At what point does hemodilution harm the brain?

Hare, Gregory M. T.

doi:10.1007/bf03021576

Cited by 3 publications

(1 citation statement)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Moreover, the occurrence of tissue hypoxia in traumatic brain injury patients with a tissue oxygenation probe was greater in patients with [Hb] of 7 g/dl vs. [Hb] of 10 g/dl (210). Whether the reduced vasomotor response and thus impaired maintenance of CDO 2 during hemodilution is implicated in risk for neurological injury in humans during major surgeries requires further investigation (68). In addition to the implications for various surgical interventions, elucidation of these mechanistic CBF relationships is paramount to our comprehension of myriad pathologies associated with arterial hypoxemia (e.g., sleep apnea, chronic lung diseases, and heart failure) and/or alterations in blood viscosity or hemoglobin levels (e.g., anemic or polycythemic pathologies including von Hippel-Landau or Chuvash diseases).…”

Section: Clinical Implications and Future Directionsmentioning

confidence: 99%

Hypoxemia, oxygen content, and the regulation of cerebral blood flow

Hoiland

Bain

Rieger

et al. 2016

American Journal of Physiology-Regulatory, Integrative and Comp

185

170

View full text Add to dashboard Cite

This review highlights the influence of oxygen (O2) availability on cerebral blood flow (CBF). Evidence for reductions in O2 content (CaO2 ) rather than arterial O2 tension (PaO2 ) as the chief regulator of cerebral vasodilation, with deoxyhemoglobin as the primary O2 sensor and upstream response effector, is discussed. We review in vitro and in vivo data to summarize the molecular mechanisms underpinning CBF responses during changes in CaO2 . We surmise that 1) during hypoxemic hypoxia in healthy humans (e.g., conditions of acute and chronic exposure to normobaric and hypobaric hypoxia), elevations in CBF compensate for reductions in CaO2 and thus maintain cerebral O2 delivery; 2) evidence from studies implementing iso- and hypervolumic hemodilution, anemia, and polycythemia indicate that CaO2 has an independent influence on CBF; however, the increase in CBF does not fully compensate for the lower CaO2 during hemodilution, and delivery is reduced; and 3) the mechanisms underpinning CBF regulation during changes in O2 content are multifactorial, involving deoxyhemoglobin-mediated release of nitric oxide metabolites and ATP, deoxyhemoglobin nitrite reductase activity, and the downstream interplay of several vasoactive factors including adenosine and epoxyeicosatrienoic acids. The emerging picture supports the role of deoxyhemoglobin (associated with changes in CaO2 ) as the primary biological regulator of CBF. The mechanisms for vasodilation therefore appear more robust during hypoxemic hypoxia than during changes in CaO2 via hemodilution. Clinical implications (e.g., disorders associated with anemia and polycythemia) and future study directions are considered.

show abstract

Section: Clinical Implications and Future Directionsmentioning

confidence: 99%