Effect of External Counterpulsation on Plasma Nitric Oxide and Endothelin-1 Levels

Akhtar, Mateen; Wu, Guifu; Du, Zhi-Min; Zhang, Zheng; Michaels, Andrew D.

doi:10.1016/j.amjcard.2006.01.053

Cited by 77 publications

(47 citation statements)

References 9 publications

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“…Both clinical investigation and animal studies from our laboratory have shown that EECP treatment increased plasma NO levels and eNOS gene expression. 22,23 In the present study, our results indicate that hypercholesterolemia markedly decreased eNOS protein level, whereas EECP significantly elevated eNOS protein expression.…”

Section: Zhang Et Al Eecp Inhibits Intimal Hyperplasia 531supporting

confidence: 62%

Enhanced External Counterpulsation Inhibits Intimal Hyperplasia by Modifying Shear Stress–Responsive Gene Expression in Hypercholesterolemic Pigs

et al. 2007

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Background-Enhanced external counterpulsation (EECP) is a circulation assist device that may improve endothelial dysfunction by increasing shear stress. Chronic exposure of vascular endothelial cells and vascular smooth muscle cells to relatively high physiological shear stress has antiproliferative and vasoprotective effects. The present study hypothesizes that EECP inhibits intimal hyperplasia and atherogenesis by modifying shear stress-responsive gene expression. Methods and Results-Thirty-five male pigs were randomly assigned to 3 groups: high-cholesterol diet (nϭ11), high-cholesterol diet plus EECP (nϭ17), and usual diet (control; nϭ7). The coronary arteries and aortas were collected for histopathological study and immunohistochemical and Western blot analysis. The peak diastolic arterial wall shear stress during EECP increased significantly compared with before EECP (49.62Ϯ10.71 versus 23.92Ϯ7.28 dyne/cm 2 ; PϽ0.001). Intimal hyperplasia was observed in the coronary arteries of the high-cholesterol diet group, whereas in animals receiving EECP, the intima-to-media area ratio was significantly decreased by 41.59% (21.27Ϯ10.00% versus 36.41Ϯ16.69%; Pϭ0.008). Hypercholesterolemia attenuated the protein expression of endothelial NO synthase and enhanced the phosphorylation of extracellular signal-regulated kinases 1/2. EECP treatment alleviated these adverse changes. Conclusions-EECP reduces hypercholesterolemia-induced endothelial damage, arrests vascular smooth muscle cell proliferation and migration, decreases proliferating cell nuclear antigen proliferative index, suppresses extracellular matrix formation, and eventually inhibits intimal hyperplasia and the development of atherosclerosis by increasing the arterial wall shear stress, which in turn activates the endothelial NO synthase/NO pathway and probably suppresses extracellular signal-regulated kinases 1/2 overactivation. (Circulation. 2007;116:526-534.)

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Section: Zhang Et Al Eecp Inhibits Intimal Hyperplasia 531supporting

confidence: 62%

Enhanced External Counterpulsation Inhibits Intimal Hyperplasia by Modifying Shear Stress–Responsive Gene Expression in Hypercholesterolemic Pigs

et al. 2007

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“…при лечении УНКП (36 часовых процедур) паци-ентов со стабильной ИБС [12]. Выявлено увеличение NOx в плазме на 62±17% по сравнению с исходным уров-нем (p<0,0001) и снижение на 36±8% ET-1 (p<0,0001).…”

Section: Enhanced External Counterpulsation In Clinical Practice усилunclassified

Possibilities of Enhanced External Counterpulsation Using in Clinical Practice

Mamieva

Лишута

Belenkov

et al. 2017

Racionalʹnaâ farmakoterapiâ v kardiologii

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Первый Московский государственный медицинский университет имени И.М. Сеченова Россия, 119991, Москва, ул. Трубецкая, 8 стр. 2 В статье рассматриваются возможности и перспективы применения в клинической практике такого метода лечения, как усиленная наружная контрпульсация (УНКП), уже давно зарекомендовавшего себя во всем мире. Рассматриваются исторические предпосылки, а также этапы раз-работки данного метода для лечения пациентов с ишемической болезнью сердца (ИБС) и хронической сердечной недостаточностью (ХСН). Детально разбирается механизм действия УНКП и основные гемодинамические, нейрогуморальные и тканевые эффекты, лежащие в осно-ве применения данного вида лечения. Отдельно рассматривается влияние УНКП на эндотелиальную функцию и коронарный резерв, нару-шение которых имеет место при большинстве сердечно-сосудистых заболеваний. Среди наиболее изученных показаний для применения УНКП является лечение пациентов с ИБС, в том числе, осложненной ХСН. В статье представлена доказательная база лечения больных этими на-рушениями с использованием УНКП. Также представлены перспективные направления применения этого метода лечения в других направ-лениях медицины.Ключевые слова: усиленная наружная контрпульсация, эндотелиальная функция, коронарный резерв, ишемическая болезнь сердца, хроническая сердечная недостаточность. Possibilities and prospects for the clinical use of enhanced external counterpulsation (EECP), which has long established itself throughout the world, are discussed in the article. Historical background, as well as the development stages of EECP for the treatment of patients with coronary heart disease (CHD) and chronic heart failure (CHF) are considered. The mechanism of action of the EECP and the main hemodynamic, neurohumoral and tissue effects that justify its use are presented. The effect of EECP on endothelial function and coronary reserve, disorders of which occurs in the majority of cardiovascular diseases, is considered separately. Treatment of patients with CHD, including complicated by CHF, are the most studied indications for EECP using in medical practice. The evidence base for treatment of patients with these disorders by EECP is presented in the article. Prospects for the EECP application in other areas of medicine are also presented.Keywords: enhanced external counterpulsation, endothelial function, coronary reserve, ischemic heart disease, chronic heart failure. ВведениеИшемическая болезнь сердца (ИБС) и сердечная не-достаточность по-прежнему сохраняют лидирующие по-зиции среди причин инвалидизации и смертности на-селения во всем мире. Несмотря на значительные до-стижения последних лет в диагностике и терапии дан-ных состояний, у определенной доли пациентов фар-макотерапия оказывается недостаточно эффективной, а использование эндоваскулярных и хирургических ме-тодов лечения не представляется возможным из-за осо-бенностей анатомии коронарного русла, предше-ствующей реваскуляризации или наличия тяжелых сопутствующих заболеваний. В этой ситуации воз-можно использование современных методов тера-

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“…117 During the course of EECP therapy in patients with CAD, plasma nitrate/ nitrite progressively increased and plasma ET-1 decreased, suggesting that EECP improves endothelial function. 118 In symptomatic patients with CAD, EECP increased flow-mediated vasodilatation and plasma levels of nitrate/nitrite and 6-keto-prostaglandin F 1a , whereas it decreased plasma levels of ET-1, ADMA, and proinflammatory cytokines. 119 Miscellaneous Treatment with the a-adrenoceptor antagonist urapidil improved coronary flow, myocardial perfusion, and left ventricular function following percutaneous coronary intervention in patients with ST-elevation acute coronary syndrome; myocardial NO concentrations in the urapidil group was higher than that of the control group.…”

Section: Herbal Agentsmentioning

confidence: 99%

Nitric Oxide-Mediated Coronary Flow Regulation in Patients with Coronary Artery Disease: Recent Advances

Toda¹,

Tanabe²,

Nakanishi³

2011

Int J Angiol

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Nitric oxide (NO) formed via endothelial NO synthase (eNOS) plays crucial roles in the regulation of coronary blood flow through vasodilatation and decreased vascular resistance, and in inhibition of platelet aggregation and adhesion, leading to the prevention of coronary circulatory failure, thrombosis, and atherosclerosis. Endothelial function is impaired by several pathogenic factors including smoking, chronic alcohol intake, hypercholesterolemia, obesity, hyperglycemia, and hypertension. The mechanisms underlying endothelial dysfunction include reduced NO synthase (NOS) expression and activity, decreased NO bioavailability, and increased production of oxygen radicals and endogenous NOS inhibitors. Atrial fibrillation appears to be a risk factor for endothelial dysfunction. Endothelial dysfunction is an important predictor of coronary artery disease (CAD) in humans. Penile erectile dysfunction, associated with impaired bioavailability of NO produced by eNOS and neuronal NOS, is also considered to be highly predictive of ischemic heart disease. There is evidence suggesting an important role of nitrergic innervation in coronary blood flow regulation. Prophylactic and therapeutic measures to eliminate pathogenic factors inducing endothelial and nitrergic nerve dysfunction would be quite important in preventing the genesis and development of CAD.KEYWORDS: Nitric oxide, constitutive nitric oxide synthase, endothelial dysfunction, coronary blood flow, coronary artery disease, asymmetric dimethylarginine Coronary blood flow is regulated through complex adjustments in the arteriolar tone and resistance of the microcirculation. Impairment of microvascular function leads to organ dysfunction in any body system including the heart. Recent evidence supports the concept that the impairment of endothelial function is an upstream event in the pathophysiology of atherosclerosis, CAD, and myocardial infarction (MI). Nitric oxide (NO) liberated as a paracrine relaxant from the vascular endothelium is known to play a pivotal role in the modulation of microvascular tone and regional blood flow.1 In addition, NO inhibits platelet aggregation and adhesion, inhibits leukocyte adhesion and migration, and reduces vascular smooth muscle proliferation, thus leading to prevention of atherosclerosis. NO produced via neuronal NO synthase (nNOS) is released from Abundant and varied data from animal and human studies, performed over the course of more than two decades, indicate that depression of synthesis and bioavailability of NO in the endothelium participates in many cardiovascular diseases, including atherosclerosis, 4 coronary heart diseases, 5 stroke, 3 renal failure, 6 and hypertension 5,7 and also in insulin resistance and diabetes mellitus.8 Mechanisms underlying impairment of NO-mediated vasodilatation and blood flow increase include the downregulation of endothelial NOS (eNOS) and nNOS expressions, generation of NOS inhibitors and NO scavengers, and upregulation of vasoconstrictor substances, such as endothelin-1 (ET-1),...

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Effect of External Counterpulsation on Plasma Nitric Oxide and Endothelin-1 Levels

Cited by 77 publications

References 9 publications

Enhanced External Counterpulsation Inhibits Intimal Hyperplasia by Modifying Shear Stress–Responsive Gene Expression in Hypercholesterolemic Pigs

Enhanced External Counterpulsation Inhibits Intimal Hyperplasia by Modifying Shear Stress–Responsive Gene Expression in Hypercholesterolemic Pigs

Possibilities of Enhanced External Counterpulsation Using in Clinical Practice

Nitric Oxide-Mediated Coronary Flow Regulation in Patients with Coronary Artery Disease: Recent Advances

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