REBUTTAL FROM DRS. DEMPSEY AND SKATRUD

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Dr. Younes claims that neuromechanical inhibition (NMI) is trivial because we do not experience apnea during exercise. How ridiculous! Of course the resulting respiratory motor output (RMO) would be the net effect of the excitatory and inhibitory influences. During sleep, on the mechanical ventilator (MV) at increased VT or pressure or at increased frequency in normocapnia, inhibitory mechanical feedback influences truly dominate, whereas during exercise, or often just in wakefulness, excitatory influences obviously dominate. All of Younes' experiments in which he attempted to test for NMI were done in wakefulness where even hypocapnia did not have consistent inhibitory effects.

We agree that when VT or pressure is increased synchronous with effort during normocapnic MV, apnea does not occur; but the amplitude of RMO is reduced during and following MV. He agrees that RMO is eliminated during and following normocapnic (and even hypercapnic) MV at slightly increased frequency. This is a powerful, nonchemical resetting of RMO.

There are no discrepancies among our previous findings. An unbiased read shows that increased pressure and/or VT, per se, on MV consistently reduced RMO amplitude and increased frequency of MV-caused apnea.

Agreed that upper airway laryngeal receptors are a potential source of NMI, but it is doubtful they are obligatory because NMI occurs with a continuous positive airway pressure (CPAP) background, with negative pressure MV, and with tracheostomy.

Younes' claims of "artifacts" are irrelevant and his citations are woefully out of date and in error. For example:

• Low levels of increased upper airway CO₂ (in the range we and others use) in unanesthetized preparations have no effect on RMO (1); increases in lung CO₂ are excitatory to RMO (2).
• Removal of oscillations in Pa_CO2 at resting carbon dioxide consumption (CO₂) have absolutely no effect on RMO (3, 4).
• NMI during MV occurs with hyperoxia or carotid body denervation.
• We and others (5) have demonstrated unequivocally that PET_CO2 represents Pa_CO2.

Certainly a 3 to 5 mm Hg fall in Pa_CO2 might explain the observed inhibitory effects of MV in sleep but the onus is clearly on Younes to locate this substantial hypocapnia. It is not to be found in his fanciful list.

When Editor Tobin invited us to write this manuscript, he said the debate would be like Cassius Clay versus Sonny Liston. Many have asked what happened to the soundly defeated Sonny Liston. The answer is now clear; he moved to Winnipeg and invented a ventilator.

Acknowledgments: Supported by NHLBI and the VA Merit Review.

Supported by the Medical research Council of Canada.

	References

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1. Lee LY, Morton RF, McIntosh MJ, Turbek JA. An isolated upper airway preparation in conscious dogs. J Appl Physiol 1986; 60: 2123-2127 [Abstract/Free Full Text].

2. Bartoli A, Cross BA, Guz A, Jain SK, Noble MIM, Trenchard DW. The effect of carbon dioxide in the airways and alveoli on ventilation: a vagal reflex studied in the dog. J Physiol (London) 1974; 240: 91-109 [Abstract/Free Full Text].

3. Takahashi E, Tateishi I, Yamamoto K, Mikami T. Effect of withdrawal of respiratory CO₂ oscillations on respiratory control at rest. J Appl Physiol 1991; 70: 1601-1606 [Abstract/Free Full Text].

4. Smith CA, Saupe KW, Henderson KW, Dempsey JA. Ventilatory effects of specific carotid body hypocapnia in dogs during wakefulness and sleep. J Appl Physiol 1995; 79: 689-699 [Abstract/Free Full Text].

5. Scheid P, Piiper J. Blood/gas equilibrium of carbon dioxide in lungs: a critical review. Respir Physiol 1980; 39: 1-31 [Medline].