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1.
J Physiol ; 593(18): 4225-43, 2015 Sep 15.
Artículo en Inglés | MEDLINE | ID: mdl-26171601

RESUMEN

We asked if the type of carotid body (CB) chemoreceptor stimulus influenced the ventilatory gain of the central chemoreceptors to CO2 . The effect of CB normoxic hypocapnia, normocapnia and hypercapnia (carotid body PCO2 ≈ 22, 41 and 68 mmHg, respectively) on the ventilatory CO2 sensitivity of central chemoreceptors was studied in seven awake dogs with vascularly-isolated and extracorporeally-perfused CBs. Chemosensitivity with one CB was similar to that in intact dogs. In four CB-denervated dogs, absence of hyper-/hypoventilatory responses to CB perfusion with PCO2 of 19-75 mmHg confirmed separation of the perfused CB circulation from the brain. The group mean central CO2 response slopes were increased 303% for minute ventilation (V̇I)(P ≤ 0.01) and 251% for mean inspiratory flow rate (VT /TI ) (P ≤ 0.05) when the CB was hypercapnic vs. hypocapnic; central CO2 response slopes for tidal volume (VT ), breathing frequency (fb ) and rate of rise of the diaphragm EMG increased in 6 of 7 animals but the group mean changes did not reach statistical significance. Group mean central CO2 response slopes were also increased 237% for V̇I(P ≤ 0.01) and 249% for VT /TI (P ≤ 0.05) when the CB was normocapnic vs. hypocapnic, but no significant differences in any of the central ventilatory response indices were found between CB normocapnia and hypercapnia. These hyperadditive effects of CB hyper-/hypocapnia agree with previous findings using CB hyper-/hypoxia.We propose that hyperaddition is the dominant form of chemoreceptor interaction in quiet wakefulness when the chemosensory control system is intact, response gains physiological, and carotid body chemoreceptors are driven by a wide range of O2 and/or CO2 .


Asunto(s)
Dióxido de Carbono/metabolismo , Cuerpo Carotídeo/metabolismo , Cuerpo Carotídeo/fisiología , Células Quimiorreceptoras/metabolismo , Células Quimiorreceptoras/fisiología , Ventilación Pulmonar/fisiología , Animales , Encéfalo/metabolismo , Encéfalo/fisiología , Perros , Femenino , Hipercapnia/metabolismo , Hipercapnia/fisiopatología , Hipocapnia/metabolismo , Hipocapnia/fisiopatología , Hipoxia/metabolismo , Hipoxia/fisiopatología , Perfusión/métodos , Respiración , Volumen de Ventilación Pulmonar/fisiología , Vigilia/fisiología
2.
J Physiol ; 588(Pt 13): 2455-71, 2010 Jul 01.
Artículo en Inglés | MEDLINE | ID: mdl-20421288

RESUMEN

We assessed the contribution of carotid body chemoreceptors to the ventilatory response to specific CNS hypercapnia in eight unanaesthetized, awake dogs. We denervated one carotid body (CB) and used extracorporeal blood perfusion of the reversibly isolated remaining CB to maintain normal CB blood gases (normoxic, normocapnic perfusate), to inhibit (hyperoxic, hypocapnic perfusate) or to stimulate (hypoxic, normocapnic perfusate) the CB chemoreflex, while the systemic circulation, and therefore the CNS and central chemoreceptors, were exposed consecutively to four progressive levels of systemic arterial hypercapnia via increased fractional inspired CO(2) for 7 min at each level. Neither unilateral CB denervation nor CB perfusion, per se, affected breathing. Relative to CB control conditions (normoxic, normocapnic perfusion), we found that CB chemoreflex inhibition decreased the slope of the ventilatory response to CNS hypercapnia in all dogs to an average of 19% of control values (range 0-38%; n = 6), whereas CB chemoreflex stimulation increased the slope of the ventilatory response to CNS hypercapnia in all dogs to an average of 223% of control values (range 204-235%; n = 4). We conclude that the gain of the CNS CO(2)/H(+) chemoreceptors in dogs is critically dependent on CB afferent activity and that CNS-CB interaction results in hyperadditive ventilatory responses to central hypercapnia.


Asunto(s)
Dióxido de Carbono/fisiología , Sistema Nervioso Central/fisiología , Células Quimiorreceptoras/fisiología , Sistema Nervioso Periférico/fisiología , Fenómenos Fisiológicos Respiratorios , Animales , Análisis de los Gases de la Sangre , Dióxido de Carbono/sangre , Cuerpo Carotídeo/irrigación sanguínea , Cuerpo Carotídeo/fisiología , Seno Carotídeo/fisiología , Desnervación , Perros , Electromiografía , Femenino , Flujo Sanguíneo Regional/fisiología , Mecánica Respiratoria/fisiología , Volumen de Ventilación Pulmonar/fisiología
3.
J Appl Physiol (1985) ; 106(5): 1564-73, 2009 May.
Artículo en Inglés | MEDLINE | ID: mdl-19246650

RESUMEN

We used extracorporeal perfusion of the reversibly isolated carotid sinus region to determine the effects of specific carotid body (CB) chemoreceptor inhibition on eupneic ventilation (Vi) in the resting, awake, intact dog. Four female spayed dogs were studied during wakefulness when CB was perfused with 1) normoxic, normocapnic blood; and 2) hyperoxic (>500 mmHg), hypocapnic ( approximately 20 mmHg) blood to maximally inhibit the CB tonic activity. We found that CB perfusion per se (normoxic-normocapnic) had no effect on Vi. CB inhibition caused marked reductions in Vi (-60%, range 49-80%) and inspiratory flow rate (-58%, range 44-87%) 24-41 s following the onset of CB perfusion. Thereafter, a partial compensatory response was observed, and a steady state in Vi was reached after 50-76 s following the onset of CB perfusion. This steady-state tidal volume-mediated hypoventilation ( approximately 31%) coincided with a significant reduction in mean diaphragm electromyogram (-24%) and increase in mean arterial pressure (+12 mmHg), which persisted for 7-25 min until CB perfusion was stopped, despite a substantial increase in CO(2) retention (+9 Torr, arterial Pco(2)) and systemic respiratory acidosis. We interpret these data to mean that CB chemoreceptors contribute more than one-half to the total eupneic drive to breathe in the normoxic, intact, awake animal. We speculate that this CB contribution consists of both the normal tonic sensory input from the CB chemoreceptors to medullary respiratory controllers, as well as a strong modulatory effect on central chemoreceptor responsiveness to CO(2).


Asunto(s)
Cuerpo Carotídeo/fisiología , Células Quimiorreceptoras/fisiología , Ventilación Pulmonar/fisiología , Animales , Presión Sanguínea/fisiología , Perros , Retroalimentación , Femenino , Hiperoxia/sangre , Hiperoxia/fisiopatología , Hipocapnia/sangre , Hipocapnia/fisiopatología , Perfusión , Vigilia/fisiología
4.
J Appl Physiol (1985) ; 103(6): 1942-9, 2007 Dec.
Artículo en Inglés | MEDLINE | ID: mdl-17932301

RESUMEN

We hypothesized that chronic intermittent hypoxia (CIH) would induce a predisposition to apnea in response to induced hypocapnia. To test this, we used pressure support ventilation to quantify the difference in end-tidal partial pressure of CO(2) (Pet(CO(2))) between eupnea and the apneic threshold ("CO(2) reserve") as an index of the propensity for apnea and unstable breathing during sleep, both before and following up to 3-wk exposure to chronic intermittent hypoxia in dogs. CIH consisted of 25 s of Pet(O(2)) = 35-40 Torr followed by 35 s of normoxia, and this pattern was repeated 60 times/h, 7-8 h/day for 3 wk. The CO(2) reserve was determined during non-rapid eye movement sleep in normoxia 14-16 h after the most recent hypoxic exposure. Contrary to our hypothesis, the slope of the ventilatory response to CO(2) below eupnea progressively decreased during CIH (control, 1.36 +/- 0.18; week 2, 0.94 +/- 0.12; week 3, 0.73 +/- 0.05 l.min(-1).Torr(-1), P < 0.05). This resulted in a significant increase in the CO(2) reserve relative to control (P < 0.05) following both 2 and 3 wk of CIH (control, 2.6 +/- 0.6; week 2, 3.7 +/- 0.8; week 3, 4.5 +/- 0.9 Torr). CIH also 1) caused no change in eupneic, air breathing Pa(CO(2)); 2) increased the slope of the ventilatory response to hypercapnia after 2 wk but not after 3 wk compared with control; and 3) had no effect on the ventilatory response to hypoxia. We conclude that 3-wk CIH reduced the sensitivity of the ventilatory response to transient hypocapnia and thereby increased the CO(2) reserve, i.e., the propensity for apnea was reduced.


Asunto(s)
Dióxido de Carbono/metabolismo , Hipocapnia/fisiopatología , Hipoxia/fisiopatología , Ventilación Pulmonar , Mecánica Respiratoria , Sistema Respiratorio/fisiopatología , Síndromes de la Apnea del Sueño/etiología , Fases del Sueño , Resistencia de las Vías Respiratorias , Animales , Presión Sanguínea , Enfermedad Crónica , Modelos Animales de Enfermedad , Perros , Femenino , Hipocapnia/complicaciones , Hipocapnia/metabolismo , Hipoxia/complicaciones , Hipoxia/metabolismo , Respiración Artificial , Sistema Respiratorio/metabolismo , Síndromes de la Apnea del Sueño/metabolismo , Síndromes de la Apnea del Sueño/fisiopatología , Factores de Tiempo
5.
J Appl Physiol (1985) ; 101(1): 76-83, 2006 Jul.
Artículo en Inglés | MEDLINE | ID: mdl-16627673

RESUMEN

Periodic breathing is commonly observed in chronic heart failure (CHF) when pulmonary capillary wedge pressure is abnormally high and there is usually concomitant tachypneic hyperventilation. We hypothesized that acute pulmonary hypertension at pressures encountered in CHF and involving all of the lungs and pulmonary vessels would predispose to apnea/unstable breathing during sleep. We tested this in a chronically instrumented, unanesthetized dog model during non-rapid eye movement (NREM) sleep. Pulmonary hypertension was created by partial occlusion of the left atrium by means of an implanted balloon catheter in the atrial lumen. Raising mean left atrial pressure by 5.7 +/- 1.1 Torr resulted immediately in tachypneic hyperventilation [breathing frequency increased significantly from 13.8 to 19.9 breaths/min; end-tidal P(CO2) (P(ET(CO2))) fell significantly from 38.5 to 35.9 Torr]. This tachypneic hyperventilation was present during wakefulness, NREM sleep, and rapid eye movement sleep. In NREM sleep, this increase in left atrial pressure increased the gain of the ventilatory response to CO2 below eupnea (1.3 to 2.2 l.min(-1).Torr(-1)) and thereby narrowed the CO2 reserve [P(ET(CO2)) (apneic threshold) - P(ET(CO2)) (eupnea)], despite the decreased plant gain resulting from the hyperventilation. We conclude that acute pulmonary hypertension during sleep results in a narrowed CO2 reserve and thus predisposes toward apnea/unstable breathing and may, therefore, contribute to the breathing instability observed in CHF.


Asunto(s)
Apnea/etiología , Apnea/fisiopatología , Función del Atrio Izquierdo/fisiología , Insuficiencia Cardíaca/complicaciones , Hipertensión Pulmonar/fisiopatología , Sueño/fisiología , Animales , Presión Sanguínea/fisiología , Dióxido de Carbono/análisis , Gasto Cardíaco/fisiología , Células Quimiorreceptoras/fisiología , Perros , Volumen de Reserva Espiratoria/fisiología , Femenino , Frecuencia Cardíaca/fisiología , Hipertensión Pulmonar/complicaciones , Hiperventilación/etiología , Hiperventilación/fisiopatología , Ventilación Pulmonar/fisiología , Mecánica Respiratoria/fisiología , Trastornos del Sueño-Vigilia/etiología , Trastornos del Sueño-Vigilia/fisiopatología , Vigilia/fisiología
6.
J Appl Physiol (1985) ; 98(5): 1732-9, 2005 May.
Artículo en Inglés | MEDLINE | ID: mdl-15591296

RESUMEN

We determined the effects of specific carotid body chemoreceptor inhibition on the propensity for apnea during sleep. We reduced the responsiveness of the carotid body chemoreceptors using intravenous dopamine infusions during non-rapid eye movement sleep in six dogs. Then we quantified the difference in end-tidal Pco(2) (Pet(CO(2))) between eupnea and the apneic threshold, the "CO(2) reserve," by gradually reducing Pet(CO(2)) transiently with pressure support ventilation at progressively increased tidal volume until apnea occurred. Dopamine infusions decreased steady-state eupneic ventilation by 15 +/- 6%, causing a mean CO(2) retention of 3.9 +/- 1.9 mmHg and a brief period of ventilatory instability. The apneic threshold Pet(CO(2)) rose 5.1 +/- 1.9 Torr; thus the CO(2) reserve was narrowed from -3.9 +/- 0.62 Torr in control to -2.7 +/- 0.78 Torr with dopamine. This decrease in the CO(2) reserve with dopamine resulted solely from the 20.5 +/- 11.3% increase in plant gain; the slope of the ventilatory response to CO(2) below eupnea was unchanged from normal. We conclude that specific carotid chemoreceptor inhibition with dopamine increases the propensity for apnea during sleep by narrowing the CO(2) reserve below eupnea. This narrowing is due solely to an increase in plant gain as the slope of the ventilatory response to CO(2) below eupnea was unchanged from normal control. These findings have implications for the role of chemoreceptor inhibition/stimulation in the genesis of apnea and breathing periodicity during sleep.


Asunto(s)
Cuerpo Carotídeo/efectos de los fármacos , Dopamina/administración & dosificación , Inhibición Neural/efectos de los fármacos , Síndromes de la Apnea del Sueño/inducido químicamente , Sueño/efectos de los fármacos , Animales , Cuerpo Carotídeo/fisiología , Perros , Dopamina/toxicidad , Femenino , Infusiones Intravenosas , Inhibición Neural/fisiología , Sueño/fisiología , Síndromes de la Apnea del Sueño/fisiopatología
7.
J Appl Physiol (1985) ; 95(3): 1159-69, 2003 Sep.
Artículo en Inglés | MEDLINE | ID: mdl-12754173

RESUMEN

In awake dogs, lactic acid was injected into the phrenic and deep circumflex iliac arteries to elicit the diaphragm and abdominal muscle metaboreflexes, respectively. At rest, injections into the phrenic or deep circumflex iliac arteries significantly increased mean arterial blood pressure 21 +/- 7% and reduced cardiac output 6 +/- 2% and blood flow to the hindlimbs 20 +/- 9%. Simultaneously, total systemic, hindlimb, and abdominal expiratory muscle vascular conductances were reduced. These cardiovascular responses were not accompanied by significant changes in the amplitude or timing of the diaphragm electromyogram. During treadmill exercise that increased cardiac output, hindlimb blood flow, and vascular conductance 159 +/- 106, 276 +/- 309, and 299 +/- 90% above resting values, lactic acid injected into the phrenic or deep circumflex iliac arteries also elicited pressor responses and reduced hindlimb blood flow and vascular conductance. Adrenergic receptor blockade at rest eliminated the cardiovascular effects of the respiratory muscle metaboreflex. We conclude that the cardiovascular effects of respiratory muscle metaboreflex activation are similar to those previously reported for limb muscles. When activated via metabolite production, the respiratory muscle metaboreflex may contribute to the increased sympathetic tone and redistribution of blood flow during exercise.


Asunto(s)
Hemodinámica/fisiología , Esfuerzo Físico/fisiología , Reflejo/fisiología , Músculos Respiratorios/metabolismo , Músculos Respiratorios/fisiología , Descanso/fisiología , Músculos Abdominales/fisiología , Animales , Presión Sanguínea/efectos de los fármacos , Presión Sanguínea/fisiología , Gasto Cardíaco/efectos de los fármacos , Gasto Cardíaco/fisiología , Diafragma/fisiología , Perros , Electromiografía , Femenino , Frecuencia Cardíaca/fisiología , Ácido Láctico/farmacología , Microesferas , Volumen Sistólico/fisiología , Sistema Nervioso Simpático/fisiología
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