TY - JOUR
T1 - Differential Sensitivity to Hypoxic Inhibition of Respiratory processes in the Anesthetized Rat
AU - Maruyama, Ryoko
AU - Yoshida, Akio
AU - Fukuda, Yasuichiro
N1 - Copyright:
Copyright 2016 Elsevier B.V., All rights reserved.
PY - 1989
Y1 - 1989
N2 - To estimate the sensitivity to hypoxic inhibition of various regulatory processes for respiration, changes in breathing pattern during hypoxic ventilatory depression (HVD) were analyzed in the halothane-anesthetized spontaneously breathing rat using a “progressive isocapnic hypoxia test.” In the carotid sinus nerve (CSN) intact rats, ventilatory augmentation was followed by depression due to reduction in respiratory frequency (f) at end-tidal [formula omitted] levels below 50–60 mmHg despite increased afferent activities from the carotid chemoreceptors. After CSN section, ventilation was progressively depressed at [formula omitted] lower than normoxic level with simultaneous decreases of f and tidal volume. An increase in CO2 stimulus or the prevention of arterial hypotension during hypoxia by infusing a vasoconstrictor agent (phenylephrine) inhibited the occurrence of ventilatory depression in both the CSN intact and denervated animals. In all cases studied, the reduction in f resulted mainly from the prolongation of expiratory time (TE). The results suggest that in the anesthetized rat the effect of respiratory stimulation from carotid chemoreceptor afferents becomes inadequate to offset the prolongation of TE due to the central hypoxia at lower [formula omitted], and that the neural process for regulating TE is the major site of deterioration during central hypoxic inhibition. Roles of CO2 stimulus and systemic circulatory conditions in the generation of HVD were also discussed.
AB - To estimate the sensitivity to hypoxic inhibition of various regulatory processes for respiration, changes in breathing pattern during hypoxic ventilatory depression (HVD) were analyzed in the halothane-anesthetized spontaneously breathing rat using a “progressive isocapnic hypoxia test.” In the carotid sinus nerve (CSN) intact rats, ventilatory augmentation was followed by depression due to reduction in respiratory frequency (f) at end-tidal [formula omitted] levels below 50–60 mmHg despite increased afferent activities from the carotid chemoreceptors. After CSN section, ventilation was progressively depressed at [formula omitted] lower than normoxic level with simultaneous decreases of f and tidal volume. An increase in CO2 stimulus or the prevention of arterial hypotension during hypoxia by infusing a vasoconstrictor agent (phenylephrine) inhibited the occurrence of ventilatory depression in both the CSN intact and denervated animals. In all cases studied, the reduction in f resulted mainly from the prolongation of expiratory time (TE). The results suggest that in the anesthetized rat the effect of respiratory stimulation from carotid chemoreceptor afferents becomes inadequate to offset the prolongation of TE due to the central hypoxia at lower [formula omitted], and that the neural process for regulating TE is the major site of deterioration during central hypoxic inhibition. Roles of CO2 stimulus and systemic circulatory conditions in the generation of HVD were also discussed.
KW - breathing pattern
KW - hypoxia
KW - rat respiration
KW - ventilatory depression
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U2 - 10.2170/jjphysiol.39.857
DO - 10.2170/jjphysiol.39.857
M3 - Article
C2 - 2698968
AN - SCOPUS:0024949977
VL - 39
SP - 857
EP - 871
JO - The Journal of Physiological Sciences
JF - The Journal of Physiological Sciences
SN - 1880-6546
IS - 6
ER -