Whole-Body Periodic Acceleration Enhances Brachial Endothelial Function

Matsumoto, Tetsuya; Fujita, Masatoshi; Tarutani, Yasuhiro; Yamane, Tetsunobu; Takashima, Hiroyuki; Nakae, Ichiro; Horie, Minoru

doi:10.1253/circj.72.139

Cited by 22 publications

(18 citation statements)

References 23 publications

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“…Our findings are also consistent with findings from the enhanced external counterpulsation data, wherein timed diastolic pulsations have been shown to improve diastolic endothelial function and NO production (2, 8,14,17,24,35). Unlike enhanced external counterpulsation, pG z is not timed to systole or diastole, but its effects on eNOS production and other beneficial endothelial-derived mediators have been established (4,36,39,48).…”

Section: Discussionsupporting

confidence: 90%

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Low-amplitude pulses to the circulation through periodic acceleration induces endothelial-dependent vasodilatation

Uryash

Wu²,

Bassuk³

et al. 2009

Journal of Applied Physiology

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Uryash A, Wu H, Bassuk J, Kurlansky P, Sackner MA, Adams JA. Low-amplitude pulses to the circulation through periodic acceleration induces endothelial-dependent vasodilatation. J Appl Physiol 106: 1840 -1847, 2009. First published March 26, 2009 doi:10.1152/japplphysiol.91612.2008.-Low-amplitude pulses to the vasculature increase pulsatile shear stress to the endothelium. This activates endothelial nitric oxide (NO) synthase (eNOS) to promote NO release and endothelial-dependent vasodilatation. Descent of the dicrotic notch on the arterial pulse waveform and a-to-b ratio (a/b; where a is the height of the pulse amplitude and b is the height of the dicrotic notch above the end-diastolic level) reflects vasodilator (increased a/b) and vasoconstrictor effects (decreased a/b) due to NO level change. Periodic acceleration (pG z) (motion of the supine body head to foot on a platform) provides systemic additional pulsatile shear stress. The purpose of this study was to determine whether or not pG z applied to rats produced endothelial-dependent vasodilatation and increased NO production, and whether the latter was regulated by the Akt/phosphatidylinositol 3-kinase (PI3K) pathway. Male rats were anesthetized and instrumented, and pG z was applied. Sodium nitroprusside, N G -nitro-L-arginine methyl ester (L-NAME), and wortmannin (WM; to block Akt/PI3K pathway) were administered to compare changes in a/b and mean aortic pressure. Descent of the dicrotic notch occurred within 2 s of initiating pG z. Dose-dependent increase of a/b and decrease of mean aortic pressure took place with SNP. L-NAME produced a dose-dependent rise in mean aortic pressure and decrease of a/b, which was blunted with pG z. In the presence of WM, pGz did not decrease aortic pressure or increase a/b. WM also abolished the pG z blunting effect on blood pressure and a/b of L-NAME-treated animals. eNOS expression was increased in aortic tissue after pG z. This study indicates that addition of low-amplitude pulses to circulation through pG z produces endothelial-dependent vasodilatation due to increased NO in rats, which is mediated via activation of eNOS, in part, by the Akt/PI3K pathway. vascular resistance; N G -nitro-L-arginine methyl ester, wortmannin; nitric oxide ADDED LOW-AMPLITUDE PULSES to the vasculature were generated with periodic acceleration (pG z ). pG z is produced by a motorized platform that repetitively moves the horizontally oriented body sinusoidally in a head to foot direction. Inertia of fluid as the body accelerates and decelerates adds a small-amplitude pulse to the circulation that is superimposed on the natural pulse, increasing pulsatile shear stress to the endothelium (3, 6, 7). In large-animal models, increased pulsatile shear stress activates endothelial nitric oxide (NO) synthase (eNOS) to release NO into the circulation, which, in turn, induces endothelial-dependent pulmonary and systemic vasodilatation, as well as increasing organ blood flows (3,5,6). pG z applied to anesthetized swine increases serum nitrite, which is ...

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Section: Discussionsupporting

confidence: 90%

“…The release of NO into the circulation with pG z has been shown to be physiologically meaningful and long lasting in a sheep model of asthma (1). Additionally, pG z applied to human subjects increases brachial flow-mediated vasodilation and induces release of NO, which is comparable to light to moderate exercise (36,47).…”

mentioning

confidence: 99%

Low-amplitude pulses to the circulation through periodic acceleration induces endothelial-dependent vasodilatation

Uryash

Wu²,

Bassuk³

et al. 2009

Journal of Applied Physiology

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“…8,22 Measurement of the brachial artery diameter before and after an increase in shear stress induced by reactive hyperemia (ie, FMD) is most frequently used in the clinical setting 8,9,22,23 (Figure 1). The increased shear stress induced by reactive hyperemia activates endothelial NO synthase (eNOS) and increases NO production in the endothelium.…”

Section: Endothelial Functionsmentioning

confidence: 99%

“…Several non-invasive methods are currently used to assess functional vascular damage, including measurement of flow-mediated vasodilatation (FMD) of the brachial artery induced by reactive hyperemia, pulse wave velocity (PWV), augmentation index (AI), central blood pressure (BP), etc and these vascular function tests have attracted attention as new tools for determining CVD risk. [8][9][10][11][12][13][14][15] In this review, we describe the pathophysiology of vascular functions, the non-invasive methods of evaluating vascular functions and the clinical applicability of these tests for CVD risk stratification. leukocyte adhesion to endothelial cells.…”

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confidence: 99%

Non-Invasive Vascular Function Tests:

Tomiyama

Yamashina

2010

Circ J

273

146

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Circulation Journal Official Journal of the Japanese Circulation Society http://www. j-circ.or.jp he clustering of conventional risk factors for cardiovascular disease (CVD) is associated with exaggerated vascular damage and poorer outcomes. 1 Therefore, clinical medicine and public health policies place significant emphasis on the modification of conventional risk factors and lifestyle behaviors to reduce the epidemic of CVD. 2 Although the population-attributable risk of major vascular risk factors is substantial, it is often difficult to distinguish those individuals with a moderate baseline risk who might benefit from aggressive risk reduction strategies. Furthermore, some studies have reported that the traditional cardiovascular risk factors account for "only 50%" of those who go on to develop coronary heart disease. 3 Therefore, additional tests to assist in the prediction of the cardiovascular risk in these individuals may be warranted. 4,5 Ultrasound examination of the carotid artery is increasingly being used as a surrogate marker of atherosclerosis and is a strong predictor of future vascular events. 6 However, evaluation of the regression of subclinical atherosclerosis by carotid arterial ultrasound examination following treatment of risk factors takes time (ie, more than 1 year is required in most cases to confirm such regression), 7 and therefore more sensitive markers to assess the effect of treatment of risk factors on vascular damage are proposed.Risk factors for CVD cause not only structural, but also functional vascular damage. Several non-invasive methods are currently used to assess functional vascular damage, including measurement of flow-mediated vasodilatation (FMD) of the brachial artery induced by reactive hyperemia, pulse wave velocity (PWV), augmentation index (AI), central blood pressure (BP), etc and these vascular function tests have attracted attention as new tools for determining CVD risk. [8][9][10][11][12][13][14][15] In this review, we describe the pathophysiology of vascular functions, the non-invasive methods of evaluating vascular functions and the clinical applicability of these tests for CVD risk stratification. Functions of ArteriesThe arterial wall has 3 layers (ie, the intima, including the endothelium, the media, and the adventitia) and each of these layers has a role in systemic circulation. Functions of the EndotheliumEndothelium regulates vascular tone, hemostasis and/or vascular permeability. 16 To exert these functions, endothelial cells biosynthesize several vasoactive substances, 17 and of these, nitric oxide (NO) in particular has a pivotal role in protecting against the initiation/progression of atherosclerosis via its vasodilatory activity and its inhibitory activity against vascular smooth muscle cell growth, nuclear transcription of cell adhesion molecules, platelet aggregation and The arterial wall has 3 layers (ie, the intima, including the endothelium, the media, and the adventitia); each of these layers has individual roles in systemic circulation. The ...

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“…61 The chronic intermittent enhancement of the pulsatile shear stress with periodic acceleration may lead to endothelial nitric oxide release via the activation of endothelial nitric oxide synthase. 59, 60 Recently, we used whole-body periodic acceleration to treat patients with chronic angina pectoris who were not indicated for percutaneous coronary intervention and/or coronary artery bypass grafting under a conceptual framework that the augmented radial shear stress at the site of pre-existing coronary collateral vessels would induce arteriogenesis. 62 In 10 patients treated with 20 sessions of 45-min whole-body periodic acceleration, myocardial perfusion in the collateral dependent area improved remarkably at rest and during adenosine infusion, indicating a significant development of collateral circulation.…”

Section: Whole-body Periodic Accelerationmentioning

confidence: 99%

Coronary Collateral Growth and Its Therapeutic Application to Coronary Artery Disease

Fujita

Sasayama

2010

Circ J

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Circulation Journal Official Journal of the Japanese Circulation Society http://www. j-circ.or.jp or a long time, the functional role of the coronary collateral circulation as a blood-conveying channel has been disputed. 1-4 Because a well-developed coronary collateral circulation is usually associated with severe coronary stenosis, some investigators assumed that the existence of collateral circulation is a marker of coronary artery disease (CAD). 1 Over the past 3 decades, accumulating evidence has documented that pre-existing well-developed coronary collateral circulation at the onset of acute myocardial infarction plays an important functional role in preserving left ventricular function, 2,5 reducing infarct size, 6 preventing left ventricular aneurysm formation 7 and survival. 2 Thus, a significant functional role of coronary collateral circulation is now well appreciated. 8 In the past decades, 9-11 we and others have emphasized the importance of arteriogenesis of the collateral vessels for enhanced coronary collateral circulation, compared with angiogenesis of the capillaries in areas perfused by occluded or critically stenosed coronary arteries. On the other hand, there has been considerable controversy concerning the stimulus for coronary collateral growth. It is now clear that long-standing high-grade coronary stenosis is mainly responsible for collateral vessel growth. 12 Severe coronary narrowing results in myocardial ischemia and a pressure gradient between the providing and receiving coronary arteries across the collateral network. New establishment of a pressure gradient leads to recruitment of collateral blood flow and increased shear stress at the site of pre-existing collateral vessels. Thus, severe coronary narrowing is inevitably accompanied by 2 potential stimuli for the development of collateral circulation, namely, myocardial ischemia and shear stress.One of the hot topics of coronary collateral growth is the role of bone-marrow-derived stem or endothelial progenitor cells in arteriogenesis. 13-16 It is still controversial whether these cells contribute to collateral growth by supplying cytokines and proteases related to arteriogenesis or by building up the collateral vessel as a result of the incorporation of these cells into vessel walls. 17 Thus, this review constitutes a summary of the historical background and current knowledge of coronary collateral growth in reference to the therapeutic potential for treating CAD. Stimulus of Coronary Collateral Growth Animal ModelsFor a long time, there was no general idea concerning the principal stimulus for coronary collateral growth. In 1967, Schaper proposed a new concept concerning the importance of mechanical factors on collateral growth. 18 He emphasized the crucial role of increased tangential (radial) shear stress at small pre-existing collateral arterioles, which results from increased intravascular pressure and arteriolar dilatation.In contrast, Scheel et al considered that myocardial ischemia is important for coronary collateral growt...

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Whole-Body Periodic Acceleration Enhances Brachial Endothelial Function

Cited by 22 publications

References 23 publications

Low-amplitude pulses to the circulation through periodic acceleration induces endothelial-dependent vasodilatation

Low-amplitude pulses to the circulation through periodic acceleration induces endothelial-dependent vasodilatation

Non-Invasive Vascular Function Tests:

Coronary Collateral Growth and Its Therapeutic Application to Coronary Artery Disease

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