Hypoxic-hypercapnic ventilatory interaction at the carotid body of awake goats

Daristotle, Leighann; Berssenbrugge, A.; Bisgard, G. E.

doi:10.1016/s0034-5687(87)80032-4

Cited by 34 publications

(31 citation statements)

References 23 publications

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“…This positive interaction has been confirmed in recent studies carried out on goats, lambs, piglets, cats, rats, and mice (Daristotle et al 1987;Wolsink et al 1992;Carroll et al 1993;Tankersley et al 1994Tankersley et al , 2004Pepper et al 1995;Calder et al 1997), although some early studies showed a negative interaction in cats (Ou et al 1976). We compared the ventilatory response to hypoxic hypercapnia between CS-and FA-exposed mice.…”

Section: Chronic Cs Exposure Produced An Abnormal Inhibitory Interactsupporting

confidence: 56%

Blunted ventilatory response to hypoxia/hypercapnia in mice with cigarette smoke-induced emphysema

Zhuang

Wang

et al. 2007

Respiratory Physiology & Neurobiology

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It has been reported that the degree of emphysema induced by chronic cigarette smoke (CS) is greater in female C3H/HeN mice as compared to other mouse strains. We hypothesized that these mice would develop the similar major characteristics seen in hypercapnic patients with chronic obstructive pulmonary disease (COPD), including emphysema, pulmonary inflammation, hypercapnia/ hypoxemia, rapid breathing, and attenuated ventilatory response (AVR). Mice were exposed either to CS or filtered air (FA) for 16 wk. After exposure, arterial blood gases and minute ventilation were measured before and during chemical challenges in anesthetized and spontaneously breathing mice. We found that as compared to FA, CS exposure caused emphysema and pulmonary inflammation associated with: (1) hypercapnia and hypoxemia, (2) rapid breathing, and (3) AVR to 25 breaths of pure N 2 , 5% CO 2 alone, and 5% CO 2 coupled with 10% O 2 . The similarity of these pathophysiological characteristics between our mouse model and COPD patients suggests that this model could be effectively applied to study COPD pathophysiology, especially central mechanisms of the AVR genesis.

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Section: Chronic Cs Exposure Produced An Abnormal Inhibitory Interactsupporting

confidence: 56%

Blunted ventilatory response to hypoxia/hypercapnia in mice with cigarette smoke-induced emphysema

Zhuang

Wang

et al. 2007

Respiratory Physiology & Neurobiology

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“…The resulting total CO2 slope, however, significantly increased from 139-2 + 51P8 at normoxaemia to 152-8 + 46-9 at moderate hypoxaemia and to 158-7 + 64-1 ml min-kPa-' kg-' at severe hypoxaemia. A positive interaction between hypoxia and hypercapnia is a well-known feature in adult man and animals (Lloyd et al 1958;VanBeek et al 1983;Daristotle et al 1987). However, in young animals and human infants the results are much more conflicting.…”

Section: Discussionmentioning

confidence: 99%

“…It is well documented that in the adult human the slope of the ventilatory response to inhaled C02 increases when the inspired 02 concentration is lowered (Lloyd, Jukes & Cunningham, 1958;Cunningham, Robbins & Wolff, 1986;Dahan, DeGoede, Berkenbosch & Olievier, 1990). From studies in adult animals it has been concluded that the positive interaction between hypoxia and hypercapnia originates at the level of the chemoreceptors of the carotid and aortic bodies (VanBeek, Berkenbosch, DeGoede & Olievier, 1983;Daristotle, Berssenbrugge & J. G. WOLSINK AND OTHERS Bisgard, 1987). In the adult cat and adult human no effect of hypoxia on the central CO2 sensitivity was found (VanBeek, Berkenbosch, DeGoede & Olievier, 1984; Dahan et al 1990).…”

Section: Introductionmentioning

confidence: 99%

The effects of hypoxia on the ventilatory response to sudden changes in CO2 in newborn piglets.

Wolsink

Berkenbosch

DeGoede

et al. 1992

The Journal of Physiology

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SUMMARY1. The ventilatory response to square-wave challenges in end-tidal partial pressure of CO2 (Pc02) was investigated at three levels of arterial Po0 (Pa°2) in nineteen anaesthetized 2-to 11-day-old piglets.2. The ventilatory responses, measured on a breath-to-breath basis, were separated into a peripheral and a central component using a two-compartment model. Both components were described by a CO2 sensitivity, a time constant, a time delay and a single offset.3. Fifty-six responses were analysed against a background ofnormoxaemia (Pa°2 = 12 70 +0O72 kPa, mean + S.D.), fifty-three against a background of moderate hypoxaemia (Pao = 8-63 +034 kPa) and fifty-one against a background of severe hypoxaemia (Pa,02 = 4-98 +030 kPa).4. The sensitivity of the peripheral chemoreceptors in mediating the response to C02 increased from 38-3 + 17-0 ml min-kPa-1 kg-1 during normoxaemia to 48-8 + 15-3 ml min-kPa-1 kg-' during moderate hypoxaemia and to 72-9 + 24-0 ml min-1 kPa-1 kg-1 at severe hypoxaemia.5. As compared with the central CO2 sensitivity during moderate hypoxaemia and normoxaemia (1040± 39-0 and 1008 + 41 6 ml min' kPa-1 kg-', respectively) it decreased to 85 9 + 54-1 ml min-' kPa-1 kg-1 at severe hypoxaemia. 6. We conclude that in newborn piglets there is a positive interaction between hypoxia and hypercapnia at the level of the peripheral chemoreceptors while severe hypoxaemia reduced the C02 sensitivity centrally.

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“…In mammals, interactive effects of O 2 and CO 2 are detectible at the level of ventilation (Nielsen and Smith, 1952), at the level of carotid sinus nerve discharge (Tenney and Brooks, 1966;Daristotle et al, 1987;Lahiri and Delaney, 1975a) and to a very small extent at the level of the increase in intracellular [Ca 2+ ], within the glomus cells, associated with chemoreceptor activation (Bamford et al, 1999;Roy et al, 2000). High levels of CO 2 increase the sensitivity of the carotid body chemoreceptors to low O 2 ; conversely, low levels of O 2 increase the sensitivity of the ventilatory response to hypercapnia (Bamford et al, 1999).…”

Section: Potential Mechanisms Underlying Interactive Effects Between mentioning

confidence: 99%

“…In mammals and some other vertebrates, hypoxic and hypercapnic stimuli often act synergistically (e.g., Tenney and Brooks, 1966;Lahiri and DeLaney, 1975a,b;Daristotle et al, 1987;West et al, 1987; see reviews by Gonzalez et al, 1994;Lahiri and Forster, 2003). Indeed, for any given level of PO 2 , there is a greater amount of carotid sinus nerve discharge when CO 2 levels are increased.…”

Section: Introductionmentioning

confidence: 99%

Reciprocal modulation of O2 and CO2 cardiorespiratory chemoreflexes in the tambaqui

Reid

Perry

Gilmour

et al. 2005

Respiratory Physiology & Neurobiology

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This study examined the effect of acute hypoxic and hypercapnic cardiorespiratory stimuli, superimposed on existing cardiorespiratory disturbances in tambaqui. In their natural habitat, these fish often encounter periods of hypoxic hypercapnia that can be acutely exacerbated by water turnover. Tambaqui were exposed to periods of normoxia, hypoxia, hyperoxia and hypercapnia during which, externally oriented O 2 and CO 2 chemoreceptors were further stimulated, by administration into the inspired water of sodium cyanide and CO 2 -equilibrated water, respectively. Hyperoxic water increased the sensitivity of the NaCN-evoked increase in breathing frequency (f R ) and decrease in heart rate. Hypoxia and hypercapnia attenuated the increase in f R but, aside from blood pressure, did not influence the magnitude of NaCN-evoked cardiovascular changes. Water PO 2 influenced the magnitude of the CO 2 -evoked cardiorespiratory changes and the sensitivity of CO 2 -evoked changes in heart rate and blood flow. The results indicate that existing respiratory disturbances modulate cardiorespiratory responses to further respiratory challenges reflecting both changes in chemosensitivity and the capacity for further change.

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Hypoxic-hypercapnic ventilatory interaction at the carotid body of awake goats

Cited by 34 publications

References 23 publications

Blunted ventilatory response to hypoxia/hypercapnia in mice with cigarette smoke-induced emphysema

Blunted ventilatory response to hypoxia/hypercapnia in mice with cigarette smoke-induced emphysema

The effects of hypoxia on the ventilatory response to sudden changes in CO2 in newborn piglets.

Reciprocal modulation of O2 and CO2 cardiorespiratory chemoreflexes in the tambaqui

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