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Related Experiment Videos

Anesthesia alters NO-mediated functional hyperemia.

R J Gerrits1, E A Stein, A S Greene

  • 1Department of Physiology, Medical College of Wisconsin, Milwaukee, WI 53226, USA.

Brain Research
|June 30, 2001
PubMed
Summary

Nitric oxide (NO) does not appear to play a primary role in functional hyperemia within the rodent whisker-barrel cortex. Previous findings suggesting NO

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Area of Science:

  • Neuroscience
  • Physiology

Background:

  • Nitric oxide (NO) is proposed to link neural activity with cerebral blood flow.
  • Evidence for NO's role in functional hyperemia is conflicting.

Purpose of the Study:

  • To investigate the role of NO in functional hyperemia in the rodent whisker-barrel cortex (WBC).
  • To test the hypothesis that NO is critical for mediating functional hyperemic responses.

Main Methods:

  • Utilized laser-Doppler flowmetry to measure blood flow changes.
  • Administered various nitric oxide synthase inhibitors (L-NAME, L-NA, 7-NI) and atropine.
  • Compared responses under different anesthetic conditions (urethane alone vs. halothane followed by urethane).

Main Results:

  • NO blockade did not alter functional hyperemia in urethane-anesthetized rats.
  • Atropine administration also had no effect on hyperemia under urethane anesthesia.
  • In halothane-pretreated rats, L-NAME significantly inhibited functional hyperemia by 33%.

Conclusions:

  • These findings do not support a primary role for NO in rat WBC functional hyperemia.
  • Anesthesia type may influence the observed effects of NO blockade on hyperemia.

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