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J Appl Physiol 97: 2303-2309, 2004. First published August 20, 2004; doi:10.1152/japplphysiol.00645.2004
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Effects on breathing of focal acidosis at multiple medullary raphe sites in awake goats

M. R. Hodges,1 P. Martino,1 S. Davis,1 C. Opansky,1 L. G. Pan,2 and H. V. Forster1,3

1Department of Physiology, Medical College of Wisconsin, 2Department of Physical Therapy, Marquette University, and 3Zablocki Veterans Affairs Medical Center, Milwaukee, Wisconsin 53226

Submitted 22 June 2004 ; accepted in final form 5 August 2004

To gain insight into why there are chemoreceptors at widespread sites in the brain, mircrotubules were chronically implanted at two or three sites in the medullary raphe nuclei of adult goats (n = 7). After >2 wk, microdialysis (MD) probes were inserted into the microtubules to create focal acidosis (FA) in the awake state using mock cerebral spinal fluid (mCSF) equilibrated with 6.4% (pH = 7.3), 50% (pH = 6.5), or 80% CO2 (pH = 6.3), where MD with 50 and 80% CO2 reduces tissue pH by 0.1 and 0.18 pH unit, respectively. There were no changes in all measured variables with MD with 6.4% at single or multiple raphe sites (P > 0.05). During FA at single raphe sites, only 80% CO2 elicited physiological changes as inspiratory flow was 16.9% above (P < 0.05) control. However, FA with 50 and 80% CO2 at multiple sites increased (P < 0.05) inspiratory flow by 18.4 and 30.1%, respectively, where 80% CO2 also increased (P < 0.05) tidal volume, heart rate, CO2 production, and O2 consumption. FA with 80% CO2 at multiple raphe sites also led to hyperventilation (–2 mmHg), indicating that FA had effects on breathing independent of an increased metabolic rate. We believe these findings suggest that the large ventilatory response to a global respiratory brain acidosis reflects the cumulative effect of stimulation at widespread chemoreceptor sites rather than a large stimulation at a single site. Additionally, focal acidification of raphe chemoreceptors appears to activate an established thermogenic response needed to offset the increased heat loss associated with the CO2 hyperpnea.

central chemoreception; control of breathing


Address for reprint requests and other correspondence: M. R. Hodges, 706 LCI, Dept. of Neurology, Yale Univ., 333 Ceder St., New Haven, CT 06520 (E-mail: hodges{at}yale.edu)




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