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Mental Stress Increases Cerebral Perfusion, More So During Hypercapnia
Author(s) -
Shoemaker Leena,
Wilson Luke,
Lucas Sam,
Machado Liana,
Cotter James
Publication year - 2018
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.2018.32.1_supplement.712.9
Subject(s) - middle cerebral artery , deoxygenated hemoglobin , hemodynamics , anesthesia , cerebral autoregulation , mean arterial pressure , transcranial doppler , cardiology , hypercapnia , oxygenation , blood pressure , cerebral perfusion pressure , cerebral blood flow , perfusion , medicine , psychology , hemoglobin , ischemia , autoregulation , heart rate , respiratory system
Acute mental stress has been shown to cause peripheral vascular dysfunction, but its effect on cerebrovasculature is unclear. Thus, the aim of this study was to examine cerebrovascular and hemodynamic responses to mental stress. Sixteen healthy participants (aged 23±4 y, 5 female) completed seated conditions of baseline, followed by low and high mental stress. Stress conditions were mental arithmetic at two levels of difficulty (i.e., counting backwards from 1000 and subtracting 13 from a frequently changing 4‐digit number), which successfully manipulated reported stress levels (p<0.001 between conditions). During each condition, end‐tidal CO 2 pressure (PETCO 2 ) was clamped at normocapnia and two elevated levels (p<0.001): 37±3, 41±1 and 46±1 mm Hg. Middle cerebral artery blood velocity (MCAv) was measured using transcranial Doppler ultrasound, and right prefrontal cortex hemodynamics measured using near‐infrared spectroscopy (NIRS). NIRS provided variables of oxygenated hemoglobin (HbO 2 ), deoxygenated hemoglobin (HHb), total hemoglobin (tHb), and depth‐resolved measures of tissue oxygenation (total oxygenation index, TOI). Blood pressure was measured beat‐by‐beat using finger photoplethysmography, to calculate mean arterial pressure (MAP). Stroke volume and cardiac output (Q̇) were derived with Modelflow. Cerebrovascular reactivity to CO 2 (CVR CO2 , ΔMCAv/ΔPETCO 2 ), cerebrovascular conductance (CVC, MCAv/MAP), and total peripheral resistance (TPR, MAP/Q̇) were calculated. Effects of mental stress and CO 2 were assessed using 2‐way repeated measures ANOVA. The acute mental stress increased MCAv, and more so at higher PETCO 2 (interaction: p=0.015). No other physiological variable showed interactive responses (p>0.069). Compared to baseline, low stress increased HR, MAP, TOI, HbO 2 , and decreased HHb (all p<0.003), but these variables were not altered thereafter with high stress (p>0.05; low vs. high stress). In contrast, CVR CO2 was elevated during high stress only (p=0.017 vs. baseline; p=0.706 for low stress vs. baseline). Finally, neither stress nor CO 2 significantly influenced TPR (p≥0.241). In conclusion, mental stress increased MCAv and this was potentiated during hypercapnia. Increased cerebral perfusion during mental stress was mediated by cardiac‐driven increases in MAP. Hypercapnic‐induced blunting of cerebral autoregulation indicates that there may be a greater risk of cerebral overperfusion (e.g., hemorrhagic stroke) as a consequence of mental stress when innate cerebral autoregulation processes are impaired (e.g. early morning). Support or Funding Information Internal postgraduate research fund ‐ The School of Physical Education, Sport and Exercise Sciences This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .