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Cerebral vasomotor reactivity: steady‐state versus transient changes in carbon dioxide tension
Author(s) -
Brothers R. Matthew,
Lucas Rebekah A. I.,
Zhu YongSheng,
Crandall Craig G.,
Zhang Rong
Publication year - 2014
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/expphysiol.2014.081190
Subject(s) - carbon dioxide , vasomotor , transient (computer programming) , reactivity (psychology) , steady state (chemistry) , tension (geology) , medicine , cardiology , chemistry , anesthesia , thermodynamics , physics , pathology , computer science , organic chemistry , alternative medicine , compression (physics) , operating system
New FindingsWhat is the central question of this study? The relationship between changes in cerebral blood flow and arterial carbon dioxide tension is used to assess cerebrovascular function. Hypercapnia is generally evoked by two methods, i.e. steady‐state and transient increases in carbon dioxide tension. In some cases, the hypercapnia is immediately preceded by a period of hypocapnia. It is unknown whether the cerebrovascular response differs between these methods and whether a period of hypocapnia blunts the subsequent response to hypercapnia.What is the main finding and its importance? The cerebrovascular response is similar between steady‐state and transient hypercapnia. However, hyperventilation‐induced hypocapnia attenuates the cerebral vasodilatory responses during a subsequent period of rebreathing‐induced hypercapnia.Cerebral vasomotor reactivity (CVMR) to changes in arterial carbon dioxide tension ( P aCO 2 ) is assessed during steady‐state or transient changes in P aCO 2 . This study tested the following two hypotheses: (i) that CVMR during steady‐state changes differs from that during transient changes in P aCO 2 ; and (ii) that CVMR during rebreathing‐induced hypercapnia would be blunted when preceded by a period of hyperventilation. For each hypothesis, end‐tidal carbon dioxide tension ( PET , CO 2 ) middle cerebral artery blood velocity (CBFV), cerebrovascular conductance index (CVCI; CBFV/mean arterial pressure) and CVMR (slope of the linear regression between changes in CBFV and CVCI versusPET , CO 2 ) were assessed in eight individuals. To address the first hypothesis, measurements were made during the following two conditions (randomized): (i) steady‐state increases in PET , CO 2of 5 and 10 Torr above baseline; and (ii) rebreathing‐induced transient breath‐by‐breath increases in PET , CO 2 . The linear regression for CBFV versusPET , CO 2( P = 0.65) and CVCI versusPET , CO 2( P = 0.44) was similar between methods; however, individual variability in CBFV or CVCI responses existed among subjects. To address the second hypothesis, the same measurements were made during the following two conditions (randomized): (i) immediately following a brief period of hypocapnia induced by hyperventilation for 1 min followed by rebreathing; and (ii) during rebreathing only. The slope of the linear regression for CBFV versusPET , CO 2( P < 0.01) and CVCI versusPET , CO 2( P < 0.01) was reduced during hyperventilation plus rebreathing relative to rebreathing only. These results indicate that cerebral vasomotor reactivity to changes in P aCO 2is similar regardless of the employed methodology to induce changes in P aCO 2and that hyperventilation‐induced hypocapnia attenuates the cerebral vasodilatory responses during a subsequent period of rebreathing‐induced hypercapnia.