Physiological and genomic consequences of intermittent hypoxia - Selected contribution: Phrenic long-term facilitation requires 5-HT receptor activation during but not following episodic hypoxia
Dd. Fuller et al., Physiological and genomic consequences of intermittent hypoxia - Selected contribution: Phrenic long-term facilitation requires 5-HT receptor activation during but not following episodic hypoxia, J APP PHYSL, 90(5), 2001, pp. 2001-2006
Episodic hypoxia evokes a sustained augmentation of respiratory motor outpu
t known as long-term facilitation (LTF). Phrenic LTF is prevented by pretre
atment with the 5-hydroxytryptamine (5-HT) receptor antagonist ketanserin.
We tested the hypothesis that 5-HT receptor activation is necessary for the
induction but not maintenance of phrenic LTF. Peak integrated phrenic nerv
e activity (integral Phr) was monitored for 1 h after three 5-min episodes
of isocapnic hypoxia (arterial PO2 = 40 +/- 2 Torr; 5-min hyperoxic interva
ls) in four groups of anesthetized, vagotomized, paralyzed, and ventilated
Sprague-Dawley rats [1) control (n = 11), 2) ketanserin pretreatment (2 mg/
kg iv; n = 7), and ketanserin treatment 0 and 45 min after episodic hypoxia
(n = 7 each)]. Ketanserin transiently decreased integral Phr, but it retur
ned to baseline levels within 10 min. One hour after episodic hypoxia, inte
gral Phr was significantly elevated from baseline in control and in the 0-
and 45-min posthypoxia ketanserin groups. Conversely, ketanserin pretreatme
nt abolished phrenic LTF. We conclude that 5-HT receptor activation is nece
ssary to initiate (during hypoxia) but not maintain (following hypoxia) phr
enic LTF.