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      Fast‐food meal reduces peripheral artery endothelial function but not cerebral vascular hypercapnic reactivity in healthy young men

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          Abstract

          Consumption of a representative fast‐food meal ( FFMeal) acutely impairs peripheral conduit artery vascular function; however, the effect on cerebral vascular function remains unknown. This study tested the hypothesis that a FFMeal would impair cerebral vascular function as indexed by an attenuated increase in cerebral vascular conductance ( CVCI) in the middle cerebral artery ( MCA) during a hypercapnic challenge. Ten healthy men (age: 24 ± 3 years, BMI: 24.3 ± 3.8 kg/m 2) were studied under two conditions; a standardized FFMeal (990 kcals, 50% fat, 36% carbohydrate, 14% protein, and 2120 mg sodium) and a fasting control condition. Basal hemodynamics, cerebral vasomotor reactivity ( CVMR), and brachial artery flow‐mediated dilation ( BA FMD) were completed after an overnight fast (Pre) and again 2 h and 4 h later both days. To assess CVMR, subjects rebreathed from a 5‐L bag while MCA velocity ( MCAV mean) was measured using transcranial Doppler ( TCD) ultrasound and converted into CVCI ( MCAV mean/mean arterial pressure). Peripheral artery endothelial function was assessed via BA FMD following a standard 5‐min occlusion protocol. As expected, BA FMD was reduced at 2 h (Pre: 6.6 ± 1.7% vs. 5.2 ± 1.8%, P = 0.01). However, despite significant impairment in BA FMD, neither peak CVCI %baseline nor CVMR was affected by the FFMeal (Control–Pre: 1.9 ± 1.1, 2 h: 2.1 ± 1.1, 4 h: 1.7 ± 1.1 ∆ CVCI%·∆ P ETCO 2 −1 vs. FFMeal–Pre: 2.1 ± 1.1, 2 h: 2.2 ± 0.7, 4 h: 1.9 ± 0.9 ∆ CVCI%·∆ P ETCO 2 −1, time × condition P = 0.88). These results suggest that cerebral vascular reactivity to hypercapnia in healthy young men is not altered by an acute FFMeal.

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          Ultrasound assessment of flow-mediated dilation.

          Developed in 1992, the flow-mediated dilation test is now the most commonly used noninvasive assessment of vascular endothelial function in humans. Since its inception, scientists have refined their understanding of the physiology, analysis, and interpretation of this measurement. Recently, a significant growth of knowledge has added to our understanding and implementation of this clinically relevant research methodology. Therefore, this tutorial provides timely insight into recent advances and practical information related to the ultrasonic assessment of vascular endothelial function in humans.
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            Computation of aortic flow from pressure in humans using a nonlinear, three-element model.

            We computed aortic flow pulsations from arterial pressure by simulating a nonlinear, time-varying three-element model of aortic input impedance. The model elements represent aortic characteristic impedance, arterial compliance, and systemic vascular resistance. Parameter values for the first two elements were computed from a published, age-dependent, aortic pressure-area relationship (G. J. Langewouters et al. J. Biomech. 17:425-435, 1984). Peripheral resistance was predicted from mean pressure and model mean flow. Model flow pulsations from aortic pressure showed the visual aspects of an aortic flow curve. For evaluation we compared model mean flow from radial arterial pressure with thermodilution cardiac output estimations, 76 times, in eight open heart surgical patients. The pooled mean difference was +7%, the SD 22%. After using one comparison per patient to calibrate the model, however, we followed quantitative changes in cardiac output that occurred either during changes in the state of the patient or subsequent to vasoactive drugs. The mean deviation from thermodilution cardiac output was +2%, the SD 8%. Given these small errors the method could monitor cardiac output continuously.
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              Assessment of middle cerebral artery diameter during hypocapnia and hypercapnia in humans using ultra-high-field MRI.

              In the evaluation of cerebrovascular CO2 reactivity measurements, it is often assumed that the diameter of the large intracranial arteries insonated by transcranial Doppler remains unaffected by changes in arterial CO2 partial pressure. However, the strong cerebral vasodilatory capacity of CO2 challenges this assumption, suggesting that there should be some changes in diameter, even if very small. Data from previous studies on effects of CO2 on cerebral artery diameter [middle cerebral artery (MCA)] have been inconsistent. In this study, we examined 10 healthy subjects (5 women, 5 men, age 21-30 yr). High-resolution (0.2 mm in-plane) MRI scans at 7 Tesla were used for direct observation of the MCA diameter during hypocapnia, -1 kPa (-7.5 mmHg), normocapnia, 0 kPa (0 mmHg), and two levels of hypercapnia, +1 and +2 kPa (7.5 and 15 mmHg), with respect to baseline. The vessel lumen was manually delineated by two independent observers. The results showed that the MCA diameter increased by 6.8 ± 2.9% in response to 2 kPa end-tidal P(CO2) (PET(CO2)) above baseline. However, no significant changes in diameter were observed at the -1 kPa (-1.2 ± 2.4%), and +1 kPa (+1.4 ± 3.2%) levels relative to normocapnia. The nonlinear response of the MCA diameter to CO2 was fitted as a continuous calibration curve. Cerebral blood flow changes measured by transcranial Doppler could be corrected by this calibration curve using concomitant PET(CO2) measurements. In conclusion, the MCA diameter remains constant during small deviations of the PET(CO2) from normocapnia, but increases at higher PET(CO2) values.
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                Author and article information

                Contributors
                matthew.brothers@uta.edu
                Journal
                Physiol Rep
                Physiol Rep
                10.1002/(ISSN)2051-817X
                PHY2
                physreports
                Physiological Reports
                John Wiley and Sons Inc. (Hoboken )
                2051-817X
                17 September 2018
                September 2018
                : 6
                : 18 ( doiID: 10.1002/phy2.2018.6.issue-18 )
                : e13867
                Affiliations
                [ 1 ] Department of Kinesiology The University of Texas at Arlington Arlington Texas
                [ 2 ] College of Nursing and Health Innovation The University of Texas at Arlington Arlington Texas
                Author notes
                [*] [* ] Correspondence

                R. M. Brothers, Department of Kinesiology, University of Texas at Arlington, Box 19259, 500 W. Nedderman Dr., 147 Maverick Activities Center, Arlington, TX 76106.

                Tel: +1 817 272 3151

                Fax: +1 817 272 3233

                E‐mail: matthew.brothers@ 123456uta.edu

                [†]

                Contributed equally to the writing of the manuscript.

                Author information
                http://orcid.org/0000-0002-3232-8639
                Article
                PHY213867
                10.14814/phy2.13867
                6139709
                30221831
                b96ddf1b-1429-44c7-8941-8022e2de9d2d
                © 2018 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society.

                This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                : 13 April 2018
                : 20 July 2018
                : 13 August 2018
                Page count
                Figures: 3, Tables: 3, Pages: 11, Words: 8010
                Categories
                Central Nervous System
                Neurological Conditions, Disorders and Treatments
                Cardiovascular Conditions, Disorders and Treatments
                Vasculature
                Nutrition
                Ageing and Degeneration
                Original Research
                Original Research
                Custom metadata
                2.0
                phy213867
                September 2018
                Converter:WILEY_ML3GV2_TO_NLMPMC version:version=5.4.7.1 mode:remove_FC converted:17.09.2018

                atherosclerosis,endothelial function,human,postprandial,western diet

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