Regulation of Breathing and Autonomic Outflows by Chemoreceptors

摘要: Lung ventilation fluctuates widely with behavior but arterial PCO2 remains stable. Under normal conditions, the chemoreflexes contribute to PaCO2 stability by producing small corrective cardiorespiratory adjustments mediated lower brainstem circuits. Carotid body (CB) information reaches respiratory pattern generator (RPG) via nucleus solitarius (NTS) glutamatergic neurons which also target rostral ventrolateral medulla (RVLM) presympathetic thereby raising sympathetic nerve activity (SNA). Chemoreceptors regulate and cardiovagal preganglionic indirectly inputs from RPG. Secondary effects of chemoreceptors on autonomic outflows result changes in lung stretch afferent baroreceptor activity. Central chemosensitivity is caused direct acid indirect CO2 astrocytes. are not definitively identified retrotrapezoid (RTN) a particularly strong candidate. The absence RTN likely causes severe central apneas congenital hypoventilation syndrome. Like other stressors, intense chemosensory stimuli produce arousal activate circuits that wake- or attention-promoting. Such pathways (e.g., locus coeruleus, raphe, orexin system) modulate state-dependent manner their activation intensifies these reflexes. In essential hypertension, obstructive sleep apnea congestive heart failure, chronically elevated CB contributes SNA breathing unchanged becomes periodic (severe CHF). Extreme CNS hypoxia produces stereotyped response (gasping, increased SNA). various pathologies networks discussed, special consideration being given interactions between peripheral chemoreflexes.