Effects of vagotomy on cardiovascular and heart rate variability alterations following chronic normobaric hypoxia in adult rabbits

BACKGROUND: chronic hypoxia increases basal ventilation and pulmonary vascular resistance, with variable changes in arterial blood pressure and heart rate, but it's impact on heart rate variability and autonomic regulation have been less well examined. We studied changes in arterial blood pressure, heart rate and heart rate variability (HRV) in rabbits subjected to chronic normobaric hypoxia (CNH; PB ~ 719 mmHg; FIO2 ~ 9.2%) for 14 days and assess the effect of autonomic control by acute bilateral vagal denervation. RESULTS: exposure to CNH stalled animal weight gain and increased the hematocrit, without affecting heart rate or arterial blood pressure. Nevertheless, Poincaré plots of the electrocardiographic R-R intervals showed a reduced distribution parallel to the line of identity, which interpreted as reduced long-term HRV. In the frequency domain, CNH reduced the very-low- (< 0.2 Hz) and high-frequency components (> 0.8 Hz) of the R-R spectrograms and produced a prominent component in the low-frequency component (0.2-0.5 Hz) of the power spectrum. In control and CNH exposed rabbits, bilateral vagotomy had no apparent effect on the short- and long-term HRV in the Poincaré plots. However, bilateral vagotomy differentially affected higher-frequency components (> 0.8 Hz); reducing it in control animals without modifying it in CNH-exposed rabbits. CONCLUSIONS: These results suggest that CNH exposure shifts the autonomic balance of heart rate towards a sympathetic predominance without modifying resting heart rate or arterial blood pressure.

Carotid body Thermoreceptors, sympathetic neural activation, and cardiometabolic disease

The carotid body (CB) is the main peripheral chemoreceptor that senses the arterial PO2, PCO2 and pH. In response to hypoxemia, hypercapnia and acidosis, carotid chemosensory discharge elicits reflex respiratory, autonomic and cardiovascular adjustments. The classical construct considers the CB as the main peripheral oxygen sensor, triggering reflex physiological responses to acute hypoxemia and facilitating the ventilatory acclimation to chronic hypoxemia at high altitude. However, a growing body of experimental evidence supports the novel concept that an abnormally enhanced CB chemosensory input to the brainstem contributes to overactivation of the sympathetic nervous system, and consequent pathology. Indeed, the CB has been implicated in several diseases associated with increases in central sympathetic outflow. These include hypertension, heart failure, sleep apnea, chronic obstructive pulmonary disease and metabolic syndrome. Indeed, ablation of the CB has been proposed for the treatment of severe and resistant hypertension in humans. In this review, we will analyze and discuss new evidence supporting an important role for the CB chemoreceptor in the progression of autonomic and cardiorespiratory alterations induced by heart failure, obstructive sleep apnea, chronic obstructive pulmonary disease and metabolic syndrome.

Fisiopatología de la hipertensión asociada al síndrome de apnea obstructiva del sueño: Evidencia de estudios clínicos y modelos animales de hipoxia crónica intermitente / Pathophysiology of obstructive sleep apnea-associated hypertension

There is a well established relationship between the obstructive sleep apnea syndrome and hypertension. Current evidence suggests that the increase in arterial pressure is secondary to an enhanced sympathetic tone through peripheral chemoreflexes triggered by intermittent hypoxic stimulation of the carotid bodies. Chronic intermittent hypoxia would activate renal and systemic vasoactive systems through potentiated hypoxic chemoreflexes. These early changes in autonomic tone can be detected through cardiovascular variability and baroreflex sensitivity analysis. Both are relatively simple and noninvasive techniques. The multiplicity of pathogenic mechanisms in obstructive sleep apnea-associated hypertension emphasizes the need of increasing diagnostic sensitivity to detect and correct this common condition, which significantly increases cardiovascular risk.