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Hemoglobin Effects on Nitric Oxide Mediated Hypoxic Vasodilation.

Zimei Rong1,2, Chris E Cooper3

  • 1Centre for English Language Education, University of Nottingham Ningbo China, Ningbo, 315100, China. zimeirong@hotmail.com.

Advances in Experimental Medicine and Biology
|January 20, 2016
PubMed
Summary

Nitric oxide (NO) concentration changes may drive the brain's blood flow response to low oxygen levels. A computational model suggests NO's role in hypoxic vasodilation, particularly its removal by oxyhemoglobin, explains the oxygen threshold.

Keywords:
HemoglobinHypoxic vasodilationNitric oxideNitriteNitrite reductase activity

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Area of Science:

  • Neuroscience
  • Physiology
  • Computational Biology

Background:

  • The brain increases cerebral blood flow (CBF) during hypoxia, but the exact mechanism and oxygen threshold remain unclear.
  • Nitric oxide (NO), an oxygen-dependent vasodilator, is a proposed key regulator of oxygen supply.
  • Existing molecular mechanisms for hypoxic vasodilation lack universal acceptance.

Purpose of the Study:

  • To computationally model and elucidate the role of nitric oxide (NO) in hypoxic vasodilation.
  • To test various NO production and removal mechanisms in relation to brain oxygen levels and CBF.
  • To refine a computational model (BRAINSIGNALS) for simulating brain blood flow and oxygen metabolism.

Main Methods:

  • Utilized the BRAINSIGNALS computational model simulating brain blood flow and oxygen metabolism.
  • Initially modeled NO production by nitric oxide synthase (NOS) and metabolism by cytochrome c oxidase (CCO).
  • Revised the model to include NO generation via deoxyhemoglobin and NO removal by oxyhemoglobin, optimizing for experimental CBF vs. PaO2 data.

Main Results:

  • The initial NOS-based model required unphysiologically low parameters to approximate experimental data.
  • Modeling NO generation via deoxyhemoglobin improved CBF vs. PaO2 curve reproduction but not the threshold.
  • Incorporating NO removal by oxyhemoglobin provided the best fit for the hypoxic vasodilation threshold phenomenon.

Conclusions:

  • Changes in nitric oxide (NO) concentration, particularly its removal by oxyhemoglobin, may be the primary driver of the relationship between oxygen partial pressure (pO2) and cerebral blood flow (CBF).
  • The revised computational model provides a plausible explanation for the threshold phenomenon in hypoxic vasodilation.
  • Further research is needed to definitively prove the causal role of NO concentration changes in regulating pO2-CBF dynamics.