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Influence of the heme-oxygenase pathway on cerebrocortical blood flow

Miriam Leszl-Ishiguro1, Béla Horváth, Robert A Johnson

  • 1Institute of Human Physiology and Clinical Experimental Research, Semmelweis University, Budapest, Hungary.

Neuroreport
|June 26, 2007
PubMed

Insights

Endogenous carbon monoxide (CO) reduces resting cerebral blood flow (CBF) by inhibiting nitric oxide synthase (NOS). Blocking CO production increases CBF, but does not affect responses to hypoxia or hypercapnia.

Area of Science:

  • Neuroscience
  • Cardiovascular Physiology
  • Biochemistry

Background:

  • Carbon monoxide (CO) is produced by heme-oxygenase (HO) in the cardiovascular and central nervous systems.
  • Endogenous CO has vascular effects and can inhibit nitric oxide synthase (NOS).

Purpose of the Study:

  • To investigate the role of endogenous CO in regulating cerebral blood flow (CBF) and its interaction with NOS.
  • To determine if CO influences CBF responses to hypoxia and hypercapnia.

Main Methods:

  • Heme-oxygenase was blocked using zinc deuteroporphyrin 2,4-bis glycol (ZnDPBG) in anesthetized rats.
  • Nitric oxide synthase was blocked using L-NAME.
  • Cerebrocortical blood flow (CBF) was measured.
  • Responses to hypoxia and hypercapnia were assessed.

Main Results:

  • Blocking HO with ZnDPBG decreased cerebral CO production and increased CBF.
  • The increase in CBF due to HO blockade was abolished by L-NAME, indicating NOS involvement.
  • CO inhibition did not affect hypoxia/hypercapnia-stimulated CBF increases.

Conclusions:

  • Endogenous CO reduces resting CBF through NOS inhibition in adult rats.
  • CO does not modulate the CBF response to hypoxia and hypercapnia.

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