Premium
Influence of cerebrovascular function on the hypercapnic ventilatory response in healthy humans
Author(s) -
Xie Ailiang,
Skatrud James B.,
Morgan Barbara,
Chenuel Bruno,
Khayat Rami,
Reichmuth Kevin,
Lin Jenny,
Dempsey Jerome A.
Publication year - 2006
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2006.110627
Subject(s) - hypercapnia , hyperventilation , hyperoxia , cerebral blood flow , anesthesia , central chemoreceptors , chemoreceptor , medicine , middle cerebral artery , hypocapnia , ventilation (architecture) , perfusion , acidosis , lung , ischemia , mechanical engineering , receptor , engineering
An important determinant of [H + ] in the environment of the central chemoreceptors is cerebral blood flow. Accordingly we hypothesized that a reduction of brain perfusion or a reduced cerebrovascular reactivity to CO 2 would lead to hyperventilation and an increased ventilatory responsiveness to CO 2 . We used oral indomethacin to reduce the cerebrovascular reactivity to CO 2 and tested the steady‐state hypercapnic ventilatory response to CO 2 in nine normal awake human subjects under normoxia and hyperoxia (50% O 2 ). Ninety minutes after indomethacin ingestion, cerebral blood flow velocity (CBFV) in the middle cerebral artery decreased to 77 ± 5% of the initial value and the average slope of CBFV response to hypercapnia was reduced to 31% of control in normoxia (1.92 versus 0.59 cm −1 s −1 mmHg −1 , P < 0.05) and 37% of control in hyperoxia (1.58 versus 0.59 cm −1 s −1 mmHg −1 , P < 0.05). Concomitantly, indomethacin administration also caused 40–60% increases in the slope of the mean ventilatory response to CO 2 in both normoxia (1.27 ± 0.31 versus 1.76 ± 0.37 l min −1 mmHg −1 , P < 0.05) and hyperoxia (1.08 ± 0.22 versus 1.79 ± 0.37 l min −1 mmHg −1 , P < 0.05). These correlative findings are consistent with the conclusion that cerebrovascular responsiveness to CO 2 is an important determinant of eupnoeic ventilation and of hypercapnic ventilatory responsiveness in humans, primarily via its effects at the level of the central chemoreceptors.