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Received March 29, 2006
Revised May 2, 2006
Accepted after revision August 22, 2006
1 University of Wisconsin, Department of Medicine
2 University of Wisconsin, Department of Medicine, and the MiddletonMemorial Veterans Hospital
3 University of Wisconsin, Dept. of Orthopeidcs and Rehabilitation
4 University of Wisconsin, Population Health Sciences
* To whom correspondence should be addressed. E-mail: axie{at}wisc.edu.
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 and/or via a reduced cerebrovascular reactivity to CO2 would lead to hyperventilation and an increased ventilatory responsiveness to CO2. We used oral indomethacin to reduce the cerebrovascular reactivity to CO2 and tested the steady-state hypercapnic ventilatory response to CO2 in nine normal awake human subjects under normoxia and hyperoxia (50% O2). Ninety minutes after indomethacin ingestion, cerebral blood flow velocity (CBFV) decreased to 77% of the initial value; and the average slope of CBFV response to hypercapnoea was reduced to 31% of control in normoxia (1.92 vs. 0.59 cm-1 sec-1 mmHg-1, p<0.05) and 37% of control in hyperoxia (1.58 vs. 0.59 cm-1 sec-1 mmHg-1 , p<0.05). Concomitantly, indomethacin administration also caused 40-60% increases in the slope of the mean ventilatory respone to CO2 in both normoxia (1.27±0.31 vs 1.76±0.37 l min-1 mmHg-1, p<0.05) and hyperoxia (1.08±22 vs 1.79±0.37 l min-1 mmHg-1, p<0.05). These correlative findings are consistent with the conclusion that cerebro-vascular responsiveness to CO2 is an important determinant of eupneic ventilation and of hypercapnic ventilatory responsiveness in humans, primarily via its effects at the level of the cental chemoreceptors.
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