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      Does External Counterpulsation Augment Mean Cerebral Blood Flow in the Healthy Brain? Effects of External Counterpulsation on Middle Cerebral Artery Flow Velocity and Cerebrovascular Regulatory Response in Healthy Subjects

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          Abstract

          Background and Purpose:External counterpulsation (ECP) noninvasively improves myocardial and organ perfusion via diastolic augmentation. The effects on cerebral blood flow velocities (CBFV) and hemodynamics are controversial. In this study, the effect of active ECP treatment on CBF in healthy subjects was continuously measured. Methods: In 9 healthy volunteers (mean age 34.1 ± 11.1 years, 4 females), 20-min active ECP treatment was performed. CBFV in the middle cerebral artery were detected via transcranial Doppler. CBFV were registered continuously before, during and after ECP. The protocol was repeated twice. Results: At onset of ECP, immediate changes in CBFV were observed: peak diastolic blood flow velocities increased from baseline to treatment (63 vs. 76 cm/s; p < 0.001) and diastolic blood flow augmentation was maintained throughout ECP. Peak systolic (87 vs. 78 cm/s; p < 0.001) and end-diastolic velocities (40 vs. 28 cm/s; p < 0.001) decreased significantly, while mean CBFV maintained constant (59 vs. 58 cm/s; not significant). The pulsatility index and resistance index as indirect parameters for peripheral vascular resistance increased during ECP (pulsatility index 0.79 vs. 0.89, p < 0.001; resistance index 0.54 vs. 0.64; p < 0.001). Conclusions: ECP did not increase mean CBFV in healthy subjects even though peak diastolic CBFV were significantly augmented. Changes in CBFV and transcranial Doppler waveform characteristics suggest that the mean flow of the middle cerebral artery is maintained stable via cerebrovascular autoregulatory mechanisms.

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          Enhanced external counterpulsation improves endothelial function in patients with symptomatic coronary artery disease.

          The goal of this study was to examine the effect of enhanced external counterpulsation (EECP) on endothelial function. Enhanced external counterpulsation improves symptoms and exercise tolerance in patients with symptomatic coronary artery disease (CAD). However, the exact mechanisms by which this technique exerts its clinical benefit are unclear. Reactive hyperemia-peripheral arterial tonometry (RH-PAT), a noninvasive method to assess peripheral endothelial function by measuring reactive hyperemic response in the finger, was performed in 23 patients with refractory angina undergoing a 35-h course of EECP. In each patient RH-PAT measurements were performed before and after the first, at midcourse, and the last EECP session. In addition, RH-PAT response was assessed one month after completion of EECP therapy; RH-PAT index, a measure of reactive hyperemia, was calculated as the ratio of the digital pulse volume during reactive hyperemia divided by that at rest. Enhanced external counterpulsation led to symptomatic improvement (>/=1 Canadian Cardiovascular Society class) in 17 (74%) patients; EECP was associated with a significant immediate increase in average RH-PAT index after each treatment (p < 0.05). In addition, average RH-PAT index at one-month follow-up was significantly higher than that before EECP therapy (p < 0.05). When patients were divided by their clinical response, RH-PAT index at one-month follow-up increased only in those patients who experienced clinical benefit. Enhanced external counterpulsation enhances peripheral endothelial function with beneficial effects persisting at one-month follow-up in patients with a positive clinical response. This suggests that improvement in endothelial function may contribute to the clinical benefit of EECP in patients with symptomatic CAD.
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            Cerebral arterial diameters during changes in blood pressure and carbon dioxide during craniotomy.

            Forty-five measurements of diameters of 12 human cerebral arteries were performed during 10 craniotomies under moderate changes in mean blood pressure and end tidal CO2. The mean change in blood pressure was 30 +/- 16 mm Hg (standard deviation) and that of end tidal CO2 was 14 +/- 6 mm Hg (standard deviation). These changes were induced with nitroprusside, phenylephrine, and adjustment of ventilator rate. Measurements were made through the operating microscope focused at the highest power, with meticulous attention to constant angle and distance from the artery. The mean diameter change in the large cerebral arteries (carotid, middle cerebral artery, vertebral artery) was less than 4%, but the smaller arteries (anterior cerebral artery, M2 segment of middle cerebral artery) showed diameter changes as large as 29% and 21% to end tidal CO2 and blood pressure changes, respectively. These data suggest that at the time of craniotomy, diameters of the large cerebral vessels do not significantly change during moderate variations in blood pressure and CO2, but that larger changes may occur in smaller vessels. This constancy of diameter suggests that the transcranial Doppler velocities obtained during intraoperative monitoring of craniotomies may closely reflect blood flow through the insonated artery.
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              Dynamic cerebral autoregulation in acute lacunar and middle cerebral artery territory ischemic stroke.

              We addressed whether dynamic cerebral autoregulation (dCA) is affected in middle cerebral artery (MCA) territory (MCAS) and lacunar ischemic stroke (LS). Blood pressure (MAP) and MCA velocity (V) were measured in 10 patients with large MCAS (National Institutes of Health Stroke score, 17+/-2; mean+/-SEM), in 10 with LS (score, 9+/-1), and in 10 reference subjects. dCA was evaluated in time (delay of the MCA Vmean counter-regulation during changes in MAP) and frequency domains (cross-spectral MCA Vmean-to-MAP phase lead). In reference subjects, latencies for MAP increments (5.3+/-0.5 seconds) and decrements (5.6+/-0.5 seconds) were comparable, and low frequency MCA Vmean-to-MAP phase lead was 56+/-5 and 59+/-5 degrees (left and right hemisphere). In MCAS, these latencies were 4.6+/-0.7 and 5.6+/-0.5 seconds in the nonischemic hemisphere and not detectable in the ischemic hemisphere. In the unaffected hemisphere, phase lead was 61+/-6 degrees versus 26+/-6 degrees on the ischemic side (P<0.05). In LS, no latency and smaller phase lead bilaterally (32+/-6 and 33+/-5 degrees) conformed to globally impaired dCA. In large MCAS infarcts, dynamic cerebral autoregulation was impaired in the affected hemisphere. In LS, dynamic cerebral autoregulation was impaired bilaterally, a finding consistent with the hypothesis of bilateral small vessel disease in patients with lacunar infarcts.
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                Author and article information

                Journal
                CED
                Cerebrovasc Dis
                10.1159/issn.1015-9770
                Cerebrovascular Diseases
                S. Karger AG
                1015-9770
                1421-9786
                2010
                November 2010
                15 October 2010
                : 30
                : 6
                : 612-617
                Affiliations
                aCenter for Stroke Research Berlin, Department of Neurology, and bArteriogenesis Research, Department of Cardiology and Center for Cardiovascular Research, Charité University Medicine Berlin, and cDepartment of Cardiology, Helios Klinikum Berlin Buch, Berlin, Germany
                Author notes
                *Gerhard J. Jungehuelsing, MD, Department of Neurology, Charité-Universitätsmedizin Berlin, Hindenburgdamm 30, DE–12203 Berlin (Germany), Tel. +49 30 8445 4080, Fax +49 30 8445 4099, E-Mail jan.jungehuelsing@charite.de
                Article
                319891 Cerebrovasc Dis 2010;30:612–617
                10.1159/000319891
                20948206
                93125e15-70e2-4de9-8623-420c3b55150d
                © 2010 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                History
                : 21 December 2009
                : 27 July 2010
                Page count
                Figures: 4, Tables: 1, Pages: 6
                Categories
                Original Paper

                Geriatric medicine,Neurology,Cardiovascular Medicine,Neurosciences,Clinical Psychology & Psychiatry,Public health
                Autoregulation,Transcranial Doppler,External counterpulsation,Cerebral blood flow

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