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Effects of CO 2 on Regional Cerebral Blood Flow Regulation During Lower‐Body Negative Pressure
Author(s) -
Thrall Scott F,
Green Chantelle,
Wynnyk Kristi,
Brandt Rachelle,
Day Trevor
Publication year - 2019
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2019.33.1_supplement.lb629
Subject(s) - normocapnia , hypocapnia , cerebral blood flow , hypercapnia , transcranial doppler , mean arterial pressure , anesthesia , hyperventilation , medicine , blood pressure , heart rate , middle cerebral artery , cardiology , posterior cerebral artery , cerebral autoregulation , hemodynamics , autoregulation , ischemia , acidosis
Cerebrovascular CO 2 reactivity (CVR) is differentially regulated between anterior and posterior cerebral circulations, where the cerebrovasculature is responsive to increases (dilation) or decreases (constriction) in arterial CO 2 . In addition, anterior and posterior cerebral blood flow (CBF) may be differentially regulated during lower body negative pressure (LNBP), where blood volume distribution is experimentally moved toward the lower extremities, imposing an acute hypovolemic and hypotensive challenge. However, the effects of steady‐state increases and decreases in CO 2 on the CBF response to LBNP‐imposed hypotension has not been investigated systematically. The aim of this study was to investigate regional CBF responses to incremental (i.e., ramp) LBNP in steady‐state hypo‐ and hypercapnia in anterior and posterior cerebral circulations. We hypothesized that posterior CBF would be better maintained during LBNP at all levels of CO 2 and that regional patterns of CBF regulation during LBNP would be unchanged by steady‐state CO 2 perturbations. In 14 healthy participants, we measured cardiovascular and cerebrovascular variables, including heart rate (HR; ECG), mean arterial pressure (MAP; finometry), and using transcranial Doppler ultrasound, cerebral blood velocity (CBV) and cerebrovascular conductance (CVC; CBV/MAP) in the middle (MCA) and posterior cerebral artery (PCA). We carried out three separate incremental LBNP protocols (−20, −40, −60 and −80 mm Hg; 3‐min each) at three randomized steady‐state levels of CO 2 : (a) hypocapnia (−8 mm Hg; i.e., coached hyperventilation), (b) normocapnia (i.e., room air), and (c) hypercapnia (+8 mm Hg; 5% inspired CO 2 ). We found that HR increased incrementally with LBNP in all CO 2 conditions (P<0.001). At −80mmHg LBNP, MAP decreased in hypo‐ (P=0.046) and normocapnia (P=0.002). MCA CBV decreased in normo‐ (P<0.001) and hypercapnia (P<0.001). PCA CBV also decreased in normo‐ (P=0.011) and hypercapnia (P=0.002). However, MCA CVC decreased in normo‐ (P=0.01) and hypercapnia (P<0.001), whereas PCA CVC did not decrease during LBNP at all levels of CO 2 . These findings demonstrate greater sensitivity in anterior cerebral circulation compared to posterior during a moderate LBNP challenge with alterations in CO 2 . Our data elucidate a comprehensive understanding of regional CVR during LBNP‐induced hypovolemia, and may be applied to understanding preferential protection of posterior brain structures during hypovolemic shock. Support or Funding Information NSERC Discovery and MRU Faculty of Science and Technology This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .