Carbon dioxide, critical closing pressure and cerebral haemodynamics prior to vasovagal syncope in humans

2001 ◽  
Vol 101 (4) ◽  
pp. 351-358 ◽  
Author(s):  
Brian J. CAREY ◽  
Penelope J. EAMES ◽  
Ronney B. PANERAI ◽  
John F. POTTER
Keyword(s):  
Carbon Dioxide ◽  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Vasovagal Syncope ◽  
Previous History ◽  
Normal Subjects ◽  
Cerebrovascular Resistance ◽  
Critical Closing Pressure ◽  
Closing Pressure

The cerebrovascular changes that occur prior to vasovagal syncope (VVS) are unclear, with both increases and decreases in cerebrovascular resistance being reported during pre-syncope. This study assessed the cerebrovascular responses, and their potential underlying mechanisms, that occurred before VVS induced by head-up tilt (HUT). Groups of 65 normal subjects with no previous history of syncope and of 16 patients with recurrent VVS were subjected to 70° HUT for up to 30min. Bilateral middle cerebral artery (MCA) cerebral blood flow velocities (CBFVs) were measured using transcranial Doppler ultrasound, along with simultaneous measures of MCA blood pressure, heart rate, and end-tidal and transcutaneous carbon dioxide concentrations. All 16 patients and 14 of the control subjects developed VVS during HUT. During pre-syncope, mean CBFV declined, due predominantly to a decrease in diastolic rather than systolic CBFV (decreases of 44.5±;19.8% and 6.3±;12.9% respectively; P < 0.0001). CO2 levels and indices of cerebrovascular resistance decreased during pre-syncope, while critical closing pressure (CrCP) increased to levels approaching MCA diastolic blood pressure before decreasing precipitously on syncope. Pre-syncopal changes were similar in syncopal patients and syncopal controls. CrCP, therefore, rises during pre-syncope, possibly related to progressive hypocapnia, and may account for the relatively greater fall in diastolic CBFV. Falls in cerebrovascular resistance, therefore, may be offset by rises in CrCP due to hypocapnia, leading to diminished cerebral blood flow during pre-syncope.

Effect of arterial carbon dioxide on cerebral blood flow in ducks

1977 ◽  
Vol 232 (6) ◽  
pp. H596-H601 ◽  
Author(s):  
B. Grubb ◽  
C. D. Mills ◽  
J. M. Colacino ◽  
K. Schmidt-Nielsen
Keyword(s):  
Carbon Dioxide ◽  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Slow Component ◽  
Avian Brain ◽  
Arterial Pco2 ◽  
Pekin Ducks ◽  
Two Component ◽  
Xenon 133

The purpose of this study was to determine the effect of arterial PCO2 on blood flow to the avian brain. Cerebral blood flow was measured on curarized, artificially ventilated Pekin ducks by the rate at which intra-arterially injected xenon-133 was cleared from the duck's brain. A two-component clearance curve resulted: the blood flow calculated from the fast and slow components was similar to the blood flow to mammalian grey and white matter, respectively. Hypercapnia markedly increased the fast component of blood flow, whereas hypocapnia had no effect on this component. These effects were not due to changes in blood pressure, which was independent of arterial PCO2. Blood flow calculated from the slow component was independent of arterial PCO2. We conclude that the lack of response to hypocapnia may contribute to the exceptional tolerance of birds to high altitude by maintaining normal cerebral blood flow.

Melatonin improves cerebral circulation security margin in rats

1998 ◽  
Vol 275 (1) ◽  
pp. H139-H144 ◽  
Author(s):  
Olivier Régrigny ◽  
Philippe Delagrange ◽  
Elizabeth Scalbert ◽  
Jeffrey Atkinson ◽  
Isabelle Lartaud-Idjouadiene
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Arterial Blood Pressure ◽  
Lower Limit ◽  
Mean Arterial Blood Pressure ◽  
Pressure Level ◽  
Cerebrovascular Resistance ◽  
Arterial Blood ◽  
Cerebral Blood Flow Autoregulation

Because melatonin is a cerebral vasoconstrictor agent, we tested whether it could shift the lower limit of cerebral blood flow autoregulation to a lower pressure level, by improving the cerebrovascular dilatory reserve, and thus widen the security margin. Cerebral blood flow and cerebrovascular resistance were measured by hydrogen clearance in the frontal cortex of adult male Wistar rats. The cerebrovasodilatory reserve was evaluated from the increase in the cerebral blood flow under hypercapnia. The lower limit of cerebral blood flow autoregulation was evaluated from the fall in cerebral blood flow following hypotensive hemorrhage. Rats received melatonin infusions of 60, 600, or 60,000 ng ⋅ kg−1 ⋅ h−1, a vehicle infusion, or no infusion ( n= 9 rats per group). Melatonin induced concentration-dependent cerebral vasoconstriction (up to 25% of the value for cerebrovascular resistance of the vehicle group). The increase in vasoconstrictor tone was accompanied by an improvement in the vasodilatory response to hypercapnia (+50 to +100% vs. vehicle) and by a shift in the lower limit of cerebral blood flow autoregulation to a lower mean arterial blood pressure level (from 90 to 50 mmHg). Because melatonin had no effect on baseline mean arterial blood pressure, the decrease in the lower limit of cerebral blood flow autoregulation led to an improvement in the cerebrovascular security margin (from 17% in vehicle to 30, 55, and 55% in the low-, medium-, and high-dose melatonin groups, respectively). This improvement in the security margin suggests that melatonin could play an important role in the regulation of cerebral blood flow and may diminish the risk of hypoperfusion-induced cerebral ischemia.

scholarly journals The C15O2 Build-up Technique to Measure Regional Cerebral Blood Flow and Volume of Distribution of Water

1989 ◽  
Vol 9 (4) ◽  
pp. 461-470 ◽  
Author(s):  
Adriaan A. Lammertsma ◽  
Richard S. J. Frackowiak ◽  
John M. Hoffman ◽  
Sung-Cheng Huang ◽  
Irving N. Weinberg ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Regional Cerebral Blood Flow ◽  
Normal Subjects ◽  
Volume Of Distribution ◽  
Regional Cerebral Blood ◽  
Arterial Concentration ◽  
Fixed Distribution

A new method to measure regional CBF (rCBF) and volume of distribution of water is presented. It centres on recording the tissue build-up and retention of 15O-labelled water during the continuous inhalation of 15O-labelled carbon dioxide. Simultaneously, the arterial concentration is continuously monitored, and corrections for delay and dispersion in the recorded response are made by curve fitting. The values for the volume of distribution of water obtained in four normal subjects were close to reported in vitro values. Using the same fixed distribution volumes for both build-up and steady-state studies resulted in comparable rCBF values for both techniques.

scholarly journals Influence of cerebrovascular resistance on the dynamic relationship between blood pressure and cerebral blood flow in humans

2014 ◽  
Vol 116 (12) ◽  
pp. 1614-1622 ◽  
Author(s):  
J. D. Smirl ◽  
Y. C. Tzeng ◽  
B. J. Monteleone ◽  
P. N. Ainslie
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Artery ◽  
Function Analysis ◽  
Flow Dynamics ◽  
Pressure Flow ◽  
Cerebrovascular Resistance ◽  
Dynamic Relationship ◽  
Transfer Function Analysis

We examined the hypothesis that changes in the cerebrovascular resistance index (CVRi), independent of blood pressure (BP), will influence the dynamic relationship between BP and cerebral blood flow in humans. We altered CVRi with (via controlled hyperventilation) and without [via indomethacin (INDO, 1.2 mg/kg)] changes in PaCO2. Sixteen subjects (12 men, 27 ± 7 yr) were tested on two occasions (INDO and hypocapnia) separated by >48 h. Each test incorporated seated rest (5 min), followed by squat-stand maneuvers to increase BP variability and improve assessment of the pressure-flow dynamics using linear transfer function analysis (TFA). Beat-to-beat BP, middle cerebral artery velocity (MCAv), posterior cerebral artery velocity (PCAv), and end-tidal Pco2 were monitored. Dynamic pressure-flow relations were quantified using TFA between BP and MCAv/PCAv in the very low and low frequencies through the driven squat-stand maneuvers at 0.05 and 0.10 Hz. MCAv and PCAv reductions by INDO and hypocapnia were well matched, and CVRi was comparably elevated ( P < 0.001). During the squat-stand maneuvers (0.05 and 0.10 Hz), the point estimates of absolute gain were universally reduced, and phase was increased under both conditions. In addition to an absence of regional differences, our findings indicate that alterations in CVRi independent of PaCO2 can alter cerebral pressure-flow dynamics. These findings are consistent with the concept of CVRi being a key factor that should be considered in the correct interpretation of cerebral pressure-flow dynamics as indexed using TFA metrics.

scholarly journals Desferroxamine infusion increases cerebral blood flow: a potential association with hypoxia-inducible factor-1

2009 ◽  
Vol 116 (10) ◽  
pp. 771-779 ◽  
Author(s):  
Farzaneh A. Sorond ◽  
Michele L. Shaffer ◽  
Andrew L. Kung ◽  
Lewis A. Lipsitz
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Lactate Dehydrogenase ◽  
Cerebral Perfusion ◽  
Hypoxia Inducible Factor ◽  
Serum Lactate ◽  
Serum Lactate Dehydrogenase ◽  
Cerebrovascular Resistance ◽  
Hypoxia Inducible Factor 1

Finding an effective means to improve cerebral perfusion during hypoxic/ischaemic stress is essential for neuroprotection. Studies in animal models of stroke have shown that desferroxamine activates HIF-1 (hypoxia-inducible factor-1), reduces brain damage and promotes functional recovery. The present study was designed to investigate the effects of desferroxamine infusion on the cerebral circulation in humans. Fifteen volunteers were enrolled in a randomized double-blind placebo-controlled crossover study. We measured cerebral blood flow velocity by transcranial Doppler ultrasonography in the middle cerebral artery, arterial blood pressure, end-tidal CO2, as well as HIF-1 protein and serum lactate dehydrogenase concentrations in response to 8 h of desferroxamine compared with placebo infusion. Cerebrovascular resistance was calculated from the ratio of steady-state beat-to-beat values for blood pressure to blood flow velocity. We found that desferroxamine infusion was associated with a significant cerebral vasodilation. Moreover, decreased cerebrovascular resistance was temporally correlated with an increased HIF-1 protein concentration as well as HIF-1 transcriptional activation, as measured by serum lactate dehydrogenase concentration. The findings of the present study provide preliminary data suggesting that activators of HIF-1, such as desferroxamine, may protect neurons against ischaemic injury by dilating cerebral vessels and enhancing cerebral perfusion.

Experimental cerebral hemodynamics

1974 ◽  
Vol 41 (5) ◽  
pp. 597-606 ◽  
Author(s):  
Richard C. Dewey ◽  
Heinz P. Pieper ◽  
William E. Hunt
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Mean Arterial Pressure ◽  
Intracranial Pressure ◽  
Perfusion Pressure ◽  
Brain Blood Flow ◽  
Vasomotor Tone ◽  
Vascular Bed ◽  
Critical Closing Pressure ◽  
Closing Pressure

✓ Application of Burton's concept of the critical closing pressure to experimental data on brain-blood flow in the monkey suggests that perfusion pressure, not vascular bed resistance, is the primary variable affecting cerebral blood flow. Perfusion pressure for the cerebral circulation is the mean arterial pressure minus the critical closing pressure (MAP — CCP). Vasomotor tone and intracranial pressure are the major determinants of the critical closing pressure. Changes in either of these variables, therefore, affect perfusion pressure and flow. Data on brain-blood flow at fixed vasomotor tone obtained over wide pressure ranges show little change in vascular bed resistance despite significant changes in flow. The diameter of resistance vessels probably does not change significantly throughout the normal physiological range of cerebral blood flow. The limits of the critical closing pressure in the anesthetized monkey are from 10 to 95 mm Hg. Using these limits, and beginning with the average values for MAP and CCP in 11 awake monkeys breathing room air, the authors present theoretical flow curves in response to changes in intracranial pressure and mean arterial pressure that closely approximate the data reported in man.

Cessation of Diastolic Cerebral Blood Flow Velocity: The Role of Critical Closing Pressure

2013 ◽  
Vol 20 (1) ◽  
pp. 40-48 ◽  
Author(s):  
Georgios V. Varsos ◽  
Hugh K. Richards ◽  
Magdalena Kasprowicz ◽  
Matthias Reinhard ◽  
Peter Smielewski ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Flow Velocity ◽  
Blood Flow Velocity ◽  
Cerebral Blood Flow Velocity ◽  
Critical Closing Pressure ◽  
Closing Pressure

scholarly journals Noninvasive optical monitoring of critical closing pressure and arteriole compliance in human subjects

2017 ◽  
Vol 37 (8) ◽  
pp. 2691-2705 ◽  
Author(s):  
Wesley B Baker ◽  
Ashwin B Parthasarathy ◽  
Kimberly P Gannon ◽  
Venkaiah C Kavuri ◽  
David R Busch ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Continuous Monitoring ◽  
Human Subjects ◽  
Correlation Spectroscopy ◽  
Invasive Technique ◽  
Windkessel Model ◽  
Arterial Blood ◽  
Critical Closing Pressure ◽  
Closing Pressure

The critical closing pressure ( CrCP) of the cerebral circulation depends on both tissue intracranial pressure and vasomotor tone. CrCP defines the arterial blood pressure ( ABP) at which cerebral blood flow approaches zero, and their difference ( ABP −  CrCP) is an accurate estimate of cerebral perfusion pressure. Here we demonstrate a novel non-invasive technique for continuous monitoring of CrCP at the bedside. The methodology combines optical diffuse correlation spectroscopy (DCS) measurements of pulsatile cerebral blood flow in arterioles with concurrent ABP data during the cardiac cycle. Together, the two waveforms permit calculation of CrCP via the two-compartment Windkessel model for flow in the cerebral arterioles. Measurements of CrCP by optics (DCS) and transcranial Doppler ultrasound (TCD) were carried out in 18 healthy adults; they demonstrated good agreement (R = 0.66, slope = 1.14 ± 0.23) with means of 11.1 ± 5.0 and 13.0 ± 7.5 mmHg, respectively. Additionally, a potentially useful and rarely measured arteriole compliance parameter was derived from the phase difference between ABP and DCS arteriole blood flow waveforms. The measurements provide evidence that DCS signals originate predominantly from arteriole blood flow and are well suited for long-term continuous monitoring of CrCP and assessment of arteriole compliance in the clinic.

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