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Isoflurane attenuates cAMP-mediated vasodilation in rat microvessels

K W Park1, H B Dai, E Lowenstein

  • 1Department of Anesthesia and Critical Care, Beth Israel Hospital, Harvard Medical School, Boston, MA 02215, USA.

Circulation
|November 1, 1995
PubMed

Insights

The inhalational anesthetic isoflurane reduces beta-adrenergic and cyclic adenosine monophosphate (cAMP)-mediated vasodilation. This impairment in blood vessel relaxation occurs downstream of adenylate cyclase activation.

Area of Science:

  • Cardiovascular Physiology
  • Anesthesiology
  • Pharmacology

Background:

  • Inhalational anesthetics like isoflurane can affect vascular function.
  • Endothelium-dependent vasodilation mediated by cyclic guanosine monophosphate (cGMP) is known to be attenuated by isoflurane.

Purpose of the Study:

  • To investigate the impact of isoflurane on beta-adrenergic and cyclic adenosine monophosphate (cAMP)-mediated vasodilation.
  • To determine the specific site of isoflurane's inhibitory action on cAMP-dependent relaxation.

Main Methods:

  • Isolated pressurized coronary arteries from Wistar rats were used.
  • Vessels were preconstricted, and concentration-response curves were generated for various vasodilators in the presence or absence of 2% isoflurane.
  • Agents included isoproterenol, sodium fluoride, forskolin, 8-Br-cAMP, and RO20-1724.

Main Results:

  • Isoflurane significantly attenuated relaxation responses to all tested agents.
  • Beta-adrenergic and cAMP-mediated vasodilation were reduced by isoflurane.
  • The inhibitory effect was observed despite normal phosphodiesterase activity.

Conclusions:

  • Isoflurane impairs cAMP-mediated vasodilation.
  • The mechanism of impairment is located downstream of adenylate cyclase activation.
  • Isoflurane does not enhance cAMP phosphodiesterase activity to cause this attenuation.
Abstract

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