2013•PubMedRequires access

[The response of cerebral blood flow and systemic arterial blood pressure to hypercapnia and hypocapnia in humans].

Vladimir P. Kulikov, D. V. Kuznetsova

Open publisher page 0 citations

Abstract

In 11 healthy volunteers 21 +/- 3.7 years old was monitored cerebral blood flow (CBF) by transcranial Doppler (TCD) of middle cerebral artery and mean hemodynamic arterial blood pressure (MAP) by continuous non-invasive measurement "beat-to-beat" at normocapnia, hypercapnia and hypocapnia. Hypercapnia was creating by rebreathing, hypocapnia was creating by spontaneous hyperventilation. The partial pressure of CO2 in alveolar air (PetCO2) was monitored by capnograph, embedded in the TCD-analyzer. During hypercapnia the velocity of CBF and PetCO2 were significantly increased already at 10 s, which was considerably earlier than the increase in the MAP (30 s). During hypocapnia velocity CBF and PetCO2 were significantly decreased at 10 s, and MAP was not changed. We have installed the threshold PetCO2 42 (41; 44) mm Hg, below which amplification CBF occurs at a constant MAP and reflects the true cerebrovascular reactivity to CO2.

About this research paper

What this paper is about

In 11 healthy volunteers 21 +/- 3.7 years old was monitored cerebral blood flow (CBF) by transcranial Doppler (TCD) of middle cerebral artery and mean hemodynamic arterial blood pressure (MAP) by continuous non-invasive measurement "beat-to-beat" at normocapnia, hypercapnia and hypocapnia. Hypercapnia was creating by rebreathing, hypocapnia was creating by spontaneous hyperventilation. The partial pressure of CO2 in alveolar air (PetCO2) was monitored by capnograph, embedded in the TCD-analyzer. During hypercapnia the velocity of CBF and PetCO2 were significantly increased already at 10 s, which was considerably earlier than the increase in the MAP (30 s). During hypocapnia velocity CBF and PetCO2 were significantly decreased at 10 s, and MAP was not changed. We have installed the threshold PetCO2 42 (41; 44) mm Hg, below which amplification CBF occurs at a constant MAP and reflects the true cerebrovascular reactivity to CO2.

Why it matters

A significance statement is not available in the OpenAlex record.

Key contribution

A contribution statement is not available in the OpenAlex record.

Method / approach

Method details are not available in the OpenAlex metadata.

Main findings

Findings are not separately available in the OpenAlex metadata.

Limitations

Limitations are not available in the OpenAlex metadata.

Applications

Application details are not available in the OpenAlex metadata.

Available abstract

In 11 healthy volunteers 21 +/- 3.7 years old was monitored cerebral blood flow (CBF) by transcranial Doppler (TCD) of middle cerebral artery and mean hemodynamic arterial blood pressure (MAP) by continuous non-invasive measurement "beat-to-beat" at normocapnia, hypercapnia and hypocapnia. Hypercapnia was creating by rebreathing, hypocapnia was creating by spontaneous hyperventilation. The partial pressure of CO2 in alveolar air (PetCO2) was monitored by capnograph, embedded in the TCD-analyzer. During hypercapnia the velocity of CBF and PetCO2 were significantly increased already at 10 s, which was considerably earlier than the increase in the MAP (30 s). During hypocapnia velocity CBF and PetCO2 were significantly decreased at 10 s, and MAP was not changed. We have installed the threshold PetCO2 42 (41; 44) mm Hg, below which amplification CBF occurs at a constant MAP and reflects the true cerebrovascular reactivity to CO2.

Key concepts: Hypocapnia, Normocapnia, Hypercapnia, Hyperventilation, Cerebral blood flow, Anesthesia, Transcranial Doppler, Hemodynamics

Related papers

Back to paper searchBrowse research topicsOriginal source
[The response of cerebral blood flow and systemic arterial blood pressure to hypercapnia and hypocapnia in humans]. — Research Paper | ScholarLens