British Journal of Anaesthesia, Vol 76, Issue 3 374-381, Copyright © 1996 by The Board of Management and Trustees of the British Journal of Anaesthesia
A. Dahan, J. van Kleef, M. van den Elsen, R. Valk and A. Berkenbosch
Short-term potentiation (STP) of breathing refers to respiratory activity
that persists at termination of a primary stimulus and is not related just
to the dynamics of chemoreceptors. In humans, STP is activated by brief
episodes of hypoxia and voluntary hyperventilation (VHV). STP exerts a
stabilizing influence on breathing pattern. To investigate the effects of a
subanaesthetic concentration of isoflurane on STP, we studied recovery from
mild and moderate hypoxic hyperpnoea and VHV. Experiments were performed in
eight healthy volunteers. If necessary, subjects were aroused to maintain a
state of wakefulness. In the hypoxic studies, a control study involved 1
min of isocapnic hypoxia (end-tidal PO2 (PE'O2 6.1) kPa) followed by sudden
transition to normoxia. In the isoflurane studies, 1 min of mild hypoxia
(Iso-1 study: PE'O2 6.2 kPa) and 1 min of moderate hypoxia (Iso-2 study:
PE'O2 5.7 kPa) were followed by sudden transition to normoxia during
inhalation of 0.1 minimum alveolar concentration (MAC) of isoflurane.
PE'CO2 was maintained at 5.9 kPa. In the VHV study, ventilatory recovery
from 1 min of normoxic VHV was monitored before and during inhalation of
0.1 MAC of isoflurane. Subjects performed multiple transitions in each
study. In the hypoxic studies, peak ventilation after 1 min of hypoxic
stimulation did not differ between treatments. The averaged responses
reached normoxic baseline after 56.3 (SEM 10.7) s in the control study (n =
47 transitions), 18.0 (3.3) s in the Iso-1 study (n = 41; P < 0.05 vs
control) and 15.3 (2.4) s in the Iso-2 study (n = 23; P < 0.05 vs
control). In the VHV studies, VE at termination of VHV was not different
from baseline after 36 s in the control study. An immediate reduction to
less than baseline ventilation, lasting 24 s, was present in the isoflurane
study. We believe that shortening of the time required to reach baseline in
the hypoxic studies, and hypoventilation at cessation of VHV in the
isoflurane studies, are related to the inability to activate STP of
breathing via an effect of isoflurane on respiratory neurones in the brain
stem. Increasing the stimulus intensity during isoflurane inhalation (Iso-2
study) did not (re)-activate STP.
CLINICAL INVESTIGATIONS
Slow ventilatory dynamics after isocapnic hypoxia and voluntary hyperventilation in humans: effects of isoflurane
Department of Anaesthesiology, Leiden University Hospital, PO Box 9600, 1200 RC Leiden, The Netherlands; Department of Physiology, Leiden University Hospital, PO Box 9600, 1200 RC Leiden, The Netherlands
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