Vascular Function In Individuals Research Articles

Postprandial Vascular Effects of a High Potassium Meal in Patients with Treated Hypertension.

There is compelling evidence of an inverse association between potassium intake and blood pressure (BP). A potential mechanism for this effect may be dietary potassium-mediated augmentation of endothelium-dependent relaxation. To date, studies have investigated potassium intake supplementation over several weeks in healthy volunteers with variable results on vascular function. There is no assessment of the acute vascular effects of potassium supplementation achieved by the ingestion of potassium-rich food in a hypertensive population. The purpose of this study was to investigate the effect of a high potassium meal on postprandial endothelial function as measured by flow-mediated dilatation (FMD). We performed an investigator-blinded randomized crossover trial in 33 treated hypertensive individuals. Participants consumed both a high (~2400 mg) and low (~543 mg) K+ meal, separated by a one-week washout period. The primary endpoint was endothelial function as assessed by FMD pre-meal and postprandially at 60 and 120 min. Meals were compared at each time point using the Hills-Armitage approach. 33 individuals were included in the study (48% male, mean age 68). In the fasting state (Baseline), and at 60 min postprandial, radial artery FMD was not significantly different between the participants after consumption of either meal (baseline: high K+ 4.2 ± 2% versus Low K+ 2.6 ± 3%, p = 0.93; 60 min: high K+ 3.8 ± 4% versus Low K+ 4.1 ± 3%, p = 0.69). However, at 120 min, FMD tended to be higher in participants after the high K+ meal (5.2 ± 4.1%) than after the low K+ meal (3.9 ± 4.1%) (p = 0.07). There were no differences in participants' radial artery diameter and blood flow between meals. This study does not support our hypothesis that a single high K+ meal improves vascular function in individuals with treated hypertension. This does not contradict the clinical evidence relating greater K+ intake with lower BP, but suggests that mechanistic investigations of increased K+ intake through diet alone and its impact on endothelial function as a mediator to reducing BP are complex and not simply due to single nutrient-mediated improvement in vascular function.

Impact of dietary supplementation of glycocalyx precursors on vascular function in type 2 diabetes.

Degradation of the endothelial glycocalyx in type 2 diabetes (T2D) is thought to contribute to impaired shear stress mechanotransduction, leading to endothelial dysfunction and the development of cardiovascular disease. Herein, we tested the hypothesis that restoration of the endothelial glycocalyx with dietary supplementation of glycocalyx precursors (DSGPs, containing glucosamine sulfate, fucoidan, superoxide dismutase, and high-molecular weight hyaluronan) improves endothelial function and other indices of vascular function in T2D. First, in db/db mice, we showed that treatment with DSGP (100 mg/kg/day) for 4 wk restored endothelial glycocalyx length, as assessed via atomic force microscopy in aortic explants. Restoration of the glycocalyx with DSGP was accompanied by improved flow-mediated dilation (FMD) and reduced arterial stiffness in isolated mesenteric arteries. Further corroborating these findings, the treatment of cultured endothelial cells with that same mixture of glycocalyx precursors promoted glycocalyx growth. Next, as an initial step to investigate the translatability of these findings, we conducted a pilot (n = 22) double-blinded randomized placebo-controlled clinical trial to assess the effects of DSGP (3,712.5 mg/day) for 8 wk on endothelial glycocalyx integrity and indices of vascular function, including FMD, in Veterans with T2D. Contrary to the hypothesis, DSGP neither enhanced endothelial glycocalyx integrity nor improved vascular function indices relative to placebo. Together, these findings conceptually support the notion that restoration of the endothelial glycocalyx can lead to improvements in vascular function in a mouse model of T2D; however, DSGP as a therapeutic strategy to enhance vascular function in individuals with T2D does not appear to be efficacious.NEW & NOTEWORTHY Endothelial glycocalyx degradation in type 2 diabetes (T2D) is thought to contribute to impaired shear stress mechanotransduction, leading to vascular dysfunction. The findings of this study support the notion that restoration of the endothelial glycocalyx using a dietary supplementation of glycocalyx precursors can lead to improvements in vascular function in diabetic mice. However, the utilized dietary supplement as a therapeutic strategy to enhance vascular function in individuals with T2D is not efficacious.

Dietary Effect on Peripheral and Cerebral Vascular Function in Adults with Non-Alcoholic Fatty Liver Disease

Objective: Non-alcoholic fatty liver disease (NAFLD) is a recognized independent risk factor for cardiovascular and cerebrovascular dysfunction. The present study evaluated the effect of dietary interventions on peripheral and cerebral vascular function in individuals with NAFLD. Methods: We studied 30 middle-aged adults (55±9 years) with NAFLD or with elevated NAFLD risk (with prediabetes symptoms). Liver fat content was assessed via 1H magnetic resonance spectroscopy. NAFLD was defined as liver fat proton density fat fraction (PDFF) exceeding 5%. Participants were randomly assigned to a low-carbohydrate diet (carbohydrate intake <30 g/d) or a low-calorie diet (30% calorie intake reduction). Arterial stiffness (via brachial-ankle pulse wave velocity-baPWV), carotid artery intima-media thickness (IMT), endothelium-dependent vasodilation (via flow-mediated dilation-FMD), cerebrovascular reactivity (CVR) in the middle cerebral artery (MCA), and blood concentrations of cardiovascular risk factors were measured before and after a two-week dietary intervention. Results: Participants with NAFLD represented 70% of the current cohort. Following the dietary interventions, participants had significant reductions in body weight (95%CI [-3.22, -1.41 kg]) and fat mass (95%CI [-1.64, -0.56 kg]), accompanied by decreased liver fat content (95%CI [-2.62, -0.79%]). These changes were only evident in the NAFLD group with no significant differences between the two dietary interventions. Systolic and diastolic blood pressure as well as pulse pressure significantly decreased in both NAFLD and non-NAFLD groups. Total cholesterol (95%CI [-22.2, -1.5 mg/dL]) and triglyceride (95%CI [-30.4, -0.9 mg/dL]) concentrations decreased in those with NAFLD assigned to the low-carbohydrate diet. baPWV decreased (95%CI [-78.6, -12.4 cm/s]) only in individuals with NAFLD assigned to the low-calorie diet. FMD significantly increased (95%CI [0.5, 5.1%]) only in individuals with NAFLD assigned to the low-carbohydrate diet. Lower baseline liver fat content was associated with greater improvement in FMD (r=-0.60, p=0.008) in the NAFLD group. Carotid IMT and cerebrovascular parameters (e.g., pulsatility index, CVR, MCA blood flow velocity) remained unchanged in any groups. Changes in vascular function were not associated with the corresponding changes in liver fat content. Conclusion: The two-week dietary intervention involving either a low-carbohydrate or low-calorie diet elicited significant reductions in liver fat content and improvements in peripheral arterial stiffness and endothelium-dependent vasodilation in adults with NAFLD. UT Aging Initiatives. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

357 Effects of Dietary Nitrate Supplementation on Vascular Function in Individuals with Prediabetes

OBJECTIVES/GOALS: Impaired vascular function, a subclinical marker of cardiovascular disease, has been identified in prediabetes. Dietary nitrate supplementation has been shown to improve vascular function. However, this has not been studied in prediabetes. The purpose was to determine the effects of dietary nitrate on vascular function in prediabetes. METHODS/STUDY POPULATION: Five individuals with prediabetes (4 men, 1 woman; 55 ± 17 yr; HbA1c = 5.8 ± 0.2) participated in a double-blind, placebo-controlled, repeated measures study. Participants were randomly assigned to a 3-day nitrate supplementation (nitrate-rich beetroot juice, 12.9 mmol, 140 mL), or a placebo supplementation (nitrate-depleted beetroot juice, 0.05 mmol, 140 mL). Following supplementation, participants reported to the lab for measures of vascular function in the lower limb. Doppler ultrasonography was used to measure flow-mediated dilation (FMD) and post-occlusive reactive hyperemia (RH) of the superficial femoral artery in response to a 5-min bout of leg ischemia. RESULTS/ANTICIPATED RESULTS: FMD did not differ between the nitrate-rich (2.87 ± 2.01%) and placebo (2.24 ± 1.69%) conditions (p = 0.48; d = 0.35). Furthermore, peak RH did not differ between the nitrate-rich (1503 ± 443 ml/min) and placebo (1762 ± 414 ml/min) conditions (p = 0.36; d = 0.46). DISCUSSION/SIGNIFICANCE: These preliminary results suggest that dietary nitrate supplementation in the form of beetroot juice does not improve vascular function in individuals with prediabetes.

Eight weeks of treatment with mineralocorticoid receptor blockade does not alter vascular function in individuals with and without type 2 diabetes.

Aldosterone has been suggested to be involved in the microvascular complications observed in type 2 diabetes. We aimed to investigate the effect of mineralocorticoid receptor (MR) blockade on endothelial function in individuals with type 2 diabetes compared to healthy controls. We included 12 participants with type 2 diabetes and 14 controls. We measured leg hemodynamics at baseline and during femoral arterial infusion of acetylcholine and sodium nitroprusside before and 8 weeks into treatment with MR blockade (eplerenone). Acetylcholine infusion was repeated with concomitant n-acetylcysteine (antioxidant) infusion. No difference in leg blood flow or vascular conductance was detected before or after the treatment with MR blockade in both groups and there was no difference between groups. Infusion of n-acetylcysteine increased baseline blood flow and vascular conductance, but did not change the vascular response to acetylcholine before or after treatment with MR blockade. Skeletal muscle eNOS content was unaltered by MR blockade and no difference between groups was detected. In conclusion, we found no effect of MR blockade endothelial function in individuals with and without type 2 diabetes. As the individuals with type 2 diabetes did not have vascular dysfunction, these results might not apply to individuals with vascular dysfunction.

Impact of Insulin-Induced Relative Hypoglycemia on Vascular Insulin Sensitivity and Central Hemodynamics in Prediabetes.

Relative hypoglycemia (RH) is linked to sympathetic responses that can alter vascular function in individuals with type 2 diabetes. However, less is known about the role of RH on hemodynamics or metabolic insulin sensitivity in prediabetes. Determine if RH alters peripheral endothelial function or central hemodynamics to a greater extent in those with prediabetes (PD) versus normoglycemia (NG). Seventy adults with obesity were classified using ADA criteria as PD (n=34 (28F); HbA1c=6.02±0.1%) or NG (n=36 (30F); HbA1c=5.4±0.0%). Brachial artery endothelial function, skeletal muscle capillary perfusion, and aortic waveforms were assessed at 0 and 120min of a euglycemic clamp (40 mU/m2/min, 90 mg/dl). Plasma nitrate/nitrite and endothelin-1 (ET-1) were measured as surrogates of nitric oxide-mediated vasodilation and vasoconstriction, respectively. RH was defined as the drop in glucose (%) from fasting to clamp steady state. There were no differences in age, weight, or VO2max between groups. PD had higher HbA1c (P<0.01) and a greater drop in glucose in response to insulin (14 vs. 8%; P=0.03). Further, heart rate (HR) increased in NG compared to PD (P<0.01), while forward wave (Pf) decreased in PD (P=0.04). Insulin also tended to reduce arterial stiffness (cfPWV) in NG versus PD (P=0.07), despite similar increases in pre-occlusion diameter (P=0.02), blood flow (P=0.02), and lower augmentation index (AIx75) (P≤0.05). Compared with NG, insulin-induced RH corresponded with a blunted rise in HR and drop in Pf during insulin infusion in adults with PD, independent of changes in peripheral endothelial function.

Hyperaemia during dynamic handgrip exercise is preserved in healthy young subjects after recovery from COVID-19.

We sought to investigate possible impaired hyperaemia during dynamic handgrip exercise (HGE) in young healthy individuals who had recovered from COVID-19. We tested the vascular function in individuals recovered from COVID-19 using a nitric oxide donor (i.e., sodium nitroprusside; SNP), which could revert a possible impaired endothelial function during HGE. Further, we tested whether individuals who recovered from COVID-19 would present exaggerated brachial vascular resistance under an adrenergic agonist (i.e., phenylephrine; PHE) stimuli during HGE. Participants were distributed into two groups: healthy controls (Control; men: n=6, 30±3years, 26±1kg/m2; and women: n=5, 25±1years, 25±1kg/m2) and subjects recovered from COVID-19 (post-COVID; men: n=6, 29±3years, 25±1kg/m2; and women: n=10, 32±4years, 22±1kg/m2). Participants in the post-COVID group tested positive (RT-PCR) 12-14weeks before the protocol. Heart rate (HR), brachial blood pressure (BP), brachial blood flow (BBF) and vascular conductance (BVC) at rest were not different between groups. The HGE increased HR (Control: Δ9±0.4bpm; and post-COVID: Δ11±0.4bpm) and BP (Control: Δ6±1mmHg; and post-COVID: Δ12±0.6mmHg) in both groups. Likewise, BBF (Control: Δ632±38ml/min; and post-COVID: Δ620±27ml/min) and BVC (Control: Δ6.6±0.4ml/min/mmHg; and post-COVID: Δ6.1±0.3ml/min/mmHg) increased during HGE. SNP did not change HGE-induced hyperaemia but did decrease BP, which induced a reflex-related increase in HR. PHE infusion also did not change the HGE-induced hyperaemia but raised BP and reduced HR. In conclusion, exercise-induced hyperaemia is preserved in healthy young subjects 12-14weeks after recovery from COVID-19 infection.

Handgrip Strength Is Associated with Specific Aspects of Vascular Function in Individuals with Metabolic Syndrome.

Metabolic syndrome (MetS) is a disorder associated with an increased risk for the development of diabetes mellitus and its complications. Lower isometric handgrip strength (HGS) is associated with an increased risk of cardiometabolic diseases. However, the association between HGS and arterial stiffness parameters, which are considered the predictors of morbidity and mortality in individuals with MetS, is not well defined. To determine the association between HGS and HGS asymmetry on components of vascular function in adults with MetS. We measured handgrip strength normalized to bodyweight (HGS/kg), HGS asymmetry, body composition, blood glucose, lipid profile, blood pressure, pulse wave velocity (PWV), reflection coefficient (RC), augmentation index @75 bpm (AIx@75) and peripheral vascular resistance (PVR) in 55 adults with a diagnosis of MetS between 25 and 54 years old. Mean age was 43.1 ± 7.0 years, 56.3% were females. HGS/kg was negatively correlated with AIx@75 (r = -0.440), p < 0.05, but these associations were not significant after adjusting for age and sex. However, when interaction effects between sex, HGS/kg and age were examined, we observed an inverse relationship between HGS/kg and AIx@75 in the older adults in the sample, whereas in the younger adults, a weak direct association was found. We also found a significant association between HGS asymmetry and PVR (beta = 30, 95% CI = 7.02; 54.2; p <0.012). Our findings suggest that in people with MetS, maintaining muscle strength may have an increasingly important role in older age in the attenuation of age-related increases in AIx@75-a marker of vascular stiffness-and that a higher HGS asymmetry could be associated with a greater vascular resistance.

Effects of L-Citrulline Supplementation and Aerobic Training on Vascular Function in Individuals with Obesity across the Lifespan.

Children with obesity are at higher risk for developing cardiometabolic diseases that once were considered health conditions of adults. Obesity is commonly associated with cardiometabolic risk factors such as dyslipidemia, hyperglycemia, hyperinsulinemia and hypertension that contribute to the development of endothelial dysfunction. Endothelial dysfunction, characterized by reduced nitric oxide (NO) production, precedes vascular abnormalities including atherosclerosis and arterial stiffness. Thus, early detection and treatment of cardiometabolic risk factors are necessary to prevent deleterious vascular consequences of obesity at an early age. Non-pharmacological interventions including L-Citrulline (L-Cit) supplementation and aerobic training stimulate endothelial NO mediated vasodilation, leading to improvements in organ perfusion, blood pressure, arterial stiffness, atherosclerosis and metabolic health (glucose control and lipid profile). Few studies suggest that the combination of L-Cit supplementation and exercise training can be an effective strategy to counteract the adverse effects of obesity on vascular function in older adults. Therefore, this review examined the efficacy of L-Cit supplementation and aerobic training interventions on vascular and metabolic parameters in obese individuals.

Traditional weight loss and dukan diets as to nutritional and laboratory results

Traditional weight loss and dukan diets as to nutritional and laboratory results

Repeated Passive Mobilization to Stimulate Vascular Function in Individuals of Advanced Age Who Are Chronically Bedridden: A Randomized Controlled Trial.

Vascular dysfunction and associated disorders are major side effects of chronic bed rest, yet passive mobilization as a potential treatment has only been theorized so far. This study investigated the effects of passive mobilization treatment on vascular function in older, chronically bedridden people. The study sample was 45 chronically bedridden people of advanced age (mean age: 87 years; 56% female; mean bed rest: 4 years) randomly assigned to a treatment (n = 23) or a control group (CTRL, n = 22). The treatment group received passive mobilization twice daily (30 minutes, 5 times/wk) for 4 weeks. A kinesiologist performed passive mobilization by passive knee flexion/extension at 1 Hz in one leg (treated leg [T-leg] vs control leg [Ctrl-leg]). The CTRL group received routine treatment. The primary outcome was changes in peak blood flow (∆peak) as measured with the single passive leg movement test at the common femoral artery. ∆Peak was increased in both legs in the Treatment group (+90.9 mL/min, p < .001, in T-leg and +25.7 mL/min, p = .039 in Ctrl-leg). No difference in peak blood flow after routine treatment was found in the CTRL group. Improvement in vascular function after 4 weeks of passive mobilization was recorded in the treatment group. Passive mobilization may be advantageously included in standard clinical practice as an effective strategy to treat vascular dysfunction in persons with severely limited mobility.

Autonomically-mediated decrease in microvascular blood flow due to mental stress and pain in sickle cell disease: A target for neuromodulatory interventions

Pain and vaso-occlusive crises (VOC) are hallmark complications of sickle cell disease (SCD) and result in significant physical and psychosocial impairment. The variability in SCD pain frequency and triggers for the transition from steady state to VOC are not well understood. This paper summarizes the harmful physiological effects of pain and emotional stressors on autonomically-mediated vascular function in individuals with SCD and the effects of a cognitive, neuromodulatory intervention (i.e. hypnosis) on microvascular blood flow. We reviewed recent studies from the authors’ vascular physiology laboratory that assessed microvascular responses to laboratory stressors in individuals with SCD. Results indicate that participants with SCD exhibit marked neurally mediated vascular reactivity in response to pain, pain-related fear, and mental stress. Further, pilot study results show that engagement in hypnosis may attenuate harmful microvascular responses to pain. The collective results demonstrate that autonomically-mediated vascular responses to pain and mental stress represent an important SCD intervention target. This ongoing work provides physiological justification for the inclusion of cognitive, neuromodulatory and complementary treatments in SCD disease management and may inform the development of targeted, integrative interventions that prevent the enhancement of autonomic vascular dysfunction in SCD.

Effects of heated water-based versus land-based exercise training on vascular function in individuals with peripheral artery disease.

Peripheral artery disease (PAD) is an atherosclerotic disease that is associated with poor vascular function, walking impairment, and reduced quality of life. Land-based exercise therapy (LBET) is frequently recommended to improve walking and reduce symptoms. Recently, evidence has suggested that heated-water exercise therapy (HWET) is an effective intervention for PAD. However, the efficacy of LBET versus HWET in PAD patients had not been elucidated. Therefore, we sought to compare effects of LBET with HWET on cardiovascular function, exercise tolerance, physical function, and body composition in PAD patients. PAD patients (n = 53) were recruited and randomly assigned to a LBET group (n = 25) or HWET group (n = 28). The LBET group performed treadmill walking, whereas the HWET group performed walking in heated water for 12 wk. Leg (legPWV) and brachial-to-ankle arterial stiffness (baPWV), blood pressure (BP), ankle-brachial index (ABI), 6-min walking distance (6MWD), claudication onset time (COT), physical function, and body composition were assessed before and after 12 wk. There were significant group-by-time interactions (P < 0.05) for legPWV, BP, 6MWD, COT, body composition, and resting metabolic rate (RMR). Both groups significantly reduced (P < 0.05) legPWV, BP, and body fat percentage, and HWET measures were significantly lower than LBET measures. Both groups significantly increased 6MWD, COT, and RMR, and HWET group measures were significantly greater than LBET measures. A time effect was noted for baPWV reduction in both groups (P < 0.05). These results suggest that both LBET and HWET improve cardiovascular function, exercise tolerance, and body composition, and HWET showed considerably greater improvements compared with LBET in patients with PAD.NEW & NOTEWORTHY The results of this study reveal for the first time that although land-based exercise therapy is effective for reducing arterial stiffness and blood pressure in patients with peripheral artery disease (PAD), heated-water exercise therapy demonstrates greater benefits on vascular function. The greater improvements in muscular strength, time to onset of claudication, and exercise tolerance after heated-water exercise therapy may have clinical implications for improving quality of life in patients with PAD. The heated-water exercise therapy intervention demonstrated relatively higher exercise training adherence (∼88%) compared with the land-based exercise intervention (∼81%).

Vascular improvements in individuals with type 2 diabetes following a 1year randomised controlled exercise intervention, irrespective of changes in cardiorespiratory fitness.

Vascular changes in individuals with type 2 diabetes mellitus majorly contribute to the development of cardiovascular disease. Increased cardiorespiratory fitness (CRF) has been associated with improvements in vascular health. Although CRF tends to improve with exercise training, there remains a portion of participants with little or no improvement. Given the importance of vascular function in individuals with type 2 diabetes, we assessed whether individuals who failed to improve CRF following a 1year exercise intervention also failed to improve arterial stiffness and structural indices. Individuals with type 2 diabetes with no major micro- and macrovascular complications and aged between 30 and 75years old (n = 63) participated in a three-arm, 1year, randomised controlled exercise intervention in Lisbon, Portugal. The study involved a non-exercise control group, a moderate continuous training combined with resistance training (RT) group and a high-intensity interval training with RT group. Allocation of participants into the intervention and control groups was done using a computer-generated list of random numbers. An improvement in CRF was defined as a change in [Formula: see text] ≥5%. Vascular stiffness and structural indices were measured using ultrasound imaging and applanation tonometry. Generalised estimating equations were used to compare changes in vascular measures across individuals in the control group (n = 22) and those in the exercise groups who either had improved CRF (CRF responders; n = 14) or whose CRF did not improve (CRF non-responders; n = 27) following 1year of exercise training. Compared with the control group, exercisers, with and without improvements in CRF, had decreased carotid intima-media thickness (IMT) (CRF responders: β = -2.84 [95% CI -5.63, -0.04]; CRF non-responders: β = -5.89 [95% CI -9.38, -2.40]) and lower-limb pulse wave velocity (PWV) (CRF responders: β = -0.14 [95% CI -0.25, -0.03]; CRF non-responders: β = -0.14 [95% CI -0.25, -0.03]), the latter being an indicator of peripheral arterial stiffness. Only CRF responders had decreased PWV of the upper limb compared with control participants (β = -0.12 [95% CI -0.23, -0.01]). As for central stiffness, CRF non-responders had increased aortic PWV compared with CRF responders (β = 0.19 [95% CI 0.07, 0.31]), whereas only the CRF non-responders had altered carotid distensibility coefficient compared with the control group (β = 0.00 [95% CI 3.01 × 10-5, 0.00]). No interaction effects between the CRF responders and non-responders vs control group were found for the remaining stiffness or haemodynamic indices (p>0.05). Regardless of improvements in CRF, individuals with type 2 diabetes had significant improvements in carotid IMT and lower-limb arterial stiffness following a 1year exercise intervention. Thus, a lack of improvement in CRF following exercise in people with type 2 diabetes does not necessarily entail a lack of improvement in vascular health. ClinicalTrials.gov NCT03144505 FUNDING: This work was supported by fellowships from the Portuguese Foundation for Science and Technology. This work is also financed by a national grant through the Fundação para a Ciência e Tecnologia (FCT), within the unit I&D 472.

Peripheral Vascular Function in Individuals with Posttraumatic Stress Disorder

THE IMPACT OF POSTTRAUMATIC STRESS DISORDER ON PERIPHERAL VASCULAR FUNCTION J. Weggen, A. Hogwood, B. Imthurn, A. McIntyre, A. Darling, K. Decker and R. Garten. Virginia Commonwealth University, Richmond, VA The physiological manifestations of posttraumatic stress disorder (PTSD) have been associated with an increase in risk of cardiovascular disease (CVD) independent of negative lifestyle factors. Peripheral vascular dysfunction may be a mechanism by which PTSD increases CVD risk via increases in oxidative stress, inflammation, and/or sympathetic nervous system activity. PURPOSE: This study sought to examine peripheral vascular function in those with PTSD compared to age-matched controls. METHODS: Eight individuals with PTSD (5 women, 3 men; age 22 ± 2 years), and sixteen healthy controls (CON; 10 women, 6 men, 23 ± 2 years), participated in the study. Leg vascular function was assessed via passive leg movement (PLM) technique and evaluated with Doppler ultrasonography. PLM-induced increases in leg blood flow were quantified as peak change in blood flow from baseline (ΔPeak LBF) and blood flow area under the curve (LBF AUC). RESULTS: Significant differences in leg vascular function were revealed between groups. The PTSD group reported significantly lower ΔPeak LBF (PTSD: 294.16 ± 54.16; CON: 594.78 ± 73.70 ml∙min-1; p = 0.01) and LBF AUC (PTSD: 57.23 ± 24.37; CON: 169.92 ± 29.84 ml; p = 0.02) when compared to the CON group. CONCLUSION: This study revealed that lower limb vascular function is impaired in individuals with PTSD when compared to healthy counterparts.

Systemic oxidoreductive balance and vascular function in individuals without clinical manifestation of atherosclerosis.

IntroductionEndothelial dysfunction is recognized as the earliest disorder in the development of atherosclerosis, in the pathogenesis of which oxidative stress plays a crucial role. The aim of this study was to determine the relationships between non-invasive parameters of vascular dysfunction and oxidative stress.Material and methodsForty-eight individuals without clinical manifestation of atherosclerosis were studied. The plasma concentrations of the following were determined in all 48 subjects: retinol, ascorbic acid, α-tocopherol and uric acid, as well as the products of oxidative DNA damage repair: 8-oxo-7,8-dihydro-2’-deoxyguanosine (8-oxodG) in blood leukocytes and urine, and 8-oxo-7,8-dihydroguanine (8-oxoGua) in urine. The following parameters of vascular dysfunction were also examined: flow- (FMD) and nitroglycerin- (NMD) mediated dilatation of the brachial artery, pulse pressure (PP), distensibility coefficient (DC), pulsation (PI) and resistance (RI) index, carotid intima-media thickness (cIMT), and ankle-brachial index (ABI).ResultsIndividuals with an FMD value of ≥ 8.8% had significantly higher blood concentrations of antioxidative vitamins and lower concentrations of 8-oxodG in their urine and blood leukocytes than their counterparts. Blood concentration of alpha-tocopherol or ascorbic acid positively correlated with FMD, PI, RI, DC and ABI and negatively with PP and cIMT. The reverse was the case for 8-oxodG in urine and leukocytes. In multiple regression analysis, markers of oxidative DNA damage positively determined the variance in PP and ABI.ConclusionsIn persons without clinical manifestation of atherosclerosis, oxidative stress was an independent factor associated with vascular wall dysfunction, and a better predictor than smoking and blood concentrations of glucose, lipids and creatinine.

Poor sleep quality related to worse vascular function in individuals with multiple sclerosis

Poor sleep quality related to worse vascular function in individuals with multiple sclerosis

Vascular function in individuals with Down syndrome

Vascular function in individuals with Down syndrome

Vascular function and brain-derived neurotrophic factor: The functional capacity factor.

Brain-derived neurotrophic factor (BDNF) is essential for neurocognitive function. This study aims at establishing a plausible link between level of serum BDNF, functional capacity (FC), and vascular function in 181 young (age 25.5±9.1 years old), apparently healthy adults. Fasting blood samples were drawn from participants' antecubital veins into plain glass tubes while they were in a sitting position to evaluate serum BDNF using enzyme-linked immunosorbent assay (ELISA). Mercury-in-silastic strain-gauge plethysmography was used to determine arterial function indices, blood flow and vascular resistance at rest and following 5 minutes of arterial ischemia. The 6-minute walk distance (6MWD) test was used to determine FC, according to the American Thoracic Society Committee on Proficiency Standards for Clinical Pulmonary Function Laboratories guidelines. It was conducted in an enclosed corridor on a flat surface with a circular track 33 meters long. The walking course was demarcated with bright colored cones. The 6MWD correlated with BDNF (r=0.3, p=0.000), as well as with forearm blood inflow (r=0.5, p=0.000) and vascular resistance (r = -0.4, p=0.000). Subsequent comparison showed that BDNF and blood inflow were greater (p<0.05) while vascular resistance was less (p<0.05) in participants who achieved a longer 6MWD. Similarly, BDNF correlated with forearm blood inflow (r=0.4, p=0.000) and vascular resistance (r = -0.4, p=0.000). Subsequent comparison showed improved vascular function (p<0.05) in the participants with greater BDNF. In conclusion, these findings might suggest that improved vascular function in individuals with greater FC is mediated, at least partially, by an enhanced serum BDNF level.

Assessment of vascular function in individuals with hyperglycemia: a cross-sectional study of glucose - induced changes in digital volume pulse.

BackgroundArterial stiffness is an independent risk factor for cardiovascular disease and its progression may be accelerated in the presence of hyperglycemia, either fasting or postprandial. The current study assessed vascular function in subjects with pre-diabetes hyperglycemia, using digital volume pulse analysis technique.MethodsWe conducted a cross-sectional study examining vascular function in the fasting and postprandial (glucose-induced) state in 44 adults, consisting of 17 subjects with pre-diabetic hyperglycemia and 27 normoglycemic volunteers. Photoplethysmography of the digital volume pulse (DVP) was used to determine stiffness index (SI) and reflective index (RI), as main measures of larger artery stiffness and vascular tone, respectively.ResultsOur results showed a significantly higher (Ln) fasting SI in the hyperglycemic group compared with the control group (2.19 ± 0.32 vs. 1.96 ± 0.22, P = 0.005). However, this pattern reversed after adjustment for potential confounders. In multiple linear regression analysis, (Ln) SI was related to age (β = 0.01, 95% CI: 0.01-0.02, P < 0.001) and systolic blood pressure (SBP) (β = 0.01, 95% CI: 0.00-0.01, P < 0.05), but not with W/H, diastolic blood pressure (DBP), fasting plasma glucose (FPG) or serum lipids. Furthermore, age (β = 0.02, 95% CI: 0.01-0.03, P < 0.001) and mean arterial pressure (MAP) (β = 0.01, 95% CI: 0.00-0.02, P < 0.05) were found as the strong predictors of fasting SI in hyperglycemic group. Neither FPG nor 2-h plasma glucose was a significant predictor for SI in hyperglycemic group, after accounting for age and MAP. Subjects with hyperglycemia had a 15% blunted change in postprandial AUCs for RI, adjusted for the respective baseline measurements (−9.40 ± 3.59 vs. -11.00 ± 2.84%) but these did not attain statistical significance.ConclusionIncreased arterial stiffness in pre-diabetic subjects is strongly associated with age and MAP. The increased DVP-derived SI reported in patients with pre-diabetic hyperglycemia may result from different frequently accompanied risk factors not just glycemic changes in this range.