Catálogo de publicaciones - libros

The petrosal ganglion (PG) that innervate the carotid body (CB) are activated by transmitters released from the CB receptor (type I, glomus) cells, resulting in the carotid nerve (CN) chemosensory activity. Although the exact transmitter(s) of this synapse is unknown, several molecules present in the CB may play a role in the generation and/or maintenance of the afferent activity (Eyzaguirre & Zapata, 1984; González et al. 1994).

Ventilation is closely tied to PaCO and PaO via a feedback control mechanism. Most importantly, changes in PCO and/or H (pH) are sensed by the central nervous system (CNS) resulting in directly related changes in ventilation. The magnitude of this response relative to the stimulus is known as, “central ventilatory chemosensitivity.” Several electrophysiological studies have demonstrated that chemosensitive neurons – i.e. neurons that change their electrical activity in response to a shift of PCO/pH – are widely distributed throughout the brainstem (Bernard and Nattie, 1996; Coates and Nattie, 1993; Dean et al., 1989, 1990; Kawai et al., 1996; Oyamada et al., 1998, 1999; Richerson, 1995), suggesting that they could be the central CO/pH sensors that regulate ventilation. In addition, PaO levels are inversely related to ventilation. The type I cells of the carotid body serve as the main sensors stimulating ventilation when PaO declines (“peripheral ventilatory chemosensitivity”). The afferent inputs from these PCO/pH- or PO-sensitive cells converge at the respiratory center located in the brainstem, where the generation of respiratory neural activity is integrated.

The systemic ventilatory and cardiovascular adjustments to hypoxia depend on the activation of peripheral chemoreceptors, mainly the carotid bodies (CBs). Intermittent hypoxia produces CB chemosensory excitation, which may participate in the pathogenesis of obstructive sleep apnea (OSA) (Narkiewicz et al., 1999). Recently, we found that chronic intermittent hypoxia (CIH) for four days enhances cat ventilatory and chemosensory responses to acute hypoxia (Rey et al., 2004). We hypothesized that the enhanced chemosensory response to hypoxia induced by CIH would be the result of an increased effect of excitatory modulators, like endothelin (ETs) peptides, and/or a decreased effect of inhibitory molecules within the CB. Thus, we studied the contribution of ETs on the enhanced chemosensory response to hypoxia in CIH-treated cats.

At the outset of these remarks I want to acknowledge Prof. Hisatake Kondo, past President of ISAC and President of XVIth ISAC Symposium for his excellent job as a host. He and his team of coworkers showed to all of us what the efficiency of organization in every regard means. I want to underline the two aspects that impressed me more: first, it was the type of punctuality in the initiation and completion of every event during the Meeting days; second, it was the sided projection that allowed every participant to be aware of coming events ahead of time. That virtue and this organizational strategy were dressed with a sincere expression of warmth that made the nearly four days of Symposium pleasant and substantial; the substance of the Meeting was provided by all symposiasts.