Cerebral oxygenation and blood flow distributions along the capillary path in awake mice (Conference Presentation)

2018 ◽  
Author(s):  
Baoqiang Li ◽  
Ikbal Sencan ◽  
Tatiana V. Esipova ◽  
Kivilcim Kilic ◽  
Mohammad Moeini ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Oxygenation

Cerebral blood flow during exercise: mechanisms of regulation

2009 ◽  
Vol 107 (5) ◽  
pp. 1370-1380 ◽  
Author(s):  
Shigehiko Ogoh ◽  
Philip N. Ainslie
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Oxygenation ◽  
Central Fatigue ◽  
Future Research ◽  
Metabolic Demand ◽  
Heavy Exercise ◽  
Peripheral Vasculature ◽  
Cerebral Vasoconstriction ◽  
Methodological Considerations

The response of cerebral vasculature to exercise is different from other peripheral vasculature; it has a small vascular bed and is strongly regulated by cerebral autoregulation and the partial pressure of arterial carbon dioxide (PaCO2). In contrast to other organs, the traditional thinking is that total cerebral blood flow (CBF) remains relatively constant and is largely unaffected by a variety of conditions, including those imposed during exercise. Recent research, however, indicates that cerebral neuronal activity and metabolism drive an increase in CBF during exercise. Increases in exercise intensity up to ∼60% of maximal oxygen uptake produce elevations in CBF, after which CBF decreases toward baseline values because of lower PaCO2 via hyperventilation-induced cerebral vasoconstriction. This finding indicates that, during heavy exercise, CBF decreases despite the cerebral metabolic demand. In contrast, this reduced CBF during heavy exercise lowers cerebral oxygenation and therefore may act as an independent influence on central fatigue. In this review, we highlight methodological considerations relevant for the assessment of CBF and then summarize the integrative mechanisms underlying the regulation of CBF at rest and during exercise. In addition, we examine how CBF regulation during exercise is altered by exercise training, hypoxia, and aging and suggest avenues for future research.

scholarly journals Cerebral blood flow regulation in end-stage kidney disease

2020 ◽  
Vol 319 (5) ◽  
pp. F782-F791
Author(s):  
Justin D. Sprick ◽  
Joe R. Nocera ◽  
Ihab Hajjar ◽  
W. Charles O’Neill ◽  
James Bailey ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Kidney Disease ◽  
Cerebral Oxygenation ◽  
Cerebrovascular Reactivity ◽  
Regulatory Mechanisms ◽  
End Stage Kidney Disease ◽  
Increased Risk ◽  
End Stage

Patients with chronic kidney disease (CKD) and end-stage kidney disease (ESKD) experience an increased risk of cerebrovascular disease and cognitive dysfunction. Hemodialysis (HD), a major modality of renal replacement therapy in ESKD, can cause rapid changes in blood pressure, osmolality, and acid-base balance that collectively present a unique stress to the cerebral vasculature. This review presents an update regarding cerebral blood flow (CBF) regulation in CKD and ESKD and how the maintenance of cerebral oxygenation may be compromised during HD. Patients with ESKD exhibit decreased cerebral oxygen delivery due to anemia, despite cerebral hyperperfusion at rest. Cerebral oxygenation further declines during HD due to reductions in CBF, and this may induce cerebral ischemia or “stunning.” Intradialytic reductions in CBF are driven by decreases in cerebral perfusion pressure that may be partially opposed by bicarbonate shifts during dialysis. Intradialytic reductions in CBF have been related to several variables that are routinely measured in clinical practice including ultrafiltration rate and blood pressure. However, the role of compensatory cerebrovascular regulatory mechanisms during HD remains relatively unexplored. In particular, cerebral autoregulation can oppose reductions in CBF driven by reductions in systemic blood pressure, while cerebrovascular reactivity to CO2 may attenuate intradialytic reductions in CBF through promoting cerebral vasodilation. However, whether these mechanisms are effective in ESKD and during HD remain relatively unexplored. Important areas for future work include investigating potential alterations in cerebrovascular regulation in CKD and ESKD and how key regulatory mechanisms are engaged and integrated during HD to modulate intradialytic declines in CBF.

Aging: Impact Upon Local Cerebral Oxygenation and Blood Flow With Acute Isovolemic Hemodilution

2006 ◽  
Vol 18 (2) ◽  
pp. 125-131 ◽  
Author(s):  
Min Li ◽  
Sarah J. Ratcliffe ◽  
Frank Knoll ◽  
Jack Wu ◽  
Beau Ances ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Oxygenation ◽  
Isovolemic Hemodilution

Cerebral Oxygenation, Blood Flow, and Oxygen Metabolism During the First Days of Life

2014 ◽  
Author(s):  
Erin M Buckley ◽  
P. Y. Lin ◽  
Katherine Hagan ◽  
Angela Fenoglio ◽  
Mathieu Dehaes ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Oxygenation ◽  
Oxygen Metabolism

Acute cocoa flavanol improves cerebral oxygenation without enhancing executive function at rest or after exercise

2016 ◽  
Vol 41 (12) ◽  
pp. 1225-1232 ◽  
Author(s):  
Lieselot Decroix ◽  
Cajsa Tonoli ◽  
Danusa D. Soares ◽  
Semah Tagougui ◽  
Elsa Heyman ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Executive Function ◽  
Cognitive Function ◽  
Near Infrared ◽  
Acute Exercise ◽  
Cerebral Oxygenation ◽  
Cognitive Task ◽  
Double Blind ◽  
Exercise Induced

Acute exercise-induced improvements in cognitive function are accompanied by increased (cerebral) blood flow and increased brain-derived neurotrophic factor (BDNF) levels. Acute cocoa flavanol (CF) intake may improve cognitive function, cerebral blood flow (in humans), and BNDF levels (in animals). This study investigated (i) the effect of CF intake in combination with exercise on cognitive function and (ii) cerebral hemodynamics and BDNF in response to CF intake and exercise. Twelve healthy men participated in this randomized, double-blind, crossover study. Participants performed a cognitive task (CT) at 100 min after acute 903-mg CF or placebo (PL) intake, followed by a 30-min time-trial. Immediately after this exercise, the same CT was performed. Prefrontal near-infrared spectroscopy was applied during CT and exercise to measure changes in oxygenated (ΔHbO2), deoxygenated (ΔHHb), and total haemoglobin (ΔHbtot) and blood samples were drawn and analyzed for BDNF. Reaction time was faster postexercise, but was not influenced by CF. ΔHbO2 during the resting CT was increased by CF, compared with PL. ΔHbO2, ΔHHb, and ΔHbtot increased in response to exercise without any effect of CF. During the postexercise cognitive task, there were no hemodynamic differences between CF or PL. Serum BDNF was increased by exercise, but was not influenced by CF. In conclusion, at rest, CF intake increased cerebral oxygenation, but not BDNF concentrations, and no impact on executive function was detected. This beneficial effect of CF on cerebral oxygenation at rest was overruled by the strong exercise-induced increases in cerebral perfusion and oxygenation.

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