Changes In Cerebral Blood Flow Regulation Research Articles

Acid-base balance and cerebrovascular regulation.

The regulation and defence of intracellular pH is essential for homeostasis. Indeed, alterations in cerebrovascular acid-base balance directly affect cerebral blood flow (CBF) which has implications for human health and disease. For example, changes in CBF regulation during acid-base disturbances are evident in conditions such as chronic obstructive pulmonary disease and diabetic ketoacidosis. The classic experimental studies from the past 75+ years are utilized to describe the integrative relationships between CBF, carbon dioxide tension (PCO2 ), bicarbonate (HCO3- ) and pH. These factors interact to influence (1) the time course of acid-base compensatory changes and the respective cerebrovascular responses (due to rapid exchange kinetics between arterial blood, extracellular fluid and intracellular brain tissue). We propose that alterations in arterial [HCO3- ] during acute respiratory acidosis/alkalosis contribute to cerebrovascular acid-base regulation; and (2) the regulation of CBF by direct changes in arterial vs. extravascular/interstitial PCO2 and pH - the latter recognized as the proximal compartment which alters vascular smooth muscle cell regulation of CBF. Taken together, these results substantiate two key ideas: first, that the regulation of CBF is affected by the severity of metabolic/respiratory disturbances, including the extent of partial/full acid-base compensation; and second, that the regulation of CBF is independent of arterial pH and that diffusion of CO2 across the blood-brain barrier is integral to altering perivascular extracellular pH. Overall, by realizing the integrative relationships between CBF, PCO2 , HCO3- and pH, experimental studies may provide insights to improve CBF regulation in clinical practice with treatment of systemic acid-base disorders.

Alterations in resting cerebrovascular regulation do not affect reactivity to hypoxia, hyperoxia or neurovascular coupling following a SCUBA dive.

What is the central question of this study? What are the characteristics of cerebral blood flow (CBF) regulation following a single SCUBA dive to a depth of 18m sea water with a 47min bottom time. What is the main finding and its importance? Acute alterations in CBF regulation at rest, including extra-cranial vasodilatation, reductions in shear patterns and elevations in intra-cranial blood velocity were observed at rest following a single SCUBA dive. These subtle changes in CBF regulation did not translate into any functional changes in cerebrovascular reactivity to hypoxia or hyperoxia, or neurovascular coupling following a single SCUBA dive. Reductions in vascular function during a SCUBA dive - due to hyperoxia-induced oxidative stress, arterial and venous gas emboli and altered endothelial integrity - may also extend to the cerebrovasculature following return to the surface. This study aimed to characterize cerebral blood flow (CBF) regulation following a single SCUBA dive to a depth of 18m sea water with a 47min bottom time. Prior to and following the dive, participants (n=11) completed (1) resting CBF in the internal carotid (ICA) and vertebral (VA) arteries (duplex ultrasound) and intra-cranial blood velocity (v) of the middle and posterior cerebral arteries (MCAv and PCAv, respectively) (transcranial Doppler ultrasound); (2) cerebrovascular reactivity to acute poikilocapnic hypoxia (i.e. , 0.10) and hyperoxia (i.e. , 1.0); and (3) neurovascular coupling (NVC; regional CBF response to local increases in cerebral metabolism). Global CBF, cerebrovascular reactivity to hypoxia and hyperoxia, and NVC were unaltered following a SCUBA dive (all P>0.05); however, there were subtle changes in other cerebrovascular metrics post-dive, including reductions in ICA (-13±8%, P=0.003) and VA (-11±14%, P=0.021) shear rate, lower ICAv (-10±9%, P=0.008) and VAv (-9±14%, P=0.028), increases in ICA diameter (+4±5%, P=0.017) and elevations in PCAv (+10±19%, P=0.047). Although we observed subtle alterations in CBF regulation at rest, these changes did not translate into any functional changes in cerebrovascular reactivity to hypoxia or hyperoxia, or NVC. Whether prolonged exposure to hyperoxia and hyperbaria during longer, deeper, colder and/or repetitive SCUBA dives would provoke changes to the cerebrovasculature requires further investigation.

Cerebral Blood Flow Regulation in Pregnancy, Hypertension, and Hypertensive Disorders of Pregnancy.

The regulation of cerebral blood flow (CBF) allows for the metabolic demands of the brain to be met and for normal brain function including cognition (learning and memory). Regulation of CBF ensures relatively constant blood flow to the brain despite changes in systemic blood pressure, protecting the fragile micro-vessels from damage. CBF regulation is altered in pregnancy and is further altered by hypertension and hypertensive disorders of pregnancy including preeclampsia. The mechanisms contributing to changes in CBF in normal pregnancy, hypertension, and preeclampsia have not been fully elucidated. This review summarizes what is known about changes in CBF regulation during pregnancy, hypertension, and preeclampsia.

Regulation of Cerebral Blood Flow after Spinal Cord Injury

Significant cardiovascular and autonomic dysfunction occurs after era spinal cord injury (SCI). Two major conditions arising from autonomic dysfunction are orthostatic hypotension and autonomic dysreflexia (i.e., severe acute hypertension). Effective regulation of cerebral blood flow (CBF) is essential to offset these drastic changes in cerebral perfusion pressure. In the context of orthostatic hypotension and autonomic dysreflexia, the purpose of this review is to critically examine the mechanisms underlying effective CBF after an SCI and propose future avenues for research. Although only 16 studies have examined CBF control in those with high-level SCI (above the sixth thoracic spinal segment), it appears that CBF regulation is markedly altered in this population. Cerebrovascular function comprises three major mechanisms: (1) cerebral autoregulation, (i.e., ΔCBF/Δ blood pressure); (2) cerebrovascular reactivity to changes in PaCO2 (i.e. ΔCBF/arterial gas concentration); and (3) neurovascular coupling (i.e., ΔCBF/Δ metabolic demand). While static cerebral autoregulation appears to be well maintained in high-level SCI, dynamic cerebral autoregulation, cerebrovascular reactivity, and neurovascular coupling appear to be markedly altered. Several adverse complications after high-level SCI may mediate the changes in CBF regulation including: systemic endothelial dysfunction, sleep apnea, dyslipidemia, decentralization of sympathetic control, and dominant parasympathetic activity. Future studies are needed to describe whether altered CBF responses after SCI aid or impede orthostatic tolerance. Further, simultaneous evaluation of extracranial and intracranial CBF, combined with modern structural and functional imaging, would allow for a more comprehensive evaluation of CBF regulatory processes. We are only beginning to understand the functional effects of dysfunctional CBF regulation on brain function on persons with SCI, which are likely to include increased risk of transient ischemic attacks, stroke, and cognitive dysfunction.

Sleep-related changes in the regulation of cerebral blood flow in newborn lambs.

The interplay between cerebral perfusion pressure (CPP) and vascular resistance leads to fluctuations in cerebral blood flow (CBF). The relationship between fluctuations in CBF and those in CPP provides insight into the impact of the regulation of vascular resistance on CBF. The aim of this work was to study sleep-related changes in CBF regulation in newborn lambs, by quantifying the extent to which variability in CBF is related to that of CPP in the different wake-sleep states. Repeated-measurement within-subject. 8 newborn lambs. Chronic instrumentation with electrodes (electrocorticogram, electrooculogram, nuchal electromyogram), an arterial catheter (arterial pressure), a subdural catheter (intracranial pressure), and an ultrasonic flow probe around the superior sagittal sinus (CBF). The CPP (difference between arterial and intracranial pressure) and CBF data sequences during quiet wakefulness, rapid-eye-movement (REM) sleep and non-REM sleep were subject to spectral analysis. The fraction of CBF variability explained by CPP variability (CPP vs CBF squared coherence in the range 0.05-0.3 Hz) was highest in REM sleep (0.653) and lowest in non-REM sleep (0.413). The CBF variability (coefficient of variation due to fluctuations in the range 0.05-0.3 Hz) was higher than CPP variability in all states, albeit not significantly in REM sleep. Results suggest that synchronized vasomotor fluctuations accounting for a quota of CBF variability not explained by CPP variability occur in all states in newborn lambs. Their relative contribution to CBF variability differs among wake-sleep states, being highest during non-REM sleep and lowest during REM sleep.