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Peripheral chemoreceptor contributions to sympathetic and cardiovascular responses during hypercapnia

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We tested the hypothesis that integrated sympathetic and cardiovascular reflexes are modulated by systemic CO2 differently in hypoxia than in hyperoxia (n = 7). Subjects performed a CO2 rebreathe protocol that equilibrates CO2 partial pressures between arterial and venous blood and that elevates end tidal CO2 (PETCO2) from ~40 to ~58 mmHg. This test was repeated under conditions where end tidal oxygen levels were clamped at 50 (hypoxia) or 200 (hyperoxia) mmHg. Heart rate (HR; EKG), stroke volume (SV; Doppler ultrasound), blood pressure (MAP; finger plethysmograph), and muscle sympathetic nerve activity (MSNA) were measured continuously during the two protocols. MAP at 40 mmHg PETCO2 (i.e., the first minute of the rebreathe) was greater during hypoxia versus hyperoxia (P < 0.05). However, the increase in MAP during the rebreathe (P < 0.05) was similar in hypoxia (16±3 mmHg) and hyperoxia (17 ± 2 mmHg PETCO2). The increase in cardiac output (Q) at 55 mmHg PETCO2 was greater in hypoxia (2.61 ± 0.7 L/min) versus hyperoxia (1.09 ± 0.44 L/min) (P < 0.05). In both conditions the increase in Q was due to elevations in both HR and SV (P < 0.05). Systemic vascular conductance (SVC) increased to similar absolute levels in both conditions but rose earlier during hypoxia (>50 mmHg PETCO2) than hyperoxia (>55 mmHg). MSNA increased earlier during hypoxic hypercapnia (>45 mmHg) compared with hyperoxic hypercapnia (>55 mmHg). Thus, in these conscious humans, the dose–response effect of PETCO2 on the integrated cardiovascular responses was shifted to the left during hypoxic hypercapnia. The combined data indicate that peripheral chemoreceptors exert important influence over cardiovascular reflex responses to hypercapnia. Key words: blood pressure, cardiac output, muscle sympathetic nerve activity, sympathetic nervous system, end tidal CO2, hypoxia.

Nous avons vérifié l'hypothèse que le CO2 systémique module les réflexes sympathiques et cardio-vasculaires de manière différente durant l'hypoxie et l'hyperoxie (n = 7). On a soumis les sujets à un protocole de réinhalation du CO2 qui équilibre les pressions partielles de CO2 entre le sang artériel et veineux et qui augmente la pression télé-expiratoire en CO2 (PTECO2) d' ~40 à ~58 mm Hg. Cet examen a été répété dans des conditions de taux d'oxygène télé-expiratoire de 50 (hypoxie) ou 200 (hyperoxie) mm Hg. La fréquence cardiaque (FC, ECG), le volume d'éjection systolique (VÉS; ultrasonographie Doppler), la pression artérielle moyenne (PAM; pléthysmo graphie du doigt) et l'activité nerveuse sympathique du muscle (ANSM) ont été mesurés en continu durant les deux protocoles. La PAM à 40 mm Hg PTECO2 (c.-à-d. la première minute de réinhalation) a été plus élevée durant l'hypoxie que durant l'hyperoxie (P < 0,05). Toutefois, l'augmentation de la PAM durant la réinhalation (P < 0,05) a été similaire en hypoxie (16±3 mm Hg) et en hyperoxie (17 ± 2 mm Hg PTECO2). L'augmentation du débit cardiaque (Q) à 55 mm Hg PTECO2 a été plus importante en hypoxie (2,61 ± 0,7 L/min) qu'en hyperoxie (1,09 ± 0,44 L/min) (P < 0,05). La conductance vasculaire systémique (CVS) a augmenté à des valeurs absolues similaires dans les deux conditions, mais elle a augmenté plus rapidement durant l'hypoxie (>50 mm Hg PTECO2) que durant l'hyperoxie (>55 mm Hg). L'ANSM a augmenté plus rapidement durant l'hypercapnie hypoxique (>45 mm Hg) que durant l'hypercapnie hyperoxique (>55 mm Hg). Ainsi, chez ces humains éveillés, l'effet dose–réponse de la PTECO2 sur les réponses
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