PubMed HealthSearch

PubMed · 8444737

Delayed poststimulus decrease of phrenic motoneuron output produced by phrenic nerve afferent stimulation.

Abstract

The immediate effects of phrenic afferent nerve activation on ventilation have been shown to be both excitatory and inhibitory. Long-lasting inhibitory effects on respiratory motoneuron output have been reported after stimulation of afferent nerves from limb muscles. However, whether respiratory muscle afferent nerves can produce this effect is unknown. We therefore hypothesized that activation of phrenic afferent nerves may produce a prolonged decrease of respiratory motoneuron output. Six alpha-chloralose-anesthetized dogs were studied after vagotomy and bilateral carotid sinus nerve section. The dogs were paralyzed, and end-tidal CO2 was controlled by mechanical ventilation. The proximal end of the cut thoracic phrenic nerve was electrically stimulated for 1 min at intensities that produced activation of thin-fiber afferents. The contralateral efferent phrenic integrated electroneurogram (ENG) was recorded. During stimulation, phrenic ENG activity increased. ENG activity was recorded during recovery and reached a peak decrease compared with control of 19 +/- 11% (SD) 9.0 +/- 6 min after stimulation and returned to control after 30 min. A qualitatively similar response was seen after stimulation of the gastrocnemius nerve. We conclude that activation of thin-fiber afferents in the phrenic nerve can produce a delayed and prolonged decrease of respiratory motoneuron output similar to that of limb muscle afferent nerves.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

J D Road, S Osborne, Y Wakai. 1993. Delayed poststimulus decrease of phrenic motoneuron output produced by phrenic nerve afferent stimulation.. https://doi.org/10.1152/jappl.1993.74.1.68

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Nitric oxide does not mediate cerebral blood flow changes during cortical spreading depression in the anaesthetised rat.

To date, the role of nitric oxide (NO) in mediation of cerebrovascular regulation during spreading depression (SD) in rats remains controversial. Studies are compromised by indirect assay of 'regional' nitric oxide synthase activity (NOS) and/or inappropriate doses of antagonists. The present study utilises direct electrochemical detection in the pia to demonstrate a local, biphasic release of NO associated with each wave of cortical depolarisation. The mean peak of SD-induced NO release was 0.35 microM, which was significantly inhibited by L-N(G)-nitroarginine methyl ester (L-NAME) pre-treatment. Changes in cerebrovascular flux remained intact following treatment with L-NAME, indicating little role for NO in mediation of rat SD blood-flux changes. Mean peak NO release was found to be lower than that observed in rat cerebral ischaemia studies (approximately 4 microM) and in SD in the cat gyrencephalic brain (approximately 0.8 microM).

Anesthesia