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J Appl Physiol 82: 371, 1997;
8750-7587/97 $5.00
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Journal of Applied Physiology
Vol. 82, No. 1, pp. 371-371, January 1997

LETTERS TO THE EDITOR

  

ABSTRACT
ARTICLE
FOOTNOTES
REFERENCES

ABSTRACT

Long, W. Q., G. G. Giesbrecht, and N. R. Anthonisen. Ventilatory response to moderate hypoxia in awake chemodenervated cats. J. Appl. Physiol. 74(2): 805-810, 1993. [Medline] ---In humans and cats the ventilatory response to 30 min of moderate hypoxia (arterial PO2 40-55 Torr) is biphasic: ventilation increases sharply for the first 5 min and then declines. In humans there is evidence that the decline is dependent on the initial increase. We therefore examined ventilatory responses to moderate isocapnic hypoxia in awake cats with and without carotid body denervation. Cats underwent denervation or a sham operation. Then they were studied in a Drorbaugh-Fenn plethysmograph while ventilation, arterial PO2, and end-tidal PO2 and PCO2 were measured. Three sham-operated and four denervated cats were studied with room air as the control. Sham animals demonstrated a biphasic response: ventilation rose to 211% of control at 5 min and fell to 114% of control at 25 min. Denervated animals showed neither the initial increase nor the subsequent decrease in ventilation. Three sham-operated and three denervated cats were studied with 2% CO2 added to the inspirate. Results were similar: intact cats showed a biphasic response to hypoxia, whereas denervated cats showed neither an increase nor a decrease in ventilation. Preliminary experiments showed that hypoxia was not associated with changes in CO2 output or systemic blood pressure in either denervated or intact animals. We conclude that depression of ventilation does not occur in awake denervated cats in response to moderate hypoxia and that the decline in ventilation that occurs in intact cats is in some way dependent on peripheral chemoreceptor output.

ARTICLE

The following is the abstract of the article discussed in the subsequent letter:

Role of carotid body activity responsible for hypoxic ventilatory decline in awake humans

To the Editor: Ventilatory response to sustained mild hypoxia is known to exhibit a biphasic profile: an initial rapid rise for ~5 min followed by gradual decline, referred to as hypoxic ventilatory decline (HVD) (1). The initial rise is derived from peripheral chemoreceptor stimulation, but the nature of the subsequent decline is the matter of current controversy (4, 7). HVD may result from waning peripheral chemoreceptor activity, and Long et al. (5) have tested this hypothesis by measuring HVD after carotid body denervation in awake cats. They found that sectioning of the carotid sinus nerve completely eliminated HVD. This finding is difficult to reconcile with the results of two studies in anesthetized animals: 1) carotid sinus nerve discharges have been observed to remain elevated during HVD (9); and 2) phrenic nerve discharges were markedly depressed during sustained 10-min hypoxia in anesthetized, paralyzed, and glomectomized cats (6).

We have previously reported studies in two patients with bilateral carotid body resection (2, 3). These human studies revealed no HVD, in agreement with the results reported in awake cats by Long et al. (5). One criticism of our data is that hypoxia caused no stimulation of breathing, and one might postulate that ventilation might have been kept at the basal control level by some other inherent control mechanism. Fortunately, however, Long et al. confirmed that hypoxic ventilation did not decline at all, even when the ventilation level was augmented by concomitant inspiration of 2% CO2. Furthermore, in neonates, HVD is more severe than in adults and often produces a ventilation that is less than the basal level (7).

In a recent Commentary, Robbins (8) suggests that attenuated peripheral chemoreceptor reflex activity in human subjects during sustained hypoxic challenge causes the ventilatory off-response to be less than the on-response and contributes to the decline in ventilatory response after repeated pulse application of hypoxia. The author also stressed the importance of the difference in ventilatory control between awake and anesthetized conditions and suggested that the findings might have been manifested only in awake subjects. We agree but also wish to point out that ventilatory output in response to carotid body stimulation in the conscious state reflects all information from the brain stem up to higher central nervous system activities. We conclude that, regarding HVD in conscious humans, the carotid body plays a pivotal role in inducing hypoxic ventilatory decline during sustained mild hypoxia.

FOOTNOTES

  
Yoshiyuki Honda
Department of Physiology
School of Medicine, Chiba University
Chiba 260

  
Horoshi Kimura
Department of Chest Medicine
School of Medicine, Chiba University
Chiba 260

  
Michiko Tanaka
School of Nursing, Immaculate Heart University
Sendai 895, Japan

REFERENCES

1. Georgopoulos, D., S. Walker, and N. R. Anthonisen. Increased chemoreceptor output and ventilatory response to sustained hypoxia. J. Appl. Physiol. 67: 1157-1163, 1989. [Abstract/Free Full Text]
2. Honda, Y. Respiratory and circulatory activities in carotid body-resected humans (Brief Review). J. Appl. Physiol. 73: 1-8, 1992. [Abstract/Free Full Text]
3. Honda, Y., and M. Tanaka. Respiratory and circulatory activities in carotid body resected humans. In: Neurobiology and Cell Physiology of Chemoreception, edited by P. G. Data, H. Acker, and S. Lahiri. New York: Plenum, 1993, p. 359-364.
4. Honda, Y. Ventilatory depression during mild hypoxia in adult humans (Review). Jpn. J. Physiol. 45: 947-959, 1995. [Medline]
5. Long, W. O., G. G. Giesbrecht, and N. R. Anthonisen. Ventilatory response to moderate hypoxia in awake chemodenervated cats. J. Appl. Physiol. 74: 805-810, 1993. [Abstract/Free Full Text]
6. Milhorn, D. E., F. L. Eldridge, J. P. Kiley, and T. G. Waldrop. Prolonged inhibition of respiration following acute hypoxia in glomectomized cats. Respir. Physiol. 57: 331-340, 1984. [Medline]
7. Neubauer, J. A., J. E. Melton, and N. H. Edelman. Modulation of respiration during brain hypoxia (Brief Review). J. Appl. Physiol. 68: 441-451, 1990. [Abstract/Free Full Text]
8. Robbins, P. A. Hypoxic ventilatory decline: site of action (Commentary). J. Appl. Physiol. 79: 373-374, 1995. [Abstract/Free Full Text]
9. Weil, J. V. Ventilatory responses to CO2 and hypoxia after sustained hypoxia in awake cats (Invited Editorial). J. Appl. Physiol. 76: 2251-2252, 1994. [Free Full Text]
0161-7567/97 $5.00 Copyright © 1997 the American Physiological Society


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