The impact of acute and chronic catecholamines on respiratory responses to hypoxic stress in the rat.

Chronic catecholamine production is associated with desensitisation and down-regulation of adrenergic receptors and occurs in conditions, such as heart failure and myocardial infarction. The effects of further acute adrenergic stimulation, which may occur during exercise, and their subsequent effects on chemosensitivity and ventilation are unclear. Chronic isoprenaline (ISO) increased ventilation by 50 % (P < 0.05) yet the sensitivity to graded hypoxia was preserved. Acute noradrenaline (NA) in control animals led to a doubling of ventilation in hyperoxia (P < 0.001), and this difference was preserved in graded hypoxia (P < 0.001). Yet, combination of NA + ISO did not increase ventilation beyond ISO at baseline or in hypoxia. ISO, NA, and NA + ISO all induced a metabolic acidosis (P < 0.05) with enhanced ventilation in partial compensation. Carotid sinus nerve (CSN) section led to a partial loss of catecholamine-induced augmentation in ventilation (P < 0.05), yet direct recording from CSN in vitro suggests catecholamine is inhibitory for CSN discharge. These observations suggest that chronic catecholamine exposure may result in decreased exercise performance as a direct consequence of the hyperpnea to compensate for an increased metabolic rate coupled with acidosis and leading to increased central chemosensitivity. A limited contribution from peripheral chemoreceptors was noted but was not a consequence of catecholamine stimulation of the carotid body.