetting obtained by spinal stimulation resulted from mass antidromic activation of the inspiratory bulbospinal neurons which thus appear to be involved in the generation of the respiratory rhythm.
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Respiration physiology · Jan 1986
The rate of oxygen release and its effect on capillary O2 tension: a mathematical analysis.
The time required by the red blood cells (RBC) to release the O2 needed by the tissues may be rate-limiting under conditions of reduced O2 supply (DO2). A time-dependent mathematical model of capillary O2 transport is developed to explore the effect of RBC deoxygenation kinetics on the intracapillary plasma PO2. The tissue capillaries are represented by a series of perfectly mixed compartments. ⋯ The discrepancy in PO2 profiles is magnified by anemia, [( Hemoglobin] = 5 g/dl), and hypoxemia, (PaO2 = 25 Torr). For these conditions of severe DO2 reduction, the end-capillary PO2 is significantly less than the venous PO2. These results suggest that (1) the kinetics of RBC deoxygenation can play an important role in the delivery of O2 to the tissues, and (2) the venous PO2 is not always an accurate measure of the end capillary PO2.
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We studied the effects of neostigmine and salbutamol on the force generated by the fatigued diaphragm in anesthetized dogs. Mechanically ventilated animals were prepared with an open thorax. A thin-walled latex balloon was positioned beneath the diaphragm to measure transdiaphragmatic pressure (Pdi) and a rigid cast was fixed around the abdomen to limit changes in diaphragmatic length and geometry during contractions. ⋯ Infusion of salbutamol had no effect on PTT, but did significantly shortened twitch half relaxation time (P less than 0.05). Salbutamol also had no effect on Pdi during stimulated and spontaneous contractions. We conclude that neostigmine improves force generated by the fatigued diaphragm by increasing twitch amplitude while salbutamol did not have a positive inotropic effect.
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Respiration physiology · May 1985
Transient PO2 and PCO2 differences between end-tidal gas and arterial blood during rebreathing in awake dogs.
O2 and CO2 partial pressures in end-tidal gas (PA) and carotid artery blood (Pa) were measured during non-steady-state gas exchange in unanesthetized dogs. In 5 experiments (A), low O2 breathing in open circuit preceded prolonged rebreathing during maintained normoxia. ⋯ This behavior of (PA-Pa)O2 could be explained by a lung model with unequal distribution of alveolar ventilation and perfusion to alveolar volume. The negative (Pa-PA)CO2 values observed during rebreathing with rapidly increasing PACO2 were in part attributable to such unequal distribution effects, in part to lung-to-carotid artery transit time effects.