| Sumario: | Chronic intermittent hypoxia (CIH), characterized by short episodes of hypoxia followed by normoxia, is a common feature of obstructive sleep apnea (OSA). It has been proposed that CIH enhances the hypoxic ventilatory response (HVR) leading to hypertension, upregulation of catecholaminergic and reninangiotensin systems (Fletcher, 2000; Prabhakar and Peng, 2004). Most of the information of the effects of CIH on peripheral chemoreflex control of cardiovascular and respiratory systems has been obtained from studies performed on OSA patients. However, conclusions from these studies are conflictive because of comorbidities associated with OSA (Narkiewicz et al., 1999). Experiments performed in rats showed that CIH enhances HVR (Ling et al., 2001) and produces long-term facilitation of respiratory motor activity (McGuire et al., 2003; Peng & Prabhakar, 2003). The facilitator effect of CIH on HVR has been attributed to a potentiation of the carotid body (CB) chemosensory responses to acute hypoxia. However, it is a matter of debate if the ventilatory potentiation induced by CIH is due to a CB enhanced activity or secondary to central facilitation of chemosensory input. Peng et al., (2001) found that basal CB discharges and chemosensory responses to acute hypoxia were enhanced in rats exposed to a pattern of 5% O2 for 15s followed by normoxia for 5 min, repeated 8 hours/day for 10 days. However, this observation has not been confirmed in other animal models of CIH. Using a protocol of short hypoxic episodes, we studied the effects of CIH on cat cardiorespiratory reflexes and CB chemosensory responses induced by hypoxia.
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