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Evaluation of Cerebral Blood Flow Autoregulation in the Rat Using Laser Doppler Flowmetry
Published on: January 19, 2020
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
Summary
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.
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