Dependence of human forearm skin postocclusive reactive hyperemia on occlusion time

Yvonne-Tee, Get Bee; Rasool, Aida Hanum Ghulam; Halim, Ahmad Sukari; Rahman, Abdul Rashid Abdul

doi:10.1016/j.vascn.2004.02.002

Cited by 74 publications

(44 citation statements)

References 18 publications

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“…In addition, our results may suggest that the structure of the blood microvessels is preserved (41,51), despite impairment of the mechanisms that contribute to the reactive hyperemia response. The exact mechanism is unknown; however, prostanoids are key players in the PORH response (21), and many factors, including metabolic and endothelial vasodilators, sensory nerves, and NO, have also been shown to be involved (23,50). In fact, abnormally elevated release of prostanoids has been observed in patients with CF (10).…”

Section: Microvascular Function In Patients With Cfmentioning

confidence: 99%

Evidence of microvascular dysfunction in patients with cystic fibrosis

Rodriguez‐Miguelez

Thomas

Seigler

et al. 2016

American Journal of Physiology-Heart and Circulatory Physiology

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Rodriguez-Miguelez P, Thomas J, Seigler N, Crandall R, McKie KT, Forseen C, Harris RA. Evidence of microvascular dysfunction in patients with cystic fibrosis. Am J Physiol Heart Circ Physiol 310: H1479 -H1485, 2016. First published April 15, 2016 doi:10.1152/ajpheart.00136.2016.-Cystic fibrosis (CF) is a genetic, multisystemic disorder with broad clinical manifestations apart from the well-characterized pulmonary dysfunction. Recent findings have described impairment in conduit vessel function in patients with CF; however, whether microvascular function is affected in this population has yet to be elucidated. Using laser-Doppler imaging, we evaluated microvascular function through postocclusive reactive hyperemia (PORH), local thermal hyperemia (LTH), and iontophoresis with acetylcholine (ACh). PORH [518 Ϯ 174% (CF) and 801 Ϯ 125% (control), P ϭ 0.039], LTH [1,338 Ϯ 436% (CF) and 1,574 Ϯ 620% (control), P ϭ 0.045], and iontophoresis with ACh [416 Ϯ 140% (CF) and 617 Ϯ 143% (control), P ϭ 0.032] were significantly lower in patients with CF than control subjects. In addition, the ratio of PORH to LTH was significantly (P ϭ 0.043) lower in patients with CF (55.3 Ϯ 5.1%) than control subjects (68.8 Ϯ 3.1%). Significant positive correlations between LTH and forced expiratory volume in 1 s (%predicted) (r ϭ 0.441, P ϭ 0.013) and between the PORH-to-LTH ratio and exercise capacity (r ϭ 0.350, P ϭ 0.049) were observed. These data provide evidence of microvascular dysfunction in patients with CF compared with control subjects. In addition, our data demonstrate a complex relationship between microvascular function and classical markers of disease severity (i.e., pulmonary function and exercise capacity) in CF. CYSTIC FIBROSIS (CF) is an inherited disorder that is predominantly characterized by pulmonary dysfunction; however, broader clinical manifestations, such as gastrointestinal, immune, endocrine, and musculoskeletal dysfunctions, are also present (36). Recently, our group reported conduit vascular endothelial dysfunction in young patients with CF (39). Importantly, this vascular impairment was observed in a population that exhibited preserved spirometric function and exercise capacity, which suggests a systemic consequence prior to the decrease in pulmonary function. Despite these recent observations, there appears to be a lack of understanding of the general functionality of the endothelium in CF.Impairments in endothelial function are highly related to a reduction in the bioavailability of nitric oxide (NO), a key vasodilator involved in the regulation of vessel tone and endothelium integrity (24). Decreases in NO balance have also been shown to contribute to impaired endothelial microvascular vasodilation (44). With use of laser-Doppler imaging technology, cutaneous blood flux can be quantified (45) to represent an accessible model of microvascular function (17). Postocclusive reactive hyperemia (PORH), local thermal hyperemia (LTH), and iontophoresis with acetylcholine (ACh), in combination with laser technology...

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Section: Microvascular Function In Patients With Cfmentioning

confidence: 99%

Evidence of microvascular dysfunction in patients with cystic fibrosis

Rodriguez‐Miguelez

Thomas

Seigler

et al. 2016

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

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“…Although to date no consensus exists about the optimal ischemia duration, an occlusion with the cuff inflated at a suprasystolic pressure (50 mm Hg above the systolic pressure) during at least 3 minutes could be performed. 44 The PORH test, which is believed to be endothelium dependent and involving both myogenic and metabolic factors, evaluates the reperfusion of the vascular beds and is characterized by a peak in the skin blood flow. 34 PORH relies mainly on adenosine, ATP-sensitive potassium channels, partial pressure of oxygen, prostaglandins, and NO.…”

Section: Porh Testmentioning

confidence: 99%

Assessment of Skin Microvascular Function and Dysfunction With Laser Speckle Contrast Imaging

Mahé

Humeau-Heurtier

Durand

et al. 2012

Circ: Cardiovascular Imaging

140

115

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“…The blood flow was measured in 2 mm depth and is expressed in arbitrary units. Given the great inter-and intra-assay variability of absolute blood flow values, a reproducible test was developed, which assesses the increase in blood flow following a 4.5-min ischemia (33). Reactive hyperemia was calculated as the ratio between the maximal postischemia and the baseline blood flow.…”

Section: Measurement Of Endothelial Functionmentioning

confidence: 99%

Benfotiamine Prevents Macro- and Microvascular Endothelial Dysfunction and Oxidative Stress Following a Meal Rich in Advanced Glycation End Products in Individuals With Type 2 Diabetes

et al. 2006

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OBJECTIVE -Diabetes is characterized by marked postprandial endothelial dysfunction induced by hyperglycemia, hypertriglyceridemia, advanced glycation end products (AGEs), and dicarbonyls (e.g., methylglyoxal [MG]). In vitro hyperglycemia-induced MG formation and endothelial dysfunction could be blocked by benfotiamine, but in vivo effects of benfotiamine on postprandial endothelial dysfunction and MG synthesis have not been investigated in humans until now.RESEARCH DESIGN AND METHODS -Thirteen people with type 2 diabetes were given a heat-processed test meal with a high AGE content (HAGE; 15.100 AGE kU, 580 kcal, 54 g protein, 17 g lipids, and 48 g carbohydrates) before and after a 3-day therapy with benfotiamine (1,050 mg/day). Macrovascular flow-mediated dilatation (FMD) and microvascular reactive hyperemia, along with serum markers of endothelial disfunction (E-selectin, vascular cell adhesion molecule-1, and intracellular adhesion molecule-1), oxidative stress, AGE, and MG were measured during both test meal days after an overnight fast and then at 2, 4, and 6 h postprandially.RESULTS -The HAGE induced a maximum reactive hyperemia decrease of Ϫ60.0% after 2 h and a maximum FMD impairment of Ϫ35.1% after 4 h, without affecting endotheliumindependent vasodilatation. The effects of HAGE on both FMD and reactive hyperemia were completely prevented by benfotiamine. Serum markers of endothelial dysfunction and oxidative stress, as well as AGE, increased after HAGE. These effects were significantly reduced by benfotiamine.CONCLUSIONS -Our study confirms micro-and macrovascular endothelial dysfunction accompanied by increased oxidative stress following a real-life, heat-processed, AGE-rich meal in individuals with type 2 diabetes and suggests benfotiamine as a potential treatment. Diabetes Care 29:2064 -2071, 2006E ndothelial dysfunction is an early marker of atherosclerosis and accompanies states showing a high cardiovascular risk, such as smoking (1), dyslipidemia (2), arterial hypertension (3), obesity (4), coronary artery disease (5), congestive heart failure (6), and type 1 (7) and type 2 (8) diabetes. Postprandial endothelial dysfunction has been proposed as the link between postprandial dysmetabolism and atherosclerosis (9) and occurs not only in patients with cardiovascular disease (10) or diabetes (11) but even in healthy subjects (12). Distinctive and cumulative (11) effects of hyperglycemia (13) and hypertriglyceridemia (14) on postprandial endothelial dysfunction have been shown. Since the postprandial state covers most of our daytime, interventions aimed at reducing postprandial endothelial dysfunction might play a decisive role in prevention of atherosclerosis. Several therapeutic approaches have been suggested for the treatment of postprandial endothelial dysfunction, including insulin, folic acid, tetrahydrobiopterin, vitamins C and E, and statins (11). These approaches aim at reducing postprandial oxidative stress (vitamins C and E, statins, and partly folic acid), postprandial hyperglycemia (insul...

show abstract

Dependence of human forearm skin postocclusive reactive hyperemia on occlusion time

Cited by 74 publications

References 18 publications

Evidence of microvascular dysfunction in patients with cystic fibrosis

Evidence of microvascular dysfunction in patients with cystic fibrosis

Assessment of Skin Microvascular Function and Dysfunction With Laser Speckle Contrast Imaging

Benfotiamine Prevents Macro- and Microvascular Endothelial Dysfunction and Oxidative Stress Following a Meal Rich in Advanced Glycation End Products in Individuals With Type 2 Diabetes

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