Protective effects of ascorbic acid on arterial hemodynamics during acute hyperglycemia

Mullan, Brian; Ennis, Ciaran N.; Fee, Howard; Young, Ian S.; McCance, David R.

doi:10.1152/ajpheart.00153.2003

Cited by 33 publications

(34 citation statements)

References 49 publications

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“…[27][28][29][30] The present findings extend these observations by demonstrating a tonic inhibitory effect of oxidative stress on carotid artery compliance in healthy estrogen-deficient postmenopausal women that is not observed in premenopausal females. Consistent with the present results in premenopausal females, our laboratory demonstrated recently that acute and chronic ascorbic acid administration have no effect on carotid artery compliance in healthy young males.…”

Section: Moreau Et Al Oxidative Stress and Arterial Stiffnesssupporting

confidence: 85%

Ascorbic Acid Selectively Improves Large Elastic Artery Compliance in Postmenopausal Women

et al. 2005

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Abstract-The compliance of large elastic arteries in the cardiothoracic region decreases with advancing age/menopause and plays an important role in the increased prevalence of cardiovascular diseases in postmenopausal women. We determined whether oxidative stress contributes to the reduced large elastic artery compliance of postmenopausal women. Carotid artery compliance was measured during acute intravenous infusions of saline (baseline control) and supraphysiological doses of the potent antioxidant ascorbic acid in premenopausal (nϭ10; 23Ϯ1; meanϮSE) and estrogen-deficient postmenopausal (nϭ21; 55Ϯ1 years) healthy sedentary women. Carotid artery compliance was 56% lower in postmenopausal compared with premenopausal women during baseline control (PϽ0.0001 ). Carotid artery diameter, blood pressure, and heart rate were unaffected by ascorbic acid. In the pooled population, the change in arterial compliance with ascorbic acid correlated with baseline waist-to-hip ratio (rϭ0.56; Pϭ0.001), plasma norepinephrine (rϭ0.58; Pϭ0.001), and LDL cholesterol (rϭ0.54; Pϭ0.001). These results suggest that oxidative stress may be an important mechanism contributing to the reduced large elastic artery compliance of sedentary, estrogen-deficient postmenopausal women. Increased abdominal fat storage, sympathetic nervous system activity, and LDL cholesterol may be mechanistically involved in oxidative stress-associated suppression of arterial compliance in postmenopausal women. Key Words: aging Ⅲ cholesterol Ⅲ oxidative stress C ardiovascular disease (CVD) is the leading cause of death in women in the United States. 1 "Vascular aging" has been emphasized recently as the major risk factor for development of CVD. 2 One clinically important change that occurs with vascular aging is a reduction in the compliance of large elastic arteries within the cardiothoracic region. In turn, this contributes to a number of adverse age-associated changes, including increased aortic impedance, left ventricular hypertrophy, and reduced cardiovagal baroreflex sensitivity. [2][3][4] As such, identifying the mechanisms that contribute to reduced large elastic artery compliance with age is an important goal. 2 Cardiovascular aging in women is unique in that it appears to be delayed or occurs at a slower rate than in men during the premenopausal years, thereafter "catching up" with men during the postmenopausal period, particularly in estrogendeficient women. [5][6][7] The mechanisms underlying the accelerated cardiovascular aging of estrogen-deficient postmenopausal women are unclear but could be related in part to the development of oxidative stress. Markers of oxidative stress are higher and endogenous antioxidant defenses lower in some estrogen-deficient postmenopausal women compared with premenopausal controls. 8,9 Because oxidative stress modulates vascular smooth muscle cell (VSMC) tone, a key determinant of large artery compliance, 10,11 we hypothesized that oxidative stress may contribute to the reduced large artery compliance of estrogen-defic...

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Section: Moreau Et Al Oxidative Stress and Arterial Stiffnesssupporting

confidence: 85%

Ascorbic Acid Selectively Improves Large Elastic Artery Compliance in Postmenopausal Women

et al. 2005

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“…Previously, it has been shown that AIx is increased during hyperglycaemia in healthy men [11]. However, this result has not been confirmed by other studies.…”

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confidence: 68%

Acute hyperglycaemia rapidly increases arterial stiffness in young patients with type 1 diabetes

et al. 2007

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Aims/hypothesis Augmentation index (AIx) and pulse wave velocity (PWV), both measures of arterial stiffness, constitute risk factors for cardiovascular disease. Notably, hyperglycaemia during an acute cardiovascular event is associated with poor prognosis. The objective of this study was to investigate whether acute hyperglycaemia increases arterial stiffness in patients with type 1 diabetes and in healthy subjects. Methods Twenty-two male patients with type 1 diabetes and thirteen healthy men, who were age-matched nonsmokers and without any diabetic complications, underwent a 120 min hyperglycaemic clamp (15 mmol/l). AIx was calculated to assess arterial stiffness. Before and during the clamp, carotid-radial (brachial) and carotid-femoral (aortic) PWV was measured. Results At baseline there was a difference in the AIx between patients with type 1 diabetes and healthy volunteers (−5±2.7 vs −20±2.8%, p<0.05). Acute hyperglycaemia rapidly increased AIx in patients with type 1 diabetes (−5±2.7 vs 8±2.5%, p<0.001) and healthy volunteers (−20±2.8 vs 6±8.8%, p<0.001). Brachial PWV increased during acute hyperglycaemia in patients with type 1 diabetes (7.1±1.2 vs 8.0±1.0 m/s, p<0.001), but not in healthy men (7.4±1.7 vs 7.3±1.4 m/s, NS). Conclusions/interpretation Acute hyperglycaemia increases the stiffness of intermediate-sized arteries and resistance arteries in young patients with type 1 diabetes and consequently emphasises the importance of strict daily glycaemic control. No change was observed in aortic PWV during the clamp, indicating that acute hyperglycaemia does not affect the large vessels.

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“…Indeed, hyperglycemia per se has been observed to negatively affect endothelium-dependent vasodilation in human arteries, 10 increase pulse wave reflections, and decrease aortic distensibility in healthy male volunteers. 29 Modest increases in postprandial glucose can acutely lower FMD in healthy subjects as well as those with impaired glucose tolerance and T2DM, though the latter groups show greater reductions. 7,8 Consistent with our results, the inverse association between FMD and plasma glucose found in these studies suggests a continuous relationship between increasing glucose concentrations and decreasing endothelial function.…”

Section: 2425mentioning

confidence: 98%

Protective Effects of Flavanol-Rich Dark Chocolate on Endothelial Function and Wave Reflection During Acute Hyperglycemia

et al. 2012

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Abstract-Nitric oxide plays a pivotal role in regulating vascular tone. Different studies show endothelial function is impaired during hyperglycemia. Dark chocolate increases flow-mediated dilation in healthy and hypertensive subjects with and without glucose intolerance; however, the effect of pretreatment with dark chocolate on endothelial function and other vascular responses to hyperglycemia has not been examined. Therefore, we aimed to investigate the effects of flavanol-rich dark chocolate administration on (1) flow-mediated dilation and wave reflections; (2) blood pressure, endothelin-1 and oxidative stress, before and after oral glucose tolerance test (OGTT 1 Atherosclerotic pathology is a common sequela to T2DM, with macrovascular and microvascular diseases being among the leading causes of morbidity and mortality in patients with T2DM.2 Even after adjustment for conventional risk factors, individuals with T2DM exhibit a 2-to 4-fold increased risk of mortality in comparison with individuals without diabetes.3 Thus, several investigations have been directed to the potential adverse effects of hyperglycemia on the arterial wall. Observational data reveal high blood glucose concentrations are a risk factor for mortality, even in nondiabetic individuals. 4 Postprandial hyperglycemia has also been implicated in the development of cardiovascular disease. Elevated postprandial glucose may have a direct toxic effect on the vascular endothelium mediated by oxidative stress, independent of other cardiovascular risk factors, such as hyperlipidemia.2,5 A highcarbohydrate meal has been described to increase oxidative stress and favor proinflammatory effects. 5Several in vivo studies have found impaired nitric oxide (NO)-mediated endothelial function during acute episodes of hyperglycemia.6-10 NO is a key endothelium-derived relaxing factor and plays a pivotal role in the maintenance of basal vascular tone and vascular responses to dilative stimuli. [11][12][13] NO acts to negate the actions of endothelium-derived contracting factors such as angiotensin II and endothelin-1 (ET-1), as well as inhibit platelet aggregability 11-13 and endothelial activation.11-13 Therefore, reduced NO bioavailability may contribute to the onset and progression of endothelial dysfunction, including impaired vasodilative and increased adhesive properties, leading to atherogenesis.11-13 Additionally, endothelium-derived NO may act to regulate arterial stiffness and wave reflec-

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Protective effects of ascorbic acid on arterial hemodynamics during acute hyperglycemia

Cited by 33 publications

References 49 publications

Ascorbic Acid Selectively Improves Large Elastic Artery Compliance in Postmenopausal Women

Ascorbic Acid Selectively Improves Large Elastic Artery Compliance in Postmenopausal Women

Acute hyperglycaemia rapidly increases arterial stiffness in young patients with type 1 diabetes

Protective Effects of Flavanol-Rich Dark Chocolate on Endothelial Function and Wave Reflection During Acute Hyperglycemia

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