Abstract
Hyperoxia, a model of oxidative stress, can disrupt brain stem function, presumably by an increase in O 2 free radicals. Breathing hyperbaric oxygen (HBO 2 ) initially causes hyperoxic hyperventilation, whereas extended exposure to HBO 2 disrupts cardiorespiratory control. Presently, it is unknown how hyperoxia affects brain stem neurons. We have tested the hypothesis that hyperoxia increases excitability of neurons of the solitary complex neurons, which is an important region for cardiorespiratory control and central CO 2 /H + chemoreception. Intracellular recordings were made in rat medullary slices during exposure to 2-3 atm of HBO 2 , HBO 2 plus antioxidant (Trolox C), and chemical oxidants ( N -chlorosuccinimide, chloramine-T). HBO 2 increased input resistance and stimulated firing rate in 38% of neurons; both effects of HBO 2 were blocked by antioxidant and mimicked by chemical oxidants. Hypercapnia stimulated 32 of 60 (53%) neurons. Remarkably, these CO 2 /H + -chemosensitive neurons were preferentially sensitive to HBO 2 ; 90% of neurons sensitive to HBO 2 and/or chemical oxidants were also CO 2 /H + chemosensitive. Conversely, only 19% of HBO 2 -insensitive neurons were CO 2 /H + chemosensitive. We conclude that hyperoxia decreases membrane conductance and stimulates firing of putative central CO 2 /H + -chemoreceptor neurons by an O 2 free radical mechanism. These findings may explain why hyperoxia, paradoxically, stimulates ventilation.
| Original language | American English |
|---|---|
| Journal | Journal of Applied Physiology |
| Volume | 95 |
| DOIs | |
| State | Published - Sep 1 2003 |
Keywords
- cardiorespiratory control
- central chemoreception
- hyperoxia
- intracellular recording
- reactive oxygen species
Disciplines
- Medical Cell Biology
- Medical Neurobiology
- Medical Physiology
- Medical Sciences
- Medicine and Health Sciences
- Neurosciences
- Physiological Processes