Artery Mean Blood Flow Velocity Research Articles

Combined Transcranial Doppler and Melatonin Levels to Predict Delayed Cerebral Ischemia After Subarachnoid Hemorrhage.

To investigate the early prediction value of transcranial Doppler ultrasound (TCD) combined with serum melatonin level for delayed cerebral ischemia (DCI) caused by subarachnoid hemorrhage (SAH). This paper is a prospective study. A total of 120 patients with SAH treated were included. The patients were divided into the DCI group (40 cases) and non-DCI group (80 cases) according to whether DCI occurred 14 days after SAH (DCI usually occurs 4 to 14d after bleeding). Baseline data, serum melatonin level, and TCD test results within 24hours after admission were compared between the 2 groups. Multivariate logistic analysis was used to analyze the factors affecting the occurrence of DCI after SAH. The value of serum melatonin level, middle cerebral artery mean blood flow velocity (MBFV) and their combination in predicting DCI in SAH patients was evaluated. Univariate analysis showed that there were statistically significant differences in the proportion of Fisher grade, Hunt-Hess grade, serum melatonin level, middle cerebral artery systolic blood flow velocity (Vs), MBFV and pulse index (PI) between the 2 groups (P<0.05). Serum melatonin levels, middle cerebral artery Vs, MBFV, and PI in the DCI group were higher than those in non-DCI group. Logistic regression (LR) analysis showed that serum melatonin level (OR=1.796, 95% CI: 1.575-4.123) and middle cerebral artery MBFV (OR=3.279, 95% CI: 2.112-4.720] were the influencing factors for DCI in SAH patients (P<0.05). Middle cerebral artery MBFV and serum melatonin levels were higher in patients with SAH complicated with DCI, and the combination of the 2 could provide a reference for early clinical prediction of DCI in patients with aneurysmal subarachnoid hemorrhage (aSAH).

The value of transcranial Doppler monitoring of cerebral blood flow changes during carotid endarterectomy performed under regional anesthesia - A case series.

Patients with unilateral hemodynamically significant carotid stenosis scheduled for elective CEAs were included. Ultrasound-guided intermediate plexus block was used for regional anesthesia. TCD monitoring of the middle cerebral artery mean blood flow velocity (MCAV) was performed throughout the procedure. MCAVs were offline analyzed during different phases of CEA: (1) resting state, before regional block, (2) after block, before incision, (3) before cross-clamp, (4) after cross-clamp, (5) 5 min after cross-clamp, (6) 10 min after cross-clamp, (7) after declamping, and (8) during the postoperative period (4-6 h). Shunt insertion based on the deterioration of neurological symptoms after cross-clamping was necessary for 11/66 patients (16.6%). In these symptomatic patients, the ipsilateral percent decrease of the MCAV was more than 70% in 8 out of 11 cases (72.7%). In asymptomatic patients, without shunt insertion, the average decrease of MCAV was less than 50%. Neurological symptoms referring to cerebral ischemia may be superior to TCD monitoring of cerebral blood flow for detecting the necessity of a shunt. Regional anesthesia enables reliable, symptom-based monitoring of CEAs.

Which repetitive transcranial magnetic stimulation modality affects vasomotor reactivity in healthy subjects and how long does it last?

Objectives The aim of our study was to evaluate the effects of low and high-frequency repetitive transcranial magnetic stimulation (rTMS) on hypoxia-induced changes in bilateral cerebrovascular reserve up to 24 h in the same individuals. Methods Right-handed ten healthy male individuals participated in the study. All participants had neither drug therapy nor a concomitant disease and none of them had a variation in the circle of Willis, intracranial stenosis, arteriovenous malformation, or aneurysm which may have an impact on transcranial doppler ultrasound (TCD) examination and transcranial magnetic stimulation (TMS) recording. Results There was a statistically significant difference in the breath‐holding index (BHI) between before and after 0, 15, 30 min after 1 Hz repetitive stimulation (p < 0.05). When applying 5 Hz repetitive stimulation there was no difference before and after BHI values (p > 0.05). There were no differences in bilateral, ipsilateral, or contralateral middle cerebral artery (MCA) mean cerebral blood flow velocity (CBFV) after low or high-frequency rTMS application (p > 0.05). Conclusion The main result of the study was that low-frequency rTMS reduced vasomotor reactivity (VMR) for the very first 30 min and then this effect disappears. And the high-frequency rTMS did not affect VMR at all. Significance The effect of rTMS on VMR may continue up to 30 min but then return to the baseline and can be used safely.

The influence of blood flow velocity changes to postoperative cognitive dysfunction development in patients undergoing heart surgery with cardiopulmonary bypass.

The aim of this study was to compare blood flow velocity changes in the middle cerebral artery before, during and after heart surgery with cardiopulmonary bypass for patients with and without postoperative cognitive dysfunction. A total of 100 patients, undergoing elective coronary artery bypass grafting or/and valve surgery enrolled in the study. A neurocognitive test evaluation included Adenbrooke, Mini-Mental State Examination and Trial Making test before and 7-10 days after surgery. Middle cerebral artery mean blood flow velocity was evaluated 1 day before the surgery, after anaesthesia induction, before cardiopulmonary bypass, at the beginning, ending and after cardiopulmonary bypass, and post surgery in intensive care unit. Blood samples for glial fibrillary acidic protein were measured after anaesthesia induction, 24 hours and 48 hours after surgery. According to neurocognitive tests results patients were divided in to two groups: patients with and without postoperative cognitive dysfunction. Of the 100, 86 patients completed investigation. After induction, blood flow velocity of the middle cerebral artery was lower in postoperative cognitive dysfunction group (41.2; min 27.91, max 49.47) than in the H group (41.2, min 21.9, max 84.3) p = 0.034, and during cardiopulmonary bypass, blood flow velocity of the middle cerebral artery was lower in the postoperative cognitive dysfunction group (37.35, min 26.6, max 44.02) than the H group (42.3, min 20.1, max 86.5), p = 0.001. After the surgery, blood flow velocity of the middle cerebral artery was lower in the postoperative cognitive dysfunction group (40.7, min 29.7, max 50.4) than in the H group (45.3, min 34.12, max 59.88), p = 0.05. Results of cognitive tests had weak correlation (rho, 0.391) with middle cerebral artery's blood flow velocity after anaesthesia induction (p = 0.001) and during bypass (p = 0.018). The receiver operating characteristic analysis showed that the blood flow velocity of the middle cerebral artery during bypass (area under the curve = 0.735) was a fair predictor for postoperative cognitive dysfunction (p = 0.001). No significant correlations were found among glial fibrillary acidic protein, middle cerebral artery blood flow velocity, and cognitive tests results. Middle cerebral artery's blood flow velocity was decreased after anaesthesia induction and during cardiopulmonary bypass for patients with postoperative cognitive dysfunction comparing with their blood flow velocity preoperatively. Blood flow velocity during bypass has diagnostic value for postoperative cognitive dysfunction. Brain biomarker glial fibrillary acidic protein is not helpful in diagnosing postoperative cognitive dysfunction.

Preoperative transcranial Doppler and cerebral oximetry as predictors of delirium following valvular heart surgery: a case-control study.

Delirium is a frequent and serious complication after cardiac surgery with cerebral hypoperfusion as one from the key pathophysiological mechanisms. Middle cerebral artery (MCA) mean blood flow velocity (MFV) measured by transcranial Doppler has been used as a marker of cerebral perfusion, and cerebral oximetry (rSO2) value as a marker of its adequacy. This prospective observational trial examined the predictive value of MCA MFV and rSO2, measured immediately before induction of anesthesia, for delirium after valvular heart surgery in elderly patients. In 113 patients, delirium was evaluated for 7days postoperatively, using the confusion assessment method for the intensive care unit. The primary endpoint was the occurrence of postoperative delirium. Overall, 16 patients (14%) exhibited delirium. MCA MVF values could not predict the development of delirium. Preoperative statin use, geriatric depression scale score, and low preoperative rSO2 (< 60%) showed association with delirium occurrence in univariable analysis. After multivariable analysis, only the low preoperative rSO2 (< 60%) (OR 6.748, 95% CI 1.647-27.652, P = 0.008) remained as an independent predictor of delirium. Preoperative MCA MFV was not significantly associated with delirium after valvular heart surgery in elderly patients, while a low baseline rSO2 value was associated with a sevenfold increased risk of delirium.

Neurovascular coupling and cerebral autoregulation in atrial fibrillation

The risk of cognitive decline and stroke is increased by atrial fibrillation (AF). We sought to determine whether neurovascular coupling and cerebral autoregulation are blunted in people with AF in comparison with age-matched, patients with hypertension and healthy controls. Neurovascular coupling was assessed using five cycles of visual stimulation for 30 s followed by 30 s with both eyes-closed. Cerebral autoregulation was examined using a sit–stand test, and a repeated squat-to-stand (0.1 Hz) manoeuvre with transfer function analysis of mean arterial pressure (MAP; input) and middle cerebral artery mean blood flow velocity (MCA Vm; output) relationships at 0.1 Hz. Visual stimulation increased posterior cerebral artery conductance, but the magnitude of the response was blunted in patients with AF (18 [8] %; mean [SD]) and hypertension (17 [8] %), in comparison with healthy controls (26 [9] %) (P < 0.05). In contrast, transmission of MAP to MCA Vm was greater in AF patients compared to hypertension and healthy controls, indicating diminished cerebral autoregulation. We have shown for the first time that AF patients have impaired neurovascular coupling responses to visual stimulation and diminished cerebral autoregulation. Such deficits in cerebrovascular regulation may contribute to the increased risk of cerebral dysfunction in people with AF.

Does respiratory drive modify the cerebral vascular response to changes in end-tidal carbon dioxide?

What is the central question of this study? There is an interaction between the regulatory systems of respiration and cerebral blood flow, because the mediator (CO2 ) is the same for both physiological systems. We examined whether the traditional method for determining cerebrovascular reactivity to CO2 is modified by changes in respiration. What is the main finding and its importance? Cerebrovascular reactivity was modified by voluntary changes in respiration during hypercapnia. This finding suggests that an alteration in the respiratory system may result in under- or overestimation of cerebrovascular reactivity determined by traditional methods in healthy adults. The cerebral vasculature is sensitive to changes in the arterial partial pressure of CO2 . This physiological mechanism has been well established as a cerebrovascular reactivity to CO2 (CVR). However, arterial CO2 may not be an independent variable in the traditional method for assessment of CVR, because the cerebral blood flow response is also affected by the activation of respiratory drive or higher centres in the brain. We hypothesized that CVR is modified by changes in respiration. To test our hypothesis, in the present study, 10 young, healthy subjects performed hyper- or hypoventilation to change end-tidal CO2 ( ) with different concentrations of CO2 in the inhaled gas (0, 2.0 and 3.5%). We measured middle cerebral artery mean blood flow velocity by transcranial Doppler ultrasonography to identify the cerebral blood flow response to change in during each set of conditions. In each set of conditions, was significantly altered by changes in ventilation, and middle cerebral artery mean blood flow velocity changed accordingly. However, the relationship between changes in middle cerebral artery mean blood flow velocity and as a response curve of CVR was reset upwards and downwards by hypo- and hyperventilation, respectively, compared with CVR during normal ventilation. The findings of the present study suggest the possibility that an alteration in respiration might lead to under- or overestimation of CVR determined by the traditional methods.

Measuring Cerebral Carbon Dioxide Reactivity With Transcranial Doppler and Near-Infrared Spectroscopy in Children With Ventricular Septal Defect

Neurologic impairment is frequently observed in children with congenital heart disease. Impairment in cerebrovascular carbon dioxide reactivity (CO2R) is related with poor neurologic outcomes. The present study examined CO2R measured with transcranial Doppler (TCD) and near-infrared spectroscopy (NIRS) in children with ventricular septal defect undergoing cardiac surgery. Prospective, paired controlled study. Operating room of a tertiary care center. Twenty children with ventricular septal defect and younger than 1 year were enrolled, and 17 children were studied (age: 6.0 ± 2.0 mo, weight 5.9 ± 1.0 kg). After induction of anesthesia and tracheal intubation, the lungs were ventilated and mechanical ventilation was initiated. Partial pressure of end-tidal carbon dioxide (PETCO2) was adjusted at 4 different levels (30, 35, 40, and 45 mmHg). Paired measurements of middle cerebral artery mean blood flow velocity (VMCA) by TCD and tissue oxygen index (TOI) by NIRS were recorded at each level of PETCO2. CO2R was calculated as the percentage change of VMCA and TOI per mmHg change in PETCO2. Systemic hemodynamic parameters were recorded. As PETCO2 rose from 30 to 45 mmHg, VMCA and TOI increased linearly (p < 0.001 for both), and CO2R-TCD and CO2R-NIRS were calculated to be 2.8% ± 0.9%/mmHg and 1.2% ± 0.3 %/mmHg, respectively. CO2R-NIRS was significantly lower compared with CO2R-TCD (p < 0.001). Significant correlations were found between VMCA and TOI (r = 0.487; p < 0.001) and between ΔVMCA and ΔTOI (r = 0.693; p < 0.001), but not between CO2R-TCD and CO2R-NIRS (r = 0.18; p = 0.24). With the increase of PETCO2, cardiac index, systemic vascular resistance index, and mean arterial pressure remained constant (p > 0.05 for all) and the heart rate decreased significantly (p = 0.018). During anesthesia, CO2R remains preserved in children with a ventricular septal defect. Even though there is lack of correlation between CO2R-TCD and CO2R-NIRS, changes in TOI and VMCA were correlated as the PETCO2 changed. NIRS may be used as a surrogate to investigate CO2R when the ultrasound window is poor.

Cardiorespiratory and Cerebrovascular Responses to Leg Cycling Exercise during Muscle Metaboreflex Activation with Blood Flow Restriction in Moderate Normobaric Hypoxia

Skeletal muscle blood flow restriction and normobaric hypoxia are strategies adopted during exercise training because the associated reductions in local or systemic oxygenation may enhance athletic performance. Both manoeuvres evoke cardiorespiratory and cerebrovascular responses but have not been studied in combination. Blood flow restriction during exercise activates metabolically sensitive group III and IV skeletal muscle afferents (i.e., muscle metaboreflex activation), while systemic hypoxia activates the peripheral chemoreflex. We sought to determine whether the cardiorespiratory and cerebrovascular response to muscle metaboreflex activation with blood flow restriction during leg cycling exercise is augmented in moderate normobaric hypoxia.Nine healthy men (age 23±2 years; mean±SE) participated in two experimental trials performed under normoxic (fraction of inspired O2 [FiO2] = 21 %) and hypoxic (FiO2 = 13.5 %; equivalent of altitude of 3500 m) conditions whilst seated in a semi‐recumbent position in an environmental chamber. Trials consisted of a resting baseline period (3 min), followed by low intensity leg cycling exercise (64±7 Watts) under free‐flow conditions (~3½ min), and then bilateral thigh cuff inflation to 100 mmHg to induce blood flow restriction and muscle metaboreflex activation (~3 ½ min). Peripheral capillary oxygen saturation (SpO2; finger pulse oximetry), mean arterial pressure (MAP; Finometer and SunTech), heart rate (HR; electrocardiogram), the partial pressure of end‐tidal carbon dioxide (PETCO2; capnography), minute ventilation (VE; pneumotachometer) and middle cerebral artery mean blood flow velocity (MCAV; transcranial Doppler) were recorded.At baseline, SpO2 was lower during hypoxia (87±1 %) than normoxia (97±1 %; P&lt;0.05), but MAP, HR, PETCO2, VE and MCAv were not different between trials (P&gt;0.05). Leg cycling under free‐flow conditions significantly increased MAP, HR, PETCO2, VE and MCAv (P&lt;0.05 vs. baseline), with no differences observed between hypoxic and normoxic trials (P&gt;0.05). MAP (Δ14±2 vs. Δ16±2 mmHg; P=0.215), HR (Δ10±2 vs. Δ8±3 b·min−1; P=0.251), PETCO2 (Δ−1.1±0.3 vs. Δ−3.4±1.8 mmHg; P=0.596), VE (Δ4±1 vs. Δ4±1 L·min−1; P=0.446) and MCAv (Δ4±2 vs. Δ4±1 cm·s−1; P=0.408) responses to blood flow restriction during leg cycling (i.e., muscle metaboreflex activation) were not different in the hypoxic and normoxic trials.These preliminary findings suggest that moderate normobaric hypoxia (FiO2 = 13.5 %) does not augment the cardiorespiratory and cerebrovascular responses to muscle metaboreflex activation with blood flow restriction during low intensity leg cycling.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Cerebral Autoregulation Is Impaired In Recurrent Syncope Patients

PURPOSE: Cerebral autoregulation is a homeostatic mechanism that serves to maintain cerebral blood flow constant over a wide range of perfusion pressure. Syncope is thought to be caused by cerebral hypoperfusion due to the transient blood pressure drop, and thus impairment of cerebral autoregulation may facilitate syncope. A previous study has reported that a past history of syncope is a strong predictor of future syncope recurrence. However, it is unclear whether impaired cerebral autoregulation would be related with recurrent syncope. The purpose of this study was to test our hypothesis that cerebral autoregulation would be impaired in syncope patients with a past history of syncope as compared with those for the first time. METHODS: We evaluated cerebral autoregulation in 24 syncope patients for the first time (age; 64±19 years old, male/ female; 15/9) and 20 syncope patients with a past history of syncope (age; 52±26 years old, male/female; 11/9). In patients with recurrent syncope, the number of past syncope was 2.9±1.6 times (range 2-7 times). Middle cerebral artery mean blood flow velocity (MCA Vmean) and mean arterial pressure (MAP) were measured by transcranial Doppler ultrasound and tonometry on right radial artery for 3 min in the supine position. In offline analysis after the measurement, the transfer function gain between MAP and MCA Vmean were calculated at very low frequency (0.023-0.07 Hz, VLF) and low frequency (0.07-0.2 Hz, LF) ranges to estimate dynamic cerebral autoregulation. RESULTS: LF gain did not differ between syncope patients with a past history of syncope and those for the first time (P=0.23). In contrast, VLF gain was significantly higher in patients with a past history of syncope than in those for the first time (1.81±1.17 cm/s/mmHg vs. 1.09±0.65 cm/s/mmHg, P=0.02). CONCLUSIONS: These data suggest that impaired cerebral autoregulation at least in part explains physiological mechanisms underlying recurrent syncope.

Increased middle cerebral artery mean blood flow velocity index after stroke thrombectomy indicates increased risk for intracranial hemorrhage

Background and purposeCerebral hyperperfusion has been related to the risk of intracranial hemorrhage (ICH) in stroke patients after vessel recanalization therapy. We hypothesized that after successful mechanical thrombectomy for acute...

Tympanic membrane temperature decreases during head up tilt: relation to frontal lobe oxygenation and middle cerebral artery mean blood flow velocity

Introduction: Changes in blood flow influence temperature of surrounding tissues. Since the internal carotid artery (ICA) and internal jugular vein (IJV) neighbor the tympanic membrane, changes in their blood flow most likely determine changes in tympanic membrane temperature (TMT). We sought to evaluate the relationship between changes during a head-up tilt (HUT) induced reduction in cerebral blood flow (CBF) and TMT.Methods: Ten male subjects (age 19–28 years) underwent 50° HUT until presyncope. A non-contact infrared sensor in the ear canal targeted the tympanic membrane. Changes in CBF were monitored by transcranial Doppler which determined the mean blood flow velocity in the middle cerebral artery (MCA Vmean) and by near infrared spectroscopy assessed frontal lobe oxygenation (ScO2), while skin blood flow (SkBF) was evaluated by laser Doppler flowmetry.Results: During HUT, TMT decreased by 0.6 °C (median; range 0.2 to 1.6 °C) related to a decrease in MCA Vmean (51.0 ± 6.7 to 34.3 ± 5.8 cm/sec (mean ± SD); r = 0.518, p = .002) and ScO2 (78.6 ± 5.4% to 69.0 ± 5.7%; r = 0.352, p = .043), but not to SkBF (120 ± 78 to 69 ± 37 PU; r = 0.245, p = .142).Conclusion: During an orthostatic challenge TMT decreases and the decrease is related to a reduction in CBF as indicated by MCA Vmean and ScO2, but not to SkBF. We consider TMT holds potential for non-invasive assessment of changes in cerebral perfusion.

Muscle oxygen saturation increases during head-up tilt-induced (pre)syncope.

To evaluate whether muscle vasodilatation plays a role for hypotension developed during central hypovolaemia, muscle oxygenation (Sm O2 ) was examined during (pre)syncope induced by head-up tilt (HUT). Skin blood flow (SkBF) and oxygenation (Sskin O2 ) were determined because evaluation of Sm O2 may be affected by superficial tissue oxygenation. Furthermore, we evaluated cerebral oxygenation (Sc O2 ) and middle cerebral artery mean blood flow velocity (MCAvmean ). Twenty healthy male volunteers (median age 24 years; range 19-38) were subjected to passive 50° HUT for 1 h or until (pre)syncope. Sc O2 and Sm O2 (near-infrared spectroscopy), MCAvmean (transcranial Doppler) along with mean arterial pressure (MAP), heart rate (HR), stroke volume (SV), cardiac output (CO) and total peripheral resistance (TPR) (Modelflow® ) were determined. (Pre)syncopal symptoms appeared in 17 subjects after 11 min (median; range 2-34) accompanied by a decrease in MAP, SV, CO and TPR, while HR remained elevated. During (pre)syncope, Sc O2 decreased [73% (71-76; mean and 95% CI) to 68% (65-71), P < 0.0001] along with MCAvmean [40 (37-43) to 32 (29-35) cm s-1 , P < 0.0001]. In contrast, Sm O2 increased [63 (56-69)% to 71% (65-78), P < 0.0001], while Sskin O2 [64% (58-69) to 53% (47-58), P < 0.0001] and SkBF [71 (44-98) compared to a baseline of 99 (72-125) units, P = 0.020] were reduced. We confirm that the decrease in MAP during HUT is associated with a reduction in indices of cerebral perfusion. (Pre)syncope was associated with an increase in Sm O2 despite reduced Sskin O2 and SkBF, supporting that muscle vasodilation plays an important role in the circulatory events leading to hypotension during HUT.

The effect of an acute increase in central blood volume on the response of cerebral blood flow to acute hypotension.

The purpose of the present study was to examine whether the response of cerebral blood flow to an acute change in perfusion pressure is modified by an acute increase in central blood volume. Nine young, healthy subjects voluntarily participated in this study. To measure dynamic cerebral autoregulation during normocapnic and hypercapnic (5%) conditions, the change in middle cerebral artery mean blood flow velocity was analyzed during acute hypotension caused by two methods: 1) thigh-cuff occlusion release (without change in central blood volume); and 2) during the recovery phase immediately following release of lower body negative pressure (LBNP; -50 mmHg) that initiated an acute increase in central blood volume. In the thigh-cuff occlusion release protocol, as expected, hypercapnia decreased the rate of regulation, as an index of dynamic cerebral autoregulation (0.236 ± 0.018 and 0.167 ± 0.025 s(-1), P = 0.024). Compared with the cuff-occlusion release, the acute increase in central blood volume (relative to the LBNP condition) with LBNP release attenuated dynamic cerebral autoregulation (P = 0.009). Therefore, the hypercapnia-induced attenuation of dynamic cerebral autoregulation was not observed in the LBNP release protocol (P = 0.574). These findings suggest that an acute change in systemic blood distribution modifies dynamic cerebral autoregulation during acute hypotension.

The Effect Of An Acute Increase In Central Blood Volume On Dynamic Cerebral Autoregulation

Previous investigations demonstrated that cerebral blood flow was influenced by changes in central blood volume and arterial blood pressure even within the range of cerebral autoregulation (60-150 mmHg). Recently, we found that during acute microgravity (parabolic flight condition), the acute increase in central blood volume decreased gradually arterial blood pressure via the arterial and cardiopulmonary baroreflexes. Despite the acute hypotension and central hypervolemia, steady-state cerebral blood flow was well maintained during this condition. However, the dynamic relationship between central blood volume and cerebrovascular control remains unclear. PURPOSE: The purpose of the present study was to examine dynamic cerebral autoregulation during an acute hypotension with central hypervolemia. METHODS: Nine young healthy subjects voluntarily participated in this study. In order to measure dynamic cerebral autoregulation, change in middle cerebral artery mean blood flow velocity (MCA Vmean) was analyzed during acute hypotension caused by two methods: 1) thigh-cuff occlusion release (without change in central blood volume) and 2) lower body negative pressure (-50 mmHg, LBNP) release (with acute increase in central blood volume). RESULTS: As expected, the thigh-cuff occlusion release caused acute hypotension and decrease in MCA Vmean accordingly, but MCA Vmean returned to the baseline value quickly. LBNP release increased and then decreased arterial blood pressure acutely. During the phase of decreased arterial blood pressure, however, the rate of regulation, as an index of dynamic cerebral autoregulation during LBNP release, was significantly lower than that during cuff release (0.112 ± 0.116 and 0.236 ± 0.053 sec-1, respectively, P=0.030). CONCLUSIONS: These findings suggest that an acute change in central blood volume modifies dynamic cerebral autoregulation.

The effect of an acute increase in central blood volume on hypercapnia‐induced attenuation in dynamic cerebral autoregulation

It is well established that hypercapnia attenuates dynamic cerebral autoregulation. The impact of central blood volume on cerebral blood flow is controversial. The purpose of the present study was to examine whether hypercapnia‐induced attenuation in dynamic cerebral autoregulation is modified by acute central hypervolemia. Nine young healthy subjects voluntarily participated in this study. In order to measure dynamic cerebral autoregulation during normocapnic and hypercapnic (5%) conditions, the change in middle cerebral artery mean blood flow velocity (MCA Vmean) was analyzed during acute hypotension caused by two methods: 1) thigh‐cuff occlusion release (without change in central blood volume) and 2) lower body negative pressure (‐50 mmHg, LBNP) release (with acute increase in central blood volume). As expected, hypercapnia decreased the rate of regulation, as an index of dynamic cerebral autoregulation (0.236±0.053 and 0.167±0.074 sec‐1, respectively, P=0.025). In contrast, this attenuation was disappeared during central hypervolemia (P=0.574). This phenomenon may be associated with hypervolemia‐induced attenuation of dynamic cerebral autoregulation (P=0.009). These findings suggest that an acute change in central blood volume modifies carbon dioxide‐induced changes in dynamic cerebral autoregulation.

Abstract WP186: Association Between Blood Pressure, Internal Carotid Artery Flow Parameters And Age-related White Matter Disease

Background: White matter lesions (WML) are associated with hypertension. Blood pressure (BP) is transmitted to the brain via the carotid arteries, and autoregulation helps protect the brain. We investigated if BP via carotid waveform parameters were associated with WML. Methods: We obtained BP measurements from a cohort of community dwelling subjects at mean ages 70±1 and 73±1 years; brain MRI and carotid artery ultrasound at mean age 73±1 years. We calculated mean values of BP (systolic, diastolic, mean, variability and pulsatility), measured WML by volume, and Fazekas scale. We calculated internal carotid artery (ICA) mean blood flow velocity, pulsatility index (PI), and resistivity index (RI). We tested associations between BP and ICA flow parameters and WML using multiple linear regression, corrected for intracranial volume (ICV), age, gender, BMI, previous MI, diabetes, hypertension, smoking, hypercholesterolaemia, PVD and stroke. Results: Amongst 694 subjects, diastolic and mean BP decreased and hence BP pulsatility increased significantly between ages 70 and 73 years. Lower diastolic BP and higher BP pulsatility were associated with higher ICA PI (standardized β, age 70= -0.24, age 73= -0.19, both p&lt;0.001; age 70 β=0.18, p&lt;0.001, age 73 β=0.10, p=0.008 respectively). WML volume was weakly associated with BP at age 70 (diastolic β=0.08, systolic β=0.08, mean β=0.09, all p&lt;0.05) but not with BP variability or pulsatility. Similar but weaker associations were seen at age 73. After adjusting for BP, larger WML volume was associated with higher ICA PI (β=0.10, p=0.012), but not any other measures. All associations were the same for WML Fazekas scores. Conclusions: The relatively weak association between BP and WML may be mediated via ICA pulsatility which is largely driven by falling diastolic BP. This questions the nature of the apparent link between BP and WML.

Transcranial Doppler Ultrasounography for Diagnosis of Cerebral Vasospasm After Aneurysmal Subarachnoid Hemorrhage: Mean Blood Flow Velocity Ratio of the Ipsilateral and Contralateral Middle Cerebral Arteries

The ratio of the ipsilateral to contralateral middle cerebral artery (MCA) mean blood flow velocity has better correlation with clinical meaningful consequences of cerebral vasospasm than absolute mean velocity in the MCA.

Both acute and prolonged administration of EPO reduce cerebral and systemic vascular conductance in humans

Administration of erythropoietin (EPO) has been linked to cerebrovascular events. EPO reduces vascular conductance, possibly because of the increase in hematocrit. Whether EPO in itself affects the vasculature remains unknown; here it was evaluated in healthy males by determining systemic and cerebrovascular variables following acute (30,000 IU/d for 3 d; n=8) and chronic (5000 IU/week for 13 wk; n=8) administration of EPO, while the responsiveness of the vasculature was challenged during cycling exercise, with and without hypoxia. Prolonged administration of EPO increased hematocrit from 42.5 ± 3.7 to 47.6 ± 4.1% (P<0.01), whereas hematocrit was unaffected following acute EPO administration. Yet, the two EPO regimes increased arterial pressure similarly (by 8±4 and 7±3 mmHg, respectively; P=0.01) through reduced vascular conductance (by 7±3 and 5±2%; P<0.05). Also, both EPO regimes widened the arterial-to-jugular O(2) differences at rest as well as during normoxic and hypoxic exercise (P<0.01), which indicated reduced cerebral blood flow despite preserved dynamic cerebral autoregulation, and an increase in middle cerebral artery mean blood flow velocity (P<0.05), therefore, reflected vasoconstriction. Thus, administration of EPO to healthy humans lowers systemic and cerebral conductance independent of its effect on hematocrit.

The distribution of blood flow in the carotid and vertebral arteries during dynamic exercise in humans

The mechanism underlying the plateau or relative decrease in cerebral blood flow (CBF) during maximal incremental dynamic exercise remains unclear. We hypothesized that cerebral perfusion is limited during high-intensity dynamic exercise due to a redistribution of carotid artery blood flow. To identify the distribution of blood flow among the arteries supplying the head and brain, we evaluated common carotid artery (CCA), internal carotid artery (ICA), external carotid artery (ECA) and vertebral artery (VA) blood flow during dynamic exercise using Doppler ultrasound. Ten subjects performed graded cycling exercise in a semi-supine position at 40, 60 and 80% of peak oxygen uptake (VO2 peak) for 5 min at each workload. The ICA blood flow increased by 23.0 ± 4.6% (mean ± SE) from rest to exercise at 60% (VO2 peak). However, at 80% (VO2 peak), ICA blood flow returned towards near resting levels (9.6 ± 4.7% vs. rest). In contrast, ECA, CCA and VA blood flow increased proportionally with workload. The change in ICA blood flow during graded exercise was correlated with end-tidal partial pressure of CO2 (r = 0.72). The change in ICA blood flow from 60% (VO2 peak) to 80% (VO2 peak) was negatively correlated with the change in ECA blood flow (r = −0.77). Moreover, there was a significant correlation between forehead cutaneous vascular conductance and ECA blood flow during exercise (r = 0.79). These results suggest that during high-intensity dynamic exercise the plateau or decrease in ICA blood flow is partly due to a large increase in ECA blood flow, which is selectively increased to prioritize thermoregulation.