scholarly journals Evaluation of the cerebral hemodynamic response to rhythmic handgrip

2000 ◽  
Vol 88 (6) ◽  
pp. 2205-2213 ◽  
Author(s):  
Cole A. Giller ◽  
Angela M. Giller ◽  
Christopher R. Cooper ◽  
Mustapha R. Hatab
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Transcranial Doppler Ultrasound ◽  
Normal Subjects ◽  
Flow Index ◽  
Luminal Area ◽  
End Tidal ◽  
Exercise Environment ◽  
Artery Flow

The response of the cerebral circulation to exercise has been studied with transcranial Doppler ultrasound (TCD) because this modality provides continuous measurements of blood velocity and is well suited for the exercise environment. The use of TCD as an index of cerebral blood flow, however, requires the assumption that the diameter of the insonated vessel is constant. Here, we examine this assumption for rhythmic handgrip using a spectral index designed to measure trends in vessel flow. Nineteen normal subjects were studied during 5 min of volitional maximum rhythmic right handgrip at 1 Hz. TCD velocities from both middle arteries (left and right), blood pressure, and end-tidal Pco 2 were recorded every 10 s. A spectral weighted sum was also calculated as a flow index (FI). Averages were computed from the last 2 min of handgrip. Relative changes in velocity, FI, and pressure were calculated. The validity of FI was tested by comparing the change in diameter derived from equations relating flow and diameter. Mean blood pressure increased 23.8 ± 17.8% (SD), and velocity increased 13.3 ± 9.8% (left) and 9.6 ± 8.3% (right). Although the mean change in FI was small [2.0 ± 18.2% (left) and 4.7 ± 29.7% (right)], the variation was high: some subjects showed a significant increase in FI and others a significant decrease. Diameter estimates from two equations relating flow and luminal area were not significantly different. Decreases in FI were associated with estimated diameter decreases of 10%. Our data suggest that the cerebral blood flow (CBF) response to rhythmic handgrip is heterogeneous and that middle cerebral artery flow can decrease in some subjects, in agreement with prior studies using the Kety-Schmidt technique. We speculate that the velocity increase is due to sympathetically mediated vasoconstriction rather than a ubiquitous flow increase. Our data suggest that the use of ordinary TCD velocities to interpret the CBF response during exercise may be invalid.

Cerebral blood flow responses to changes in oxygen and carbon dioxide in humans

2002 ◽  
Vol 80 (8) ◽  
pp. 819-827 ◽  
Author(s):  
Andrea Vovk ◽  
David A Cunningham ◽  
John M Kowalchuk ◽  
Donald H Paterson ◽  
James Duffin
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Middle Cerebral Artery ◽  
Arterial Blood Pressure ◽  
Cerebral Artery ◽  
Mean Arterial Blood Pressure ◽  
Transcranial Doppler Ultrasound ◽  
Arterial Blood ◽  
End Tidal

This study characterized cerebral blood flow (CBF) responses in the middle cerebral artery to PCO2ranging from 30 to 60 mmHg (1 mmHg = 133.322 Pa) during hypoxia (50 mmHg) and hyperoxia (200 mmHg). Eight subjects (25 ± 3 years) underwent modified Read rebreathing tests in a background of constant hypoxia or hyperoxia. Mean cerebral blood velocity was measured using a transcranial Doppler ultrasound. Ventilation (VE), end-tidal PCO2 (PETCO2), and mean arterial blood pressure (MAP) data were also collected. CBF increased with rising PETCO2 at two rates, 1.63 ± 0.21 and 2.75 ± 0.27 cm·s–1·mmHg–1 (p < 0.05) during hypoxic and 1.69 ± 0.17 and 2.80 ± 0.14 cm·s–1·mmHg–1 (p < 0.05) during hyperoxic rebreathing. VE also increased at two rates (5.08 ± 0.67 and 10.89 ± 2.55 L·min–1·mmHg–1 and 3.31 ± 0.50 and 7.86 ± 1.43 L·min–1·mmHg–1) during hypoxic and hyperoxic rebreathing. MAP and PETCO2 increased linearly during both hypoxic and hyperoxic rebreathing. The breakpoint separating the two-component rise in CBF (42.92 ± 1.29 and 49.00 ± 1.56 mmHg CO2 during hypoxic and hyperoxic rebreathing) was likely not due to PCO2 or perfusion pressure, since PETCO2 and MAP increased linearly, but it may be related to VE, since both CBF and VE exhibited similar responses, suggesting that the two responses may be regulated by a common neural linkage. Key words: brain blood flow, middle cerebral artery, ventilation, mean arterial blood pressure.

The relationship of blood flow velocity fluctuations to intracranial pressure B waves

1992 ◽  
Vol 76 (3) ◽  
pp. 415-421 ◽  
Author(s):  
David W. Newell ◽  
Rune Aaslid ◽  
Renate Stooss ◽  
Hans J. Reulen
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Intracranial Pressure ◽  
Arterial Blood Pressure ◽  
Wave Amplitude ◽  
Transcranial Doppler Ultrasound ◽  
Normal Subjects ◽  
Content Type ◽  
Arterial Blood ◽  
Flow Fluctuations

✓ Intracranial pressure (ICP) and continuous transcranial Doppler ultrasound signals were monitored in 20 head-injured patients and simultaneous synchronous fluctuations of middle cerebral artery (MCA) velocity and B waves of the ICP were observed. Continuous simultaneous monitoring of MCA velocity, ICP, arterial blood pressure, and expired CO2 revealed that both velocity waves and B waves occurred despite a constant CO2 concentration in ventilated patients and were usually not accompanied by fluctuations in the arterial blood pressure. Additional recordings from the extracranial carotid artery during the ICP B waves revealed similar synchronous fluctuations in the velocity of this artery, strongly supporting the hypothesis that blood flow fluctuations produce the velocity waves. The ratio between ICP wave amplitude and velocity wave amplitude was highly correlated to the ICP (r = 0.81, p < 0.001). Velocity waves of similar characteristics and frequency, but usually of shorter duration, were observed in seven of 10 normal subjects in whom MCA velocity was recorded for 1 hour. The findings in this report strongly suggest that B waves in the ICP are a secondary effect of vasomotor waves, producing cerebral blood flow fluctuations that become amplified in the ICP tracing, in states of reduced intracranial compliance.

Direct Cerebral Vasodilatory Effects of Sevoflurane and Isoflurane 

1999 ◽  
Vol 91 (3) ◽  
pp. 677-677 ◽  
Author(s):  
Basil F. Matta ◽  
Karen J. Heath ◽  
Kate Tipping ◽  
Andrew C. Summors
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Middle Cerebral Artery ◽  
Flow Velocity ◽  
Cerebral Artery ◽  
Blood Flow Velocity ◽  
End Tidal

Background The effect of volatile anesthetics on cerebral blood flow depends on the balance between the indirect vasoconstrictive action secondary to flow-metabolism coupling and the agent's intrinsic vasodilatory action. This study compared the direct cerebral vasodilatory actions of 0.5 and 1.5 minimum alveolar concentration (MAC) sevoflurane and isoflurane during an propofol-induced isoelectric electroencephalogram. Methods Twenty patients aged 20-62 yr with American Society of Anesthesiologists physical status I or II requiring general anesthesia for routine spinal surgery were recruited. In addition to routine monitoring, a transcranial Doppler ultrasound was used to measure blood flow velocity in the middle cerebral artery, and an electroencephalograph to measure brain electrical activity. Anesthesia was induced with propofol 2.5 mg/kg, fentanyl 2 micro/g/kg, and atracurium 0.5 mg/kg, and a propofol infusion was used to achieve electroencephalographic isoelectricity. End-tidal carbon dioxide, blood pressure, and temperature were maintained constant throughout the study period. Cerebral blood flow velocity, mean blood pressure, and heart rate were recorded after 20 min of isoelectric encephalogram. Patients were then assigned to receive either age-adjusted 0.5 MAC (0.8-1%) or 1.5 MAC (2.4-3%) end-tidal sevoflurane; or age-adjusted 0.5 MAC (0.5-0.7%) or 1.5 MAC (1.5-2%) end-tidal isoflurane. After 15 min of unchanged end-tidal concentration, the variables were measured again. The concentration of the inhalational agent was increased or decreased as appropriate, and all measurements were repeated again. All measurements were performed before the start of surgery. An infusion of 0.01% phenylephrine was used as necessary to maintain mean arterial pressure at baseline levels. Results Although both agents increased blood flow velocity in the middle cerebral artery at 0.5 and 1.5 MAC, this increase was significantly less during sevoflurane anesthesia (4+/-3 and 17+/-3% at 0.5 and 1.5 MAC sevoflurane; 19+/-3 and 72+/-9% at 0.5 and 1.5 MAC isoflurane [mean +/- SD]; P&lt;0.05). All patients required phenylephrine (100-300 microg) to maintain mean arterial pressure within 20% of baseline during 1.5 MAC anesthesia. Conclusions In common with other volatile anesthetic agents, sevoflurane has an intrinsic dose-dependent cerebral vasodilatory effect. However, this effect is less than that of isoflurane.

scholarly journals Adenosine receptor-dependent signaling is not obligatory for normobaric and hypobaric hypoxia-induced cerebral vasodilation in humans

2017 ◽  
Vol 122 (4) ◽  
pp. 795-808 ◽  
Author(s):  
Ryan L. Hoiland ◽  
Anthony R. Bain ◽  
Michael M. Tymko ◽  
Mathew G. Rieger ◽  
Connor A. Howe ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
High Altitude ◽  
Sea Level ◽  
Adenosine Receptor ◽  
Hypobaric Hypoxia ◽  
End Tidal ◽  
Double Blinded

Hypoxia increases cerebral blood flow (CBF) with the underlying signaling processes potentially including adenosine. A randomized, double-blinded, and placebo-controlled design, was implemented to determine if adenosine receptor antagonism (theophylline, 3.75 mg/Kg) would reduce the CBF response to normobaric and hypobaric hypoxia. In 12 participants the partial pressures of end-tidal oxygen ([Formula: see text]) and carbon dioxide ([Formula: see text]), ventilation (pneumotachography), blood pressure (finger photoplethysmography), heart rate (electrocardiogram), CBF (duplex ultrasound), and intracranial blood velocities (transcranial Doppler ultrasound) were measured during 5-min stages of isocapnic hypoxia at sea level (98, 90, 80, and 70% [Formula: see text]). Ventilation, [Formula: see text] and [Formula: see text], blood pressure, heart rate, and CBF were also measured upon exposure (128 ± 31 min following arrival) to high altitude (3,800 m) and 6 h following theophylline administration. At sea level, although the CBF response to hypoxia was unaltered pre- and postplacebo, it was reduced following theophylline ( P < 0.01), a finding explained by a lower [Formula: see text] ( P < 0.01). Upon mathematical correction for [Formula: see text], the CBF response to hypoxia was unaltered following theophylline. Cerebrovascular reactivity to hypoxia (i.e., response slope) was not different between trials, irrespective of [Formula: see text]. At high altitude, theophylline ( n = 6) had no effect on CBF compared with placebo ( n = 6) when end-tidal gases were comparable ( P > 0.05). We conclude that adenosine receptor-dependent signaling is not obligatory for cerebral hypoxic vasodilation in humans. NEW & NOTEWORTHY The signaling pathways that regulate human cerebral blood flow in hypoxia remain poorly understood. Using a randomized, double-blinded, and placebo-controlled study design, we determined that adenosine receptor-dependent signaling is not obligatory for the regulation of human cerebral blood flow at sea level; these findings also extend to high altitude.

scholarly journals Features of cerebral blood flow in patients with chronic obstructive pulmonary disease associated with hypertension

2021 ◽  
Vol 26 (6) ◽  
pp. 676-687
Author(s):  
N. B. Poletaeva ◽  
O. V. Teplyakova ◽  
I. F. Grishina ◽  
A. A. Klepikova
Keyword(s):  
Blood Pressure ◽  
Chronic Obstructive Pulmonary Disease ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Carotid Artery ◽  
Blood Flow Velocity ◽  
Flow Index ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Blood Flow Index

Objective. The aim of the work was to study the features of cerebral blood flow in patients with chronic obstructive pulmonary disease (COPD) associated with hypertension (HTN). Design and methods. A crosssectional study was conducted, which included 90 males 40–60 years old. Of these, 30 patients with chronic COPD associated with HTN (COPD + HTN) were included in the study group, 30 individuals with isolated COPD were in the comparison group, 30 healthy volunteers were included in the control group. All participants underwent physical examination, spirography, 24-hour blood pressure monitoring and ultrasound examination of cerebral vessels. Results. Patients with COPD + HTN in comparison with the control showed an increase in the diameter (p = 0,018) and complex of the intima-media of the common carotid artery (p = 0,003) while the velocities, resistance index (RI) and pulsation index (PI) did not change. In the basin of the internal carotid artery an increase in RI values was noted (p = 0,018). At the intracranial level there was a decrease in the end-diastolic velocity (p = 0,03) and the time-averaged average blood flow velocity (TAV) (p = 0,033) without due changes RI and PI. At the same time no changes in speed indicators and indices were noted in the vertebral artery basin. Among the indicators of cerebral perfusion in patients with COPD + HTN, hydrodynamic resistance (p = 0,0015), intracranial pressure (ICP) (p = 0,0048) significantly increased, and the cerebral blood flow index was comparable with the control. Assessment of venous cerebral blood flow showed an increase in the diameter of the internal jugular vein (p = 0,021) with unchanged TAV together with an increase in ICP indicating the formation of venous dysfunction. It was shown that the body mass index, forced expiratory volume at the first second, systolic and diastolic blood pressure together determine the peak systolic blood flow velocity from the midbrain artery. Conclusions. The cerebral blood flow in patients with COPD + HTN is characterized by a change in arterial blood flow at the level of both intra- and extracranial vessels, while maintaining a normal cerebral blood flow index, as well as the formation of arteriovenous dyshemia against the background of remodeling of the cerebral vascular bed.

Ventilatory, cerebrovascular, and cardiovascular interactions in acute hypoxia: regulation by carbon dioxide

2004 ◽  
Vol 97 (1) ◽  
pp. 149-159 ◽  
Author(s):  
Philip N. Ainslie ◽  
Marc J. Poulin
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Blood Flow Velocity ◽  
Acute Hypoxia ◽  
Random Order ◽  
Transcranial Doppler Ultrasound ◽  
Individual Variability ◽  
Cerebral Vasoconstriction ◽  
Arterial Blood ◽  
End Tidal

This study examined the effect of high, normal, and uncontrolled end-tidal Pco2 (PetCO2) on the ventilatory, peak cerebral blood flow velocity ( V̄p), and mean arterial blood pressure (MAP) responses to acute hypoxia. Nine healthy subjects undertook, in random order, three hypoxic protocols (end-tidal Po2 was held at eight steps between 300 and 45 Torr) in conditions of hypercapnia, isocapnia, or poikilocapnia (PetCO2 +7.5 Torr, +1.0 Torr, or uncontrolled, respectively). Transcranial Doppler ultrasound was used to measure V̄p in the middle cerebral artery. The slopes of the linear regressions of ventilation, V̄p, and MAP with arterial O2 saturation were significantly greater in hypercapnia than in both isocapnia and poikilocapnia ( P < 0.05). Strong, significant correlations were observed between ventilation, V̄p, and MAP with each PetCO2 condition. These data suggest that 1) a high acute hypoxic ventilatory response (AHVR) decreases the acute hypoxic cerebral blood flow responses during poikilocapnia hypoxia, due to hypocapnic-induced cerebral vasoconstriction; and 2) in hypercapnic hypoxia, a high AHVR is associated with a high acute hypoxic cerebral blood flow response, demonstrating a linkage of individual sensitivities of ventilation and cerebral blood flow to the interaction of PetCO2 and hypoxia. In summary, the between-individual variability in AHVR is shown to be firmly linked to the variability in V̄p and MAP responses to hypoxia. Individuals with a high AHVR are found also to have high V̄p and MAP responses to hypoxia.

scholarly journals Animal model of assessing cerebrovascular functional reserve by imaging photoplethysmography

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Oleg V. Mamontov ◽  
Alexey Y. Sokolov ◽  
Maxim A. Volynsky ◽  
Anastasija V. Osipchuk ◽  
Valery V. Zaytsev ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Animal Model ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Systemic Blood Pressure ◽  
Functional Reserve ◽  
Systemic Blood ◽  
Flow Reserve ◽  
Custom Made ◽  
End Tidal

Abstract Assessment of the cerebral blood-flow-reserve in patients with cerebrovascular diseases is extremely important in terms of making prognosis, determining treatment tactics, and controlling the revascularization outcome in the case of reconstructive interventions on the brain vessels. However, there is no easy-to-use, contactless method for either assessing the functional reserve of the cortical vascular network or intraoperative monitoring of surgical intervention. Our study aims to demonstrate feasibility of green-light imaging photoplethysmography (iPPG) to estimate cerebrovascular functional reserve in animal model of craniosurgical intervention. Custom-made iPPG system was exploited to visualize intracranial vessels in anesthetized Wistar rats (n = 15). Video frames of rat’s cortex were recorded concurrently with systemic blood pressure, end-tidal CO2, and electrocardiogram. We found that injection of dorzolamide (carbonic-anhydrase inhibitor) significantly increased the blood-pulsations amplitude in all animals by 35 ± 19% (p < 0.001). Such an increase negatively correlated with significant decrease in end-tidal CO2 by 32 ± 7% (p < 0.001). It is noteworthy that the dorzolamide injection did not lead to significant changes in systemic blood pressure. Concluding, pulsations amplitude is a marker of the vascular tone that can be used to evaluate the functional cerebrovascular reserve. Imaging PPG is a simple and convenient method to assess cerebral blood flow, including during various neurosurgical interventions.

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.

scholarly journals Cerebral blood flow regulation in women across menstrual phase: differential contribution of cyclooxygenase to basal, hypoxic, and hypercapnic vascular tone

2016 ◽  
Vol 311 (2) ◽  
pp. R222-R231 ◽  
Author(s):  
Garrett L. Peltonen ◽  
John W. Harrell ◽  
Benjamin P. Aleckson ◽  
Kaylie M. LaPlante ◽  
Meghan K. Crain ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Menstrual Cycle ◽  
Transcranial Doppler Ultrasound ◽  
Follicular Phase ◽  
Cerebrovascular Reactivity ◽  
Menstrual Phase ◽  
Arterial Blood ◽  
End Tidal ◽  
Late Follicular Phase

In healthy young women, basal cerebral blood flow (CBF) and cerebrovascular reactivity may change across the menstrual cycle, but mechanisms remain untested. When compared with the early follicular phase of the menstrual cycle, we hypothesized women in late follicular phase would exhibit: 1) greater basal CBF, 2) greater hypercapnic increases in CBF, 3) greater hypoxic increases in CBF, and 4) increased cyclooxygenase (COX) signaling. We measured middle cerebral artery velocity (MCAv, transcranial Doppler ultrasound) in 11 healthy women (23 ± 1 yr) during rest, hypoxia, and hypercapnia. Subjects completed four visits: two during the early follicular (∼ day 3) and two during the late follicular (∼ day 14) phases of the menstrual cycle, with and without COX inhibition (oral indomethacin). Isocapnic hypoxia elicited an SPO2 = 90% and SPO2 = 80% for 5 min each. Separately, hypercapnia increased end-tidal CO2 10 mmHg above baseline. Cerebral vascular conductance index (CVCi = MCAv/MABP·100, where MABP is mean arterial blood pressure) was calculated and a positive change reflected vasodilation (ΔCVCi). Basal CVCi was greater in the late follicular phase ( P < 0.001). Indomethacin decreased basal CVCi (∼37%) and abolished the phase difference ( P < 0.001). Hypoxic ΔCVCi was similar between phases and unaffected by indomethacin. Hypercapnic ΔCVCi was similar between phases, and indomethacin decreased hypercapnic ΔCVCi (∼68%; P < 0.001) similarly between phases. In summary, while neither hypercapnic nor hypoxic vasodilation is altered by menstrual phase, increased basal CBF in the late follicular phase is fully explained by a greater contribution of COX. These data provide new mechanistic insight into anterior CBF regulation across menstrual phases and contribute to our understanding of CBF regulation in women.

Caffeine and Cerebral Blood Flow

1983 ◽  
Vol 143 (6) ◽  
pp. 604-608 ◽  
Author(s):  
Roy J. Mathew ◽  
Deborah L. Barr ◽  
Maxine L. Weinman
Keyword(s):  
Carbon Dioxide ◽  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Respiratory Rate ◽  
Regional Cerebral Blood Flow ◽  
Inhalation Technique ◽  
Regional Cerebral Blood ◽  
End Tidal Carbon Dioxide ◽  
End Tidal

SummaryTwo groups of normal volunteers had regional cerebral blood flow (rCBF) measured, by the 133Xenon inhalation technique, before and 30 minutes after 250 mg or 500 mg caffeine given orally. rCBF was measured in a third group of subjects, twice, at a similar interval under identical laboratory conditions. Subjects who received caffeine showed significant decreases in rCBF while the others showed no rCBF change from the first to the second measurement. However, the two caffeine groups did not differ in degrees of rCBF reduction. There were no regional variations in the post-caffeine decrease in cerebral blood flow. The three groups did not show significant changes in end-tidal carbon dioxide, pulse rate, blood pressure, forehead skin temperature and respiratory rate.

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