Spinal serotonin receptor activation modulates the exercise ventilatory response with increased dead space in goats

G. S. Mitchell, D. L. Turner, D. R. Henderson, Kevin Foley

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

Small increases in respiratory dead space (VD) augment the exercise ventilatory response by a serotonin-dependent mechanism known as short-term modulation (STM). We tested the hypotheses that the relevant serotonin receptors for STM are in the spinal cord, and are of the 5-HT 2 -receptor subtype. After preparing adult female goats with a mid-thoracic (T6-T8) subarachnoid catheter, ventilation and arterial blood gases were measured at rest and during treadmill exercise (4.8 km/h; 5% grade) with and without an increased VD (0.2-0.3 L). Measurements were made before and after spinal or intravenous administration of a broad-spectrum serotonin receptor antagonist (methysergide, 1-2 mg total) and a selective 5-HT 2 -receptor antagonist (ketanserin, 5-12 mg total). Although spinal methysergide had no effect on the exercise ventilatory response in control conditions, the augmented response with increased VD was impaired, allowing P a C O2 to increase from rest to exercise. Spinal methysergide diminished both mean inspiratory flow and frequency responses to exercise with increased VD. Spinal ketanserin impaired P a C O2 regulation with increased VD, although its ventilatory effects were less clear. Intrathecal dye injections indicated CSF drug distribution was caudal to the upper cervical spinal cord and intravenous drugs at the same total dose did not affect STM. We conclude that spinal 5-HT 2 receptors modulate the exercise ventilatory response with increased VD in goats.

Original languageEnglish (US)
Pages (from-to)230-238
Number of pages9
JournalRespiratory Physiology and Neurobiology
Volume161
Issue number3
DOIs
StatePublished - May 31 2008
Externally publishedYes

Fingerprint

Serotonin 5-HT2 Receptors
Methysergide
Serotonin Receptors
Goats
Ketanserin
Respiratory Dead Space
Spinal Injections
Serotonin Antagonists
Pharmaceutical Preparations
Intravenous Administration
Ventilation
Serotonin
Spinal Cord
Coloring Agents
Thorax
Catheters
Gases

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)
  • Physiology
  • Pulmonary and Respiratory Medicine

Cite this

Spinal serotonin receptor activation modulates the exercise ventilatory response with increased dead space in goats. / Mitchell, G. S.; Turner, D. L.; Henderson, D. R.; Foley, Kevin.

In: Respiratory Physiology and Neurobiology, Vol. 161, No. 3, 31.05.2008, p. 230-238.

Research output: Contribution to journalArticle

@article{4fbaebd606e840ebbcea68ef6949983a,
title = "Spinal serotonin receptor activation modulates the exercise ventilatory response with increased dead space in goats",
abstract = "Small increases in respiratory dead space (VD) augment the exercise ventilatory response by a serotonin-dependent mechanism known as short-term modulation (STM). We tested the hypotheses that the relevant serotonin receptors for STM are in the spinal cord, and are of the 5-HT 2 -receptor subtype. After preparing adult female goats with a mid-thoracic (T6-T8) subarachnoid catheter, ventilation and arterial blood gases were measured at rest and during treadmill exercise (4.8 km/h; 5{\%} grade) with and without an increased VD (0.2-0.3 L). Measurements were made before and after spinal or intravenous administration of a broad-spectrum serotonin receptor antagonist (methysergide, 1-2 mg total) and a selective 5-HT 2 -receptor antagonist (ketanserin, 5-12 mg total). Although spinal methysergide had no effect on the exercise ventilatory response in control conditions, the augmented response with increased VD was impaired, allowing P a C O2 to increase from rest to exercise. Spinal methysergide diminished both mean inspiratory flow and frequency responses to exercise with increased VD. Spinal ketanserin impaired P a C O2 regulation with increased VD, although its ventilatory effects were less clear. Intrathecal dye injections indicated CSF drug distribution was caudal to the upper cervical spinal cord and intravenous drugs at the same total dose did not affect STM. We conclude that spinal 5-HT 2 receptors modulate the exercise ventilatory response with increased VD in goats.",
author = "Mitchell, {G. S.} and Turner, {D. L.} and Henderson, {D. R.} and Kevin Foley",
year = "2008",
month = "5",
day = "31",
doi = "10.1016/j.resp.2008.02.007",
language = "English (US)",
volume = "161",
pages = "230--238",
journal = "Respiratory Physiology and Neurobiology",
issn = "1569-9048",
publisher = "Elsevier",
number = "3",

}

TY - JOUR

T1 - Spinal serotonin receptor activation modulates the exercise ventilatory response with increased dead space in goats

AU - Mitchell, G. S.

AU - Turner, D. L.

AU - Henderson, D. R.

AU - Foley, Kevin

PY - 2008/5/31

Y1 - 2008/5/31

N2 - Small increases in respiratory dead space (VD) augment the exercise ventilatory response by a serotonin-dependent mechanism known as short-term modulation (STM). We tested the hypotheses that the relevant serotonin receptors for STM are in the spinal cord, and are of the 5-HT 2 -receptor subtype. After preparing adult female goats with a mid-thoracic (T6-T8) subarachnoid catheter, ventilation and arterial blood gases were measured at rest and during treadmill exercise (4.8 km/h; 5% grade) with and without an increased VD (0.2-0.3 L). Measurements were made before and after spinal or intravenous administration of a broad-spectrum serotonin receptor antagonist (methysergide, 1-2 mg total) and a selective 5-HT 2 -receptor antagonist (ketanserin, 5-12 mg total). Although spinal methysergide had no effect on the exercise ventilatory response in control conditions, the augmented response with increased VD was impaired, allowing P a C O2 to increase from rest to exercise. Spinal methysergide diminished both mean inspiratory flow and frequency responses to exercise with increased VD. Spinal ketanserin impaired P a C O2 regulation with increased VD, although its ventilatory effects were less clear. Intrathecal dye injections indicated CSF drug distribution was caudal to the upper cervical spinal cord and intravenous drugs at the same total dose did not affect STM. We conclude that spinal 5-HT 2 receptors modulate the exercise ventilatory response with increased VD in goats.

AB - Small increases in respiratory dead space (VD) augment the exercise ventilatory response by a serotonin-dependent mechanism known as short-term modulation (STM). We tested the hypotheses that the relevant serotonin receptors for STM are in the spinal cord, and are of the 5-HT 2 -receptor subtype. After preparing adult female goats with a mid-thoracic (T6-T8) subarachnoid catheter, ventilation and arterial blood gases were measured at rest and during treadmill exercise (4.8 km/h; 5% grade) with and without an increased VD (0.2-0.3 L). Measurements were made before and after spinal or intravenous administration of a broad-spectrum serotonin receptor antagonist (methysergide, 1-2 mg total) and a selective 5-HT 2 -receptor antagonist (ketanserin, 5-12 mg total). Although spinal methysergide had no effect on the exercise ventilatory response in control conditions, the augmented response with increased VD was impaired, allowing P a C O2 to increase from rest to exercise. Spinal methysergide diminished both mean inspiratory flow and frequency responses to exercise with increased VD. Spinal ketanserin impaired P a C O2 regulation with increased VD, although its ventilatory effects were less clear. Intrathecal dye injections indicated CSF drug distribution was caudal to the upper cervical spinal cord and intravenous drugs at the same total dose did not affect STM. We conclude that spinal 5-HT 2 receptors modulate the exercise ventilatory response with increased VD in goats.

UR - http://www.scopus.com/inward/record.url?scp=43149096034&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=43149096034&partnerID=8YFLogxK

U2 - 10.1016/j.resp.2008.02.007

DO - 10.1016/j.resp.2008.02.007

M3 - Article

VL - 161

SP - 230

EP - 238

JO - Respiratory Physiology and Neurobiology

JF - Respiratory Physiology and Neurobiology

SN - 1569-9048

IS - 3

ER -