Journal of Applied Physiology
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J Appl Physiol 94: 1883-1895, 2003; doi:10.1152/japplphysiol.01103.2002
8750-7587/03 $5.00
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Vol. 94, Issue 5, 1883-1895, May 2003

Prolongation of the laryngeal chemoreflex after inhibition of the rostral ventral medulla in piglets: a role in SIDS?

Liesbeth van der Velde1, Aidan K. Curran1, James J. Filiano2, Robert A. Darnall1,2, Donald Bartlett Jr.1, and J. C. Leiter1,3

Departments of 1 Physiology, 3 Medicine, and 2 Pediatrics, Dartmouth Medical School, Lebanon, New Hampshire 03756

We tested the hypothesis that inhibition of neurons within the rostral ventral medulla (RVM) would prolong the laryngeal chemoreflex (LCR), a putative stimulus in the sudden infant death syndrome (SIDS). We studied the LCR in 19 piglets, age 3-16 days, by injecting 0.05 ml of saline or water into the larynx during wakefulness, non-rapid eye movement (NREM) sleep, and REM sleep, before and after 1 or 10 mM muscimol dialysis in the RVM. Muscimol prolonged the LCR (P < 0.05), and the prolongation was greater when the LCR was stimulated with water compared with saline (P < 0.02). The LCR was longer during NREM sleep than during wakefulness and longest during REM sleep (REM compared with wakefulness). Muscimol had no effect on the likelihood of arousal from sleep after LCR stimulation. We conclude that the RVM provides a tonic facilitatory drive to ventilation that limits the duration of the LCR, and loss of this drive may contribute to the SIDS when combined with stimuli that inhibit respiration.

sudden infant death syndrome; sleep


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