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[Intrathecal midazolam attenuates renal sympathetic nerve activity in rabbits]

K Hashimoto1, F Karasawa, T Satoh

  • 1Department of Anesthesiology, National Defense Medical College, Tokorozawa.

Masui. the Japanese Journal of Anesthesiology
|August 1, 1997
PubMed

Insights

Intrathecal midazolam (IT M) at high concentrations significantly reduces renal sympathetic nerve activity (RSNA) in rabbits by acting on spinal cord benzodiazepine receptors (BZR). This effect is reversed by flumazenil, confirming the BZR involvement.

Area of Science:

  • Neuroscience
  • Pharmacology
  • Physiology

Context:

  • The central nervous system regulates sympathetic nerve activity, influencing cardiovascular function.
  • Spinal cord benzodiazepine receptors (BZR) are implicated in modulating autonomic outflow.
  • Intrathecal (IT) administration allows direct targeting of spinal cord mechanisms.

Purpose:

  • To investigate the effect of intrathecal midazolam (IT M) on renal sympathetic nerve activity (RSNA).
  • To determine if the effects of IT M on RSNA are mediated by spinal cord BZR.
  • To elucidate the role of spinal BZR in the regulation of sympathetic nerve activity.

Summary:

  • High-concentration intrathecal midazolam (0.5%) significantly decreased mean arterial pressure (MAP) and attenuated renal sympathetic nerve activity (RSNA) in rabbits.
  • These effects were observed in both neuraxis-intact and sino-aortic denervated rabbits.
  • Intravenous flumazenil administration reversed the decrease in MAP and RSNA induced by IT midazolam, indicating mediation via BZR.

Impact:

  • This study demonstrates that high-dose intrathecal midazolam attenuates RSNA through spinal BZR.
  • Findings suggest a potential role for spinal BZR in modulating sympathetic tone.
  • Highlights the importance of considering the site of action for drugs affecting autonomic function.

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