Attenuation of reflex pressor and ventilatory responses to static muscular contraction by intrathecal opioids

J. M. Hill, M. P. Kaufman

Research output: Contribution to journalArticle

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Abstract

We have tested the hypothesis that intrathecal injections of opioid peptides attenuate the reflex pressor and ventilatory responses to static contraction of the triceps surae muscles of chloralose-anesthetized cats. We found that before intrathecal injections of [D-Ala2]Met-enkephalinamide (100 μg in 0.2 ml), static contraction increased mean arterial pressure and ventilation by 32 ± 5 (SE) mmHg and 227 ± 61 (SE) ml/min, whereas after injection of this opioid peptide, static contraction increased mean arterial pressure and ventilation by only 15 ± 5 mmHg and 37 ± 33 ml/min, respectively. The attenuation of both the pressor and ventilatory responses to static contraction by [D-Ala2]Met-enkephalinamide were statistically significant (P < 0.05). Moreover, the attenuation was probably not caused by an opioid-induced withdrawal of sympathetic outflow because [D-Ala2]Met-enkephalinamide had no effect on the pressor and ventilatory responses evoked by high-intensity electrical stimulation of the central cut end of the sciatic nerve. In addition, intrathecal injection of peptides that were highly selective agonists for either the opioid μ- or δ-receptor attenuated the reflex response to static contraction. Naloxone (1,000 μg), injected intrathecally, prevented the attenuation of the reflex responses to contraction by opioid peptides. We speculate that the opioid-induced attenuation of the reflex pressor and ventilatory responses to static contraction may have been due to suppression of substance P release from group III and IV muscle afferents.

Original languageEnglish (US)
Pages (from-to)2466-2472
Number of pages7
JournalJournal of applied physiology
Volume68
Issue number6
StatePublished - Jan 1 1990

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Muscle Contraction
Spinal Injections
Opioid Analgesics
Opioid Peptides
Reflex
Ventilation
Arterial Pressure
Muscles
Chloralose
Opioid Receptors
Sciatic Nerve
Substance P
Naloxone
Electric Stimulation
Cats
Peptides
Injections
Met-enkephalinamide

All Science Journal Classification (ASJC) codes

  • Physiology
  • Physiology (medical)

Cite this

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abstract = "We have tested the hypothesis that intrathecal injections of opioid peptides attenuate the reflex pressor and ventilatory responses to static contraction of the triceps surae muscles of chloralose-anesthetized cats. We found that before intrathecal injections of [D-Ala2]Met-enkephalinamide (100 μg in 0.2 ml), static contraction increased mean arterial pressure and ventilation by 32 ± 5 (SE) mmHg and 227 ± 61 (SE) ml/min, whereas after injection of this opioid peptide, static contraction increased mean arterial pressure and ventilation by only 15 ± 5 mmHg and 37 ± 33 ml/min, respectively. The attenuation of both the pressor and ventilatory responses to static contraction by [D-Ala2]Met-enkephalinamide were statistically significant (P < 0.05). Moreover, the attenuation was probably not caused by an opioid-induced withdrawal of sympathetic outflow because [D-Ala2]Met-enkephalinamide had no effect on the pressor and ventilatory responses evoked by high-intensity electrical stimulation of the central cut end of the sciatic nerve. In addition, intrathecal injection of peptides that were highly selective agonists for either the opioid μ- or δ-receptor attenuated the reflex response to static contraction. Naloxone (1,000 μg), injected intrathecally, prevented the attenuation of the reflex responses to contraction by opioid peptides. We speculate that the opioid-induced attenuation of the reflex pressor and ventilatory responses to static contraction may have been due to suppression of substance P release from group III and IV muscle afferents.",
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Attenuation of reflex pressor and ventilatory responses to static muscular contraction by intrathecal opioids. / Hill, J. M.; Kaufman, M. P.

In: Journal of applied physiology, Vol. 68, No. 6, 01.01.1990, p. 2466-2472.

Research output: Contribution to journalArticle

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N2 - We have tested the hypothesis that intrathecal injections of opioid peptides attenuate the reflex pressor and ventilatory responses to static contraction of the triceps surae muscles of chloralose-anesthetized cats. We found that before intrathecal injections of [D-Ala2]Met-enkephalinamide (100 μg in 0.2 ml), static contraction increased mean arterial pressure and ventilation by 32 ± 5 (SE) mmHg and 227 ± 61 (SE) ml/min, whereas after injection of this opioid peptide, static contraction increased mean arterial pressure and ventilation by only 15 ± 5 mmHg and 37 ± 33 ml/min, respectively. The attenuation of both the pressor and ventilatory responses to static contraction by [D-Ala2]Met-enkephalinamide were statistically significant (P < 0.05). Moreover, the attenuation was probably not caused by an opioid-induced withdrawal of sympathetic outflow because [D-Ala2]Met-enkephalinamide had no effect on the pressor and ventilatory responses evoked by high-intensity electrical stimulation of the central cut end of the sciatic nerve. In addition, intrathecal injection of peptides that were highly selective agonists for either the opioid μ- or δ-receptor attenuated the reflex response to static contraction. Naloxone (1,000 μg), injected intrathecally, prevented the attenuation of the reflex responses to contraction by opioid peptides. We speculate that the opioid-induced attenuation of the reflex pressor and ventilatory responses to static contraction may have been due to suppression of substance P release from group III and IV muscle afferents.

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