Flow-mediated vasodilation of human epicardial coronary arteries: effect of inhibition of nitric oxide synthesis

Shiode, Nobuo; Morishima, Nobuyuki; Nakayama, Kensyo; Yamagata, Togo; Matsuura, Hideo; Kajiyama, Goro

doi:10.1016/0735-1097(95)00465-3

Cited by 73 publications

(45 citation statements)

References 30 publications

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“…These stressors induce coronary vasodilatation by a primarily endothelium-independent mechanism. In fact, only the subsequent increment in coronary blood flow triggers further flow-induced vasodilation, which is endothelium-dependent (13). In the present study, we demonstrate that the non-pharmacological stressor CPT is able to reveal a reduced CFR in SHypo patients.…”

Section: Discussionsupporting

confidence: 53%

“…In the second study, dipyridamole infusion induced a similar reduction of hyperemic coronary flow, and thus of CFR, in patients with SHypo and in normal subjects (12). It is noteworthy that both adenosine and dipyridamole induce a hyperemic stimulus that relaxes vascular smooth muscle cells in a fashion only partially dependent on endothelial function (13).…”

Section: Introductionmentioning

confidence: 92%

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Endothelial-mediated coronary flow reserve in patients with mild thyroid hormone deficiency

Biondi

Galderisi²,

Pagano³

et al. 2009

European Journal of Endocrinology

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Context: Although coronary flow reserve (CFR) is reduced in patients with subclinical hypothyroidism (SHypo), the endothelial response of coronary vasomotion has never been explored in this clinical setting. Objective: To investigate the endothelial response of coronary flow in young and middle-aged patients with SHypo, without associated cardiovascular risk factors compared with healthy control subjects. Patients and methods:The study population consisted of 20 women (mean age 38.4C12.1 years) with newly diagnosed, untreated and persistent SHypo due to Hashimoto's thyroiditis. A total of 15 volunteers served as controls. Age, gender, body surface area, glucose, insulin levels, heart rate, systolic, diastolic, and mean blood pressure were similar in patients and controls. Body mass index was significantly higher in SHypo patients. Total cholesterol and low-density lipoprotein cholesterol, despite not significant, tended to be higher, and high-density lipoprotein cholesterol to be lower in SHypo. Coronary blood flow velocities were recorded in patients at rest and after the cold pressor test (CPT), a stimulus that can be considered totally endothelium-dependent. CFR was calculated as the ratio of hyperemic-to-resting diastolic peak velocities. Results: Coronary diastolic peak velocities at rest did not differ between the two groups but were significantly lower after CPT in patients with SHypo, thereby resulting in a lower CFR. The difference remained significant after adjusting resting and CPT velocities for the respective mean blood pressures. TSH was inversely correlated with CFR in the pooled population. Conclusion: Patients with SHypo without associated cardiovascular risk factors have a coronary endothelial dysfunction that appears in response to a physiological stimulus (the CPT).

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Section: Discussionsupporting

confidence: 53%

Section: Introductionmentioning

confidence: 92%

Endothelial-mediated coronary flow reserve in patients with mild thyroid hormone deficiency

Biondi

Galderisi²,

Pagano³

et al. 2009

European Journal of Endocrinology

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“…12 Such an adenosine-induced increase in sympathetic nervous activity might be particularly marked with the large dose of adenosine used in our study. This is in contrast to studies in which small amounts of adenosine have been administered directly into the coronary arteries, 23,24 not yielding systemic concentrations high enough to increase sympathetic nervous activity. Therefore, a low level of sympathetic nervous activity could be an explanation for the lack of effect of NO synthase inhibition on adenosine-induced coronary vascular resistance observed in these studies.…”

Section: Discussionmentioning

confidence: 42%

Influence of Nitric Oxide Synthase and Adrenergic Inhibition on Adenosine-Induced Myocardial Hyperemia

et al. 2001

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Background-Myocardial perfusion during adenosine-induced hyperemia is used both in clinical diagnosis of coronary heart disease and for scientific investigations of the myocardial microcirculation. The objective of this study was to clarify whether adenosine-induced hyperemia is dependent on endothelial NO production or is influenced by adrenergic mechanisms. Methods and Results-In 12 healthy men, myocardial perfusion was measured with PET in 2 protocols performed in random order, each including 3 perfusion measurements. First, perfusion was measured at rest. Second, either saline or the NO synthase inhibitor N G -nitro-L-arginine methyl ester (L-NAME, 4 mg/kg) was infused, and perfusion during adenosine-induced hyperemia was determined. Last, in both protocols, the ␣-receptor blocker phentolamine was infused, and perfusion during adenosine-induced hyperemia was determined again. Resting perfusion was similar in the 2 protocols (0.69Ϯ0.14 and 0.66Ϯ0.18 mL · min Ϫ1 · g Ϫ1 ). L-NAME increased mean arterial blood pressure by 12Ϯ7 mm Hg (PϽ0.01) and reduced heart rate by 16Ϯ7 bpm (PϽ0.01). Adenosine-induced hyperemia (1.90Ϯ0.33 mL · min Ϫ1 · g

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“…ATP is a potent vasodilator of the coronary microvasculature, 1 but also dilates epicardial coronary arteries, through flowmediated vasodilation. 24 In addition, ATP infusion did not cause any significant changes in ST deviation or changes in the double (rate-pressure) product in the present study. Second, it has been shown that the presence of coronary endothelial dysfunction at the level of resistance vessels and/or conduit vessels can cause perfusion defects in patients without significant coronary stenosis.…”

Section: Mechanisms Responsible For Reversible Defects In Patients Wisupporting

confidence: 44%

Coronary Vasospasm Produces Reversible Perfusion Defects Observed During Adenosine Triphosphate Stress Myocardial Single‐photon Emission Computed Tomography

Teragawa¹,

Ueda²,

Okuhara³

et al. 2008

Clinical Cardiology

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Background: Adenosine triphosphate stress thallium-201 single-photon emission computed tomography (ATP-SPECT) is useful for diagnosing coronary artery disease (CAD), although sometimes false positive results are observed. It has not been established whether a coronary spasm is responsible for the false positive findings during ATP-SPECT. Hypothesis: We investigated whether coronary spasm is one of the factors which produces reversible defects on ATP-SPECT. Methods: Eighty-six patients (mean age: 62 y; 58 men) who underwent both spasm-provocation testing by coronary angiography and ATP-SPECT, were selected for the study. Patients with coronary narrowing (>30%), myocardial infarction, or heart failure were excluded. Patients were divided into 2 groups based on whether the spasm-provocation test result was positive (vasospastic angina [VSA] group, n = 46) or negative (non-VSA group, n = 39). Results: The body mass index was lower in the VSA group than in the non-VSA group (p = 0.005). On ATP-SPECT imaging, any type of reversible defect was observed more frequently in the VSA group (68%) than in the non-VSA group (36%, p = 0.0027). Logistic regression analysis demonstrated that the presence of reversible defects was one of the factors accounting for the presence of coronary vasospasm (p = 0.0022, R 2 = 0.172). Conclusions:The findings suggest that reversible defects on ATP-SPECT imaging are frequently present in patients with coronary vasospasm. Coronary spasm may be considered as 1 of the factors, which produce reversible defects on ATP-SPECT, observed in patients with chest symptoms and angiographically normal coronary arteries.

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Flow-mediated vasodilation of human epicardial coronary arteries: effect of inhibition of nitric oxide synthesis

Abstract: Our data suggest that nitric oxide modulates basal coronary artery tone but that mediators other than nitric oxide may be responsible for the flow-mediated vasodilation of human epicardial coronary arteries.

Cited by 73 publications

References 30 publications

Endothelial-mediated coronary flow reserve in patients with mild thyroid hormone deficiency

Endothelial-mediated coronary flow reserve in patients with mild thyroid hormone deficiency

Influence of Nitric Oxide Synthase and Adrenergic Inhibition on Adenosine-Induced Myocardial Hyperemia

Coronary Vasospasm Produces Reversible Perfusion Defects Observed During Adenosine Triphosphate Stress Myocardial Single‐photon Emission Computed Tomography

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