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Abstract
Increased body temperature stimulates hyperventilation in man but little is known
about its effects on ventilatory responsiveness to hypoxia. Hence this study examined
the effects of hyperthermia on hypoxic ventilatory response (HVR), hypercapnic ventilatory
response (HCVR), and oxygen consumption (V̇o2). Six fasting subjects had these variables measured under basal conditions and at
two levels of hyperthermia. Hypoxic ventilatory response was measured as the shape
parameter A of the V̇e/Pao2 curves. Since hyperthermia produces hyperventilation and, therefore, hypocapnia,
HVR was measured at the hyperthermic (hypocapnic) alveolar CO2 tension (PaCO2) and at the basal (normothermic) paCO2. Hypoxic ventilatory response (A) increased when measured at basal PaCO2 levels, from 113 ± 8.8 (S.E.M.) to 189 ± 21.8 at +0.7 °C. and 240 ± 34.0 at +1.40
°C. (P < 0.005). HVR measured during hyperthermic hypocapnia also increased at each
temperature level but did not reach statistical significance (P = 0.1). Hypercapnic
ventilatory response, as measured by the slope S of V̇e/PaCO2 lines, increased significantly at each temperature elevation (P < 0.025). We conclude
that raising body temperature causes a significant augmentation of ventilatory responses
to hypoxia (during normothermic PaCO2 conditions) and to hypercapnia.
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Article info
Publication history
Accepted:
June 2,
1976
Received:
April 8,
1976
Footnotes
☆This study was supported by NIH Grant No. HL 14985. Dr. Weil is the recipient of an NIH Research Career Development Award No. HL 133742. Dr. Zwillich is the recipient of an NIH Research Career Development Award No. HL 00225.
Identification
Copyright
© 1977 Published by Elsevier Inc.
