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Effects of chemoreflexes on hyperthermic hyperventilation and cerebral blood velocity in resting heated humans
Author(s) -
Fujii Naoto,
Honda Yasushi,
Hayashi Keiji,
Kondo Narihiko,
Koga Shunsaku,
Nishiyasu Takeshi
Publication year - 2008
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/expphysiol.2008.042143
Subject(s) - hyperventilation , medicine , cardiology , resting heart rate , blood pressure , heart rate
We tested the hypothesis that hyperthermic hyperventilation in part reflects enhanced chemoreceptor ventilatory O 2 drive, and that the resultant hypocapnia attenuates ventilatory responses and/or middle cerebral artery mean blood velocity (MCA V mean ) in resting humans. Eleven healthy subjects were passively heated for 50–80 min, causing oesophageal temperature ( T oes ) to increase by 1.6°C. During heating, minute ventilation increased ( P < 0.05), while end‐tidal CO 2 pressure ( P ET,CO 2) and MCA V mean declined. A hyperoxia test in which three breaths of hyperoxic air were inspired was performed once before heating and three times during the heating. When we observed hypocapnia ( P ET,CO 2below 40 mmHg), P ET,CO 2was restored to the eucapnic level by adding 100% CO 2 to the inspired air immediately before the last two tests. Minute ventilation was significantly reduced by hyperoxia, and that reduction gradually increased with increasing T oes . However, the percentage decrease in from the normoxic level was small (20–29%) and unchanged during heating. When P ET,CO 2was restored to eucapnic levels, was unchanged, but MCA V mean was partly restored to the level seen prior to heating (28.1% restoration at T oes 37.6°C and 38.1% restoration at T oes 38.0°C). These findings suggest that although hyperthermia increases chemoreceptor ventilatory O 2 drive in resting humans, the relative contribution of the chemoreceptor ventilatory O 2 drive to hyperthermic hyperventilation is small (∼20%) and unaffected by increasing core temperature. Moreover, hypocapnia induced by hyperthermic hyperventilation reduces cerebral blood flow but not ventilatory responses.