Brachial Artery Endothelial Function Research Articles

The effects of menstrual phase on brachial artery endothelial function after mental stress in young women

The changes in ovarian hormones throughout the menstrual cycle have direct actions on endothelial function. However, very limited human data are available regarding the alterations in endothelial function at baseline or after mental stress during the discrete phases of the menstrual cycle. We examined whether the menstrual cycle influences the endothelial function after mental stress in young women. Female university students were tested during three phases of a normal menstrual cycle. Delineation of the three phases occurred as follows: (1) the early follicular phase; (2) the late follicular phase; (3) the middle luteal phase. Non-invasive measurement of peripheral endothelial function was determined by flow-mediated dilation (FMD) testing in the brachial artery during reactive hyperemia using echo and Doppler ultrasound. After the measurements of basal levels, they were subjected to mental stress evoked by the modified Stroop Color Word Test (CWT) in 10 min. The CWT induced arterial pressure and heart rate (HR) elevations, and a slight vasoconstriction of brachial artery. The measurements of flow-mediated dilation (FMD) and maximal blood flow (%) were repeated at 5 min and 30 min after the CWT. Basal FMD and FMD after the CWT tended to vary during the three phases cyclically.These findings suggest the importance of menstrual phase in the interpretation of data on endothelial function.

Impaired brachial artery endothelial function in young healthy women following an acute painful stimulus

Impaired endothelial function has been observed during and immediately following an acutely painful stimulus. However, the extent to which this persists following pain dissipation is unclear. To determine whether painful ischemic handgrip exercise (pain task) causes impaired flow-mediated dilation (FMD) after the sensation of pain and hemodynamic responses have abated. A second purpose was to determine whether the response to pain differed with a predisposition to magnify, ruminate, and feel helpless about pain (pain catastrophizing status). Brachial artery FMD stimulated by reactive hyperemia was assessed via ultrasound in 18 (9 high catastrophizing) healthy, women (20 ± 1 years) before and 15 min after a 3 min pain task. The shear stress stimulus for FMD was estimated as shear rate (blood velocity/brachial artery diameter). RESULTS (MEAN ± SD): None of the variables were significantly impacted by pain catastrophizing status and are presented pooled across group. The pain task increased pain ratings [1 ± 1-6 ± 3 (0-10 scale) (p < 0.001)], mean arterial pressure (MAP) (p < 0.001) and heart rate (HR) (p < 0.001), all returning to pre-pain levels ≤2-min post-pain task (pre-pain vs. 2-min post-pain: pain rating p = 1.000; MAP p = 0.142; HR p = 0.992). The shear rate stimulus was not different between pre- and post-pain task FMD tests (p = 0.200). FMD decreased post-pain task (10.8 ± 4.6 vs. 7.0 ± 2.7 %, p < 0.001). These results indicate that, regardless of pain catastrophizing status, painful ischemic handgrip exercise has a deleterious impact on endothelial function that persists after the pain sensation and hemodynamic responses have abated.

Elevation in blood flow and shear rate prevents hyperglycemia-induced endothelial dysfunction in healthy subjects and those with type 2 diabetes

Hyperglycemia, commonly present after a meal, causes transient impairment in endothelial function. We examined whether increases in blood flow (BF) protect against the hyperglycemia-mediated decrease in endothelial function in healthy subjects and patients with type 2 diabetes mellitus (T2DM). Ten healthy subjects and 10 age- and sex-matched patients with T2DM underwent simultaneous bilateral assessment of brachial artery endothelial function by means of flow-mediated dilation (FMD) using high-resolution echo-Doppler. FMD was examined before and 60, 120, and 150 min after a 75-g oral glucose challenge. We unilaterally manipulated BF by heating one arm between minute 30 and minute 60. Oral glucose administration caused a statistically significant, transient increase in blood glucose in both groups (P < 0.001). Forearm skin temperature, brachial artery BF, and shear rate significantly increased in the heated arm (P < 0.001), and to a greater extent compared with the nonheated arm in both groups (interaction effect P < 0.001). The glucose load caused a transient decrease in FMD% (P < 0.05), whereas heating significantly prevented the decline (interaction effect P < 0.01). Also, when correcting for changes in diameter and shear rate, we found that the hyperglycemia-induced decrease in FMD can be prevented by local heating (P < 0.05). These effects on FMD were observed in both groups. Our data indicate that nonmetabolically driven elevation in BF and shear rate can similarly prevent the hyperglycemia-induced decline in conduit artery endothelial function in healthy volunteers and in patients with type 2 diabetes. Additional research is warranted to confirm that other interventions that increase BF and shear rate equally protect the endothelium when challenged by hyperglycemia.

Systemic sclerosis induces pronounced peripheral vascular dysfunction characterized by blunted peripheral vasoreactivity and endothelial dysfunction.

Systemic sclerosis (SSc) vasculopathy can result in a digital ulcer (DU) and/or pulmonary arterial hypertension (PAH). We hypothesized that bedside brachial artery flow-mediated dilation (FMD) testing with duplex ultrasound could be used in SSc patients to identify features of patients at risk for DU or PAH. Thirty-eight SSc patients were compared to 52 age-matched healthy controls from the VAMC Utah Vascular Research Laboratory. Peripheral hemodynamics, arterial structure, and endothelial function were assessed by duplex ultrasound. A blood pressure cuff was applied to the forearm and 5-min ischemia was induced. Post-occlusion, brachial artery vascular reactivity (peak hyperemia/area under the curve [AUC]), shear rate, and endothelial function (FMD) were measured. SSc patients had smaller brachial artery diameters (p < 0.001) and less reactive hyperemia (p < 0.001), peak shear rate (p = 0.03), and brachial artery FMD (p < 0.001) compared with healthy controls. Brachial artery FMD was lower (p < 0.05) in SSc patients with DU. Tertile analysis suggested the 2 lower FMD tertiles (<5.40 %) had a 40-50 % chance of presenting with DU while the SSc patients with highest FMD tertile (>5.40 %) had less than 15 % chance of DU. All brachial artery FMD measurements were similar between SSc patients with and without PAH (all p > 0.05). Compared to healthy controls, SSc patients had significantly smaller brachial artery diameter and blunted peripheral vascular reactivity and endothelial function. SSc patients with DU have even greater impairments in endothelial function compared to those without DU. FMD testing has clinical utility to identify SSc patients at risk for DU.

Interval exercise, but not endurance exercise, prevents endothelial ischemia-reperfusion injury in healthy subjects.

Endothelial ischemia-reperfusion (I/R) injury importantly contributes to the poor prognosis during ischemic (myocardial) events. Preconditioning, i.e., repeated exposure to short periods of ischemia, effectively reduces endothelial I/R injury. In the present study, we examined the hypothesis that exercise has preconditioning effects on endothelial I/R injury. Therefore, we studied whether an acute bout of endurance or interval exercise is able to protect against endothelial I/R injury. In 17 healthy young subjects, we examined changes in brachial artery endothelial function using flow-mediated dilation (FMD) before and after a bout of high-intensity interval exercise, moderate-intensity endurance exercise, or a control intervention. Subsequently, I/R injury was induced by inflation of a blood pressure cuff around the upper arm to 220 mmHg for 20 min and 20 min of reperfusion followed by another FMD measurement. Near-infrared spectrometry was used to examine local tissue oxygenation during exercise. No differences in brachial artery FMD were found at baseline for the three conditions. I/R induced a significant decline in FMD (7.1±2.3 to 4.3±2.3, P<0.001). When preceded by the interval exercise bout, no change in FMD was present after I/R (7.7±3.1 to 7.2±3.1, P=0.56), whereas the decrease in FMD after I/R could not be prevented by the endurance exercise bout (7.8±3.1 to 3.8±1.7, P<0.001). In conclusion, a single bout of lower limb interval exercise, but not moderate-intensity endurance exercise, effectively prevents brachial artery endothelial I/R injury. This indicates the presence of a remote preconditioning effect of exercise, which is selectively present after short-term interval but not continuous exercise in healthy young subjects.

The Effect of Androgen Deprivation Therapy in Arterial Stiffness of the Aorta and the Endothelial Function of Peripheral Arteries

Objective: To study the effect of androgen deprivation therapy (ADT) is using an LHRH agonist in arterial stiffness and endothelial function of peripheral arteries as a possible mechanism increasing their cardiovascular risk. Material and Methods: This pilot study is a prospective analysis of 32 patients with metastatic prostate cancer who received androgen deprivation therapy (ADT) using an LHRH agonist. We evaluated the endothelial function of brachial artery through ultrasound and measurement of Flow Mediated Dilatation (FMD) and we assessed the central arterial stiffness of the aorta by measuring Augmentation index (AIX) and velocity of the aortic pulse wave (PWV). The measurements were performed one day before starting treatment and then three months and six months after the initiation of treatment. Results: PWV increased significantly by 8.26% from three to six months of follow up (p=0.037). FMD was found slightly elevated from baseline to 6 months of follow up by 7.18% (p>0.99), but AI was increased significantly (15.53%, p=0.007) at six months as compared with baseline measures. Glucose, LDL, Triglycerides were increased by 15.23% (p=0.002) 14.34% (p<0.001), and 13.46 %( p<0.001) respectively at 6 months follow up and these values increased significantly between all other time points. HDL was decreased statistically significantly by 14.56 %( p<0.001) during the follow up of 6 months. Conclusion: We found that these agents cause changes in arterial stiffness of the aorta and the endothelial function of peripheral arteries and we proposed them as a possible mechanism of increasing their cardiovascular risk.

Exercise training reverses endothelial dysfunction in nonalcoholic fatty liver disease.

Nonalcoholic fatty liver disease (NAFLD) is an independent risk factor for cardiovascular disease (CVD). Endothelial dysfunction is an early manifestation of atherosclerosis and an important prognostic marker for future cardiovascular events. The aim of this study was twofold: to examine 1) the association between liver fat, visceral adipose tissue (VAT), and endothelial dysfunction in obese NAFLD patients and 2) the impact of supervised exercise training on this vascular defect. Brachial artery endothelial function was assessed by flow-mediated dilatation (FMD) in 34 obese NAFLD patients and 20 obese controls of similar age and cardiorespiratory fitness [peak oxygen uptake (V̇o2 peak)] (48 ± 2 vs. 47 ± 2 yr; 27 ± 1 vs. 26 ± 2 ml·kg−1·min−1−1). Magnetic resonance imaging and spectroscopy quantified abdominal and liver fat, respectively. Twenty-one NAFLD patients completed either 16 wk of supervised moderate-intensity exercise training (n = 13) or conventional care (n = 8). Differences between NAFLD and controls were compared using independent t-tests and effects of interventions by analysis of covariance. NAFLD patients had higher liver fat [11.6% (95% CI = 7.4, 18.1), P < 0.0005] and VAT [1.6 liters (95% CI = 1.2, 2.0), P < 0.0001] than controls and exhibited impaired FMD compared with controls [−3.6% (95% CI = −4.9, −2.2), P < 0.0001]. FMD was inversely correlated with VAT (r = −0.54, P = 0.001) in NAFLD, although the impairment in FMD remained following covariate adjustment for VAT [3.1% (95% CI = 1.8, 4.5), P < 0.001]. Exercise training, but not conventional care, significantly improved V̇o2 peak [9.1 ml·kg−1·min−1 (95% CI = 4.1, 14.1); P = 0.001] and FMD [3.6% (95% CI = 1.6, 5.7), P = 0.002]. Endothelial dysfunction in NAFLD cannot be fully explained by excess VAT but can be reversed with exercise training; this has potential implications for the primary prevention of CVD in NAFLD.

Randomized controlled trial using bosentan to enhance the impact of exercise training in subjects with type 2 diabetes mellitus.

In type2 diabetes patients, endothelin (ET) receptor blockade may enhance blood flow responses to exercise training. The combination of exercise training and ET receptor blockade may represent a more potent stimulus than training alone to improve vascular function, physical fitness and glucose homeostasis. We assessed the effect of an 8week exercise training programme combined with either ET blockade or placebo on vasculature, fitness and glucose homeostasis in people with type2 diabetes. In a double-blind randomized controlled trial, brachial endothelium-dependent and ‑independent dilatation (using flow-mediated dilatation and glyceryl trinitrate, respectively), glucose homeostasis (using Homeostasis Model Assessment for Insulin Resistance (HOMA-IR)) and physical fitness (maximal cycling test) were assessed in 18 men with type2 diabetes (60±6years old). Subjects underwent an 8week exercise training programme, with half of the subjects receiving ET receptor blockade (bosentan) and the other half a placebo, followed by reassessment of the tests above. Exercise training improved physical fitness to a similar extent in both groups, but we did not detect changes in vascular function in either group. This study suggests that there is no adaptation in brachial and femoral artery endothelial function after 8weeks of training in type2 diabetes patients. Endothelin receptor blockade combined with exercise training does not additionally alter conduit artery endothelial function or physical fitness in type2 diabetes.

Dyslipidemia and endothelial function in women with metabolic syndrome associated with autoimmune thyroiditis

The research objectives are lipid spectrum and endothelial function (EF) in women with metabolic syndrome (MS) associated with autoimmune thyroiditis (AIT) against the background of non-compensated with L-thyroxin subclinical hypothyroidism (SH). Groups of women with MS associated with AIT and euthyroidism, women with MS associated with SH and women with MS without any thyroid disorders were observed. Complex «intima media» and endothelial function of brachial artery were evaluated by ultrasound method. It was indicated that dyslipidemia was more significant in women with MS associated with AIT and SH. But there were no abnormalities in complex «intima media» and EF. The cause of it is that the diabetes mellitus occurred two times rarely in this group in comparison with the other groups as well as the high sensitivity to the L-thyroxin. The results of the study demonstrate the necessary prescription of adequate dose of L-thyroxin to compensate SH completely.

Time-course of vascular adaptations during 8 weeks of exercise training in subjects with type 2 diabetes and middle-aged controls.

Exercise training in healthy volunteers rapidly improves vascular function, preceding structural remodelling. No study examined the time-course of such adaptations in subjects with a priori endothelial dysfunction. We examined brachial artery endothelial and smooth muscle function using flow-mediated dilation (FMD) and glyceryl trinitrate (GTN) administration in 13 type 2 diabetes patients (59 ± 6 years) and 10 healthy subjects (58 ± 7 years) before, during (2-weekly) and after an 8-week training programme. Arterial structure was assessed via peak blood flow and artery diameter. Training increased peak oxygen uptake (P = 0.03), comparable between groups (P = 0.276). We observed a similar impact of training on brachial artery vasomotor function across the training period in diabetes patients and controls (FMD/GTN-ratio), with a higher FMD/GTN-ratio at 2, 6 and 8 weeks (P = 0.036). Artery diameter, peak blood flow or peak diameter had not changed after training. Training leads to rapid improvement in brachial artery vascular function in diabetes patients and controls. In contrast to previous observations in healthy young subjects, the increase in function was preserved after 8 weeks of training in middle-aged diabetes patients and controls, suggesting a different time-course in vascular adaptations in subjects with endothelial dysfunction.

Impact of endothelin blockade on acute exercise-induced changes in blood flow and endothelial function in type 2 diabetes mellitus.

Positive vascular effects of exercise training are mediated by acute increases in blood flow. Type2 diabetes patients show attenuated exercise-induced increases in blood flow, possibly mediated by the endothelin pathway, preventing an optimal stimulus for vascular adaptation. We examined the impact of endothelin receptor blockade (bosentan) on exercise-induced blood flow in the brachial artery and on pre- and postexercise endothelial function in type2 diabetes patients (n=9, 60±7years old) and control subjects (n=10, 60±5years old). Subjects reported twice to the laboratory to perform hand-grip exercise in the presence of endothelin receptor blockade or placebo. We examined brachial artery endothelial function (via flow-mediated dilatation) before and after exercise, as well as blood flow during exercise. Endothelin receptor blockade resulted in a larger increase in blood flow during exercise in type2 diabetes patients (P=0.046), but not in control subjects (P=0.309). Exercise increased shear rate across the exercise protocol, unaffected by endothelin receptor blockade. Exercise did not alter brachial artery diameter in either group, but endothelin receptor blockade resulted in a larger brachial artery diameter in type2 diabetes patients (P=0.033). Exercise significantly increased brachial artery flow-mediated dilatation in both groups, unaffected by endothelin receptor blockade. Endothelin receptor blockade increased exercise-induced brachial artery blood flow in type2 diabetes patients, but not in control subjects. Despite this effect of endothelin receptor blockade on blood flow, we found no impact on baseline or post-exercise endothelial function in type2 diabetes patients or control subjects, possibly related to normalization of the shear stimulus during exercise. The successful increase in blood flow during exercise in type2 diabetes patients through endothelin receptor blockade may have beneficial effects in repeated exercise training.

Retrograde shear rate in formerly preeclamptic and healthy women before and after exercise training: relationship with endothelial function

Blood flow patterns in conduit arteries characterized by high levels of retrograde shear stress can be detrimental for vascular health. In this study we examined whether retrograde shear rate and endothelial function are related in healthy and formerly preeclamptic (PE) women and whether this relationship is altered by exercise training. Formerly PE women (32 ± 4 yr, n = 20) and controls (32 ± 4 yr, n = 20), all 6-12 mo postpartum, performed 12-wk aerobic exercise training. We measured brachial artery shear rate (SR) and endothelial function by flow-mediated dilation (FMD, echo-Doppler). We additionally performed power spectral analysis of heart rate variability and calculated low-frequency/high-frequency (LF/HF) ratio. Antegrade SR was not different between groups, while retrograde SR was significantly higher and FMD% lower in PE women compared with controls (both P < 0.05). Retrograde shear correlated strongly with FMD% in PE women and controls (P < 0.05). LF/HF ratio inversely correlated with brachial artery retrograde SR and FMD% (both P < 0.05) in PE women and controls. Exercise training reduced retrograde shear, improved FMD%, and reduced LF/HF ratios similarly in both groups (all P < 0.05). Training-induced changes in retrograde SR correlated with changes in FMD% and LF/HF ratio. A higher brachial artery retrograde SR relates to lower brachial artery endothelial function, in both controls and formerly PE women. Exercise training improves retrograde SR, while the magnitude of this change correlated strongly with improvements in FMD and reductions in LF/HF ratio. Therefore, the impact of PE and exercise training on endothelial health may, at least partly, be related to retrograde shear rate.

Does Brachial Artery Endothelial Function Represent The Endothelial Function During Prolonged Sitting?

Does Brachial Artery Endothelial Function Represent The Endothelial Function During Prolonged Sitting?

Systemic inflammation and brachial artery endothelial function in the Multi-Ethnic Study of Atherosclerosis (MESA)

Background and objectiveInflammation and endothelial dysfunction have been implicated in the pathogenesis of atherosclerotic vascular disease. Brachial artery flow-mediated dilation (FMD) is a reliable, non-invasive method of assessing endothelial function....

Seven-Day Remote Ischemic Preconditioning Improves Local and Systemic Endothelial Function and Microcirculation in Healthy Humans

Ischemic preconditioning (IPC) protects tissue against ischemia-induced injury inside and outside ischemic areas. The purpose was to examine the hypothesis that daily IPC leads to improvement in endothelial function and skin microcirculation not only in the arm exposed to IPC but also in the contralateral arm. Thirteen healthy, young, normotensive male individuals (aged 22±2 years) were assigned to 7-day daily exposure of the arm to IPC (4×5 minutes). Assessment of brachial artery endothelial function (using flow-mediated dilation (FMD)) and forearm microcirculation (cutaneous vascular conductance (CVC) at baseline and during local heating) was performed before and after 7 days to examine the local (i.e., intervention arm) and remote (i.e., control arm) effect of IPC. We repeated the assessment tests 8 days after the intervention (Post+8). FMD increased after repeated IPC (P = 0.03) and remained significantly elevated at Post+8 in the intervention (5.0±2.2%, 6.1±2.2%, and 6.6±2.3%) and contralateral arms (5.4±2.2%, 6.0±2.2%, and 7.5±2.2%). Forearm CVC also increased following repeated IPC (P = 0.006) and remained elevated at Post+8 in both arms (intervention: 0.12±0.03, 0.14±0.04, 0.16±0.04 mV/mm Hg; contralateral: 0.14±0.04, 0.015±0.04, 0.17±0.07). No interaction between IPC arm and time was evident for FMD and CVC (both P > 0.05). IPC intervention did not alter CVC responses to local heating (P > 0.05). Daily exposure to IPC for 7 days leads to local and remote improvements in brachial artery FMD and resting skin microcirculation that remain after cessation of the intervention and beyond the late phase of protection. These findings may have clinical relevance for micro- and macrovascular improvements.

Repeated core temperature elevation induces conduit artery adaptation in humans

Shear stress is a known stimulus to vascular adaptation in humans. However, it is not known whether thermoregulatory reflex increases in blood flow and shear can induce conduit artery adaptation. Ten healthy young volunteers therefore underwent 8 weeks of 3 × weekly bouts of 30 min lower limb heating (40 °C) during which the upper body was not directly heated. Throughout each leg heating session, a pneumatic cuff was placed on one forearm and inflated to unilaterally restrict reflex-mediated blood flow responses. Each bout of leg heating significantly increased brachial artery shear rate in the uncuffed arm (96 ± 97 vs 401 ± 96 l/s, P < 0.01), whereas no change was apparent in the cuffed arm (83 ± 69 vs 131 ± 76 l/s, P = 0.67). Repeated episodic exposure to leg heating enhanced brachial artery endothelial function (measured by flow-mediated dilation) in the uncuffed arm from week 0 (5.2 ± 1.9 %) to week 4 (7.7 ± 2.6 %, P < 0.05), before returning to baseline levels by week 8. No adaptation was evident in the cuffed arm. We conclude that repeated increases in core temperature, induced via lower limb heating, resulted in upper limb conduit artery vascular adaptation which was dependent upon increases in shear stress. To our knowledge this is the first study to establish a beneficial systemic impact of thermoregulatory reflexes on conduit artery function in humans.

Endothelial function increases after a 16-week diet and exercise intervention in overweight and obese young women.

Weight loss improves endothelial function in overweight individuals. The effects of weight loss through combined aerobic and resistance training and caloric restriction on in vivo vascular measures and blood markers associated with the regulation of endothelial function have not been comprehensively examined. Therefore, we investigated brachial artery endothelial function and potential regulatory blood markers in twenty overweight women (30.3 ± 2.0 years) who participated in 16 weeks of aerobic (5 d/wk) and resistance training (2 d/wk) (combined: ≥250 kcal/d) and caloric restriction (−500 kcal/d versus requirement). Resting brachial artery flow mediated dilation (FMD) and circulating endothelin-1 (ET-1) and interleukin-6 (IL-6) were assessed at baseline and following the intervention. Relative and absolute FMD increased (before: 4.0 ± 0.5% versus after: 6.9 ± 0.6%, P < 0.05, and before: 0.14 ± 0.02 mm versus after: 0.23 ± 0.02 mm, P < 0.05, resp.), while body mass decreased (before: 86.9 ± 2.4 kg versus after: 81.1 ± 2.4 kg, P < 0.05) following the intervention. There were no changes in either blood marker (IL-6: before: 1.5 ± 0.2 pg/mL versus after: 1.5 ± 0.1 pg/mL, P > 0.05, and ET-1: before: 0.55 ± 0.05 pg/mL versus after: 0.59 ± 0.09 pg/mL, P > 0.05). 16 weeks of combined aerobic/resistance training and diet-induced weight loss improved endothelial function in overweight and obese young women, but this increase was not associated with changes in blood markers of vasoconstriction or inflammation.

Exercise Training in Polycystic Ovarian Syndrome Enhances Flow-Mediated Dilation in the Absence of Changes in Fatness

Polycystic ovarian syndrome (PCOS) is associated with an adverse cardiovascular disease (CVD) profile. A surrogate marker for CVD risk is endothelial dysfunction. Limited studies exist examining the cardiovascular and metabolic effects of exercise in PCOS and specifically its impact on endothelial function. Therefore, the aim of the current study was to investigate the impact of exercise on endothelial function, in parallel with body composition, insulin resistance, and cardiopulmonary fitness in PCOS. Ten women with PCOS (27 yr, 95% confidence interval [CI] = 23-32; 31 kg·m⁻², 95% CI = 28-34) completed a 16-wk exercise (EX) program, and seven women with PCOS (29 yr, 95% CI = 24-35; 35 kg·m⁻², 95% CI = 31-40) undertook conventional care (CC) following lifestyle advice. Brachial artery endothelial function was assessed pre- and postintervention using flow-mediated dilation adjusted for variability in baseline diameter. Visceral and abdominal subcutaneous adipose tissue was assessed using whole-body magnetic resonance imaging and ¹H magnetic resonance spectroscopy quantified liver fat. Cardiorespiratory fitness, glycemic control, hormone, and lipid profiles were also assessed. Data were analyzed using covariate-controlled generalized estimating equations. At follow-up, EX improved flow-mediated dilation by 3.6% (95% CI = 0.5-6.7, P = 0.03) more than CC. There was a parallel improvement in cardiorespiratory fitness of 4.7 mL·kg⁻¹·min⁻¹ (95% CI = 1.4-7.9, P < 0.001) with EX versus CC. These changes were not explained by changes in visceral adipose tissue, subcutaneous adipose tissue, liver fat or insulin resistance. Supervised exercise in women with PCOS improves endothelial function, an adaptation associated with reduced CVD risk. This change occurs independent of changes in body weight or composition. The success of public health interventions in this patient group should not be solely judged by weight loss.

Abstract 18776: Endothelial Function is Not Affected by Fresh or Storage-Aged Autologous Blood Transfusions in Healthy Individuals

Background: Red cells play a modulating role in nitric oxide (NO)-mediated signaling and hypoxic vasodilation that may be influenced by blood transfusions, particularly with storage-aged blood (pRBCs). We have shown that brachial artery endothelial function, measured as flow-mediated vasodilation (FMD) is adversely affected in patients receiving aged compared to fresh pRBCs. Here we investigated endothelial NO activity in healthy subjects receiving autologous pRBCs with the hypothesis that aged pRBCs will impair endothelial conductance vessel and microvascular function. Methods: Sixteen healthy participants (aged 31±10 years, 38% female) were transfused 1 unit of fresh (aged 3-7 days) and subsequently with storage-aged (35-42 days) autologous pRBCs. Endothelial function was measured using FMD and reactive hyperemia index (RHI), a measure of microvascular function, was measured using pulsatile arterial tonometry (Itamar Inc., n=7), before, 1 hour, and 24 hours after transfusion. Data were analyzed by repeated measures ANOVA. Results: Hemoglobin was similar before both transfusions (p=0.066) and increased by 1.02±1.0 g/dL (±SD) and 1.2±1.2 g/dL with fresh and storage-aged transfusions, respectively. The FMD before, 1 hr and 24 hr after transfusion of fresh pRBCs (7.8±6.9%, 8.2±4.8% and 6.9±4.3%) or stored pRBCs (7.1±5.5%, 7.4±4.7% and 8.5±4.9%) was similar,( p=0.45). The RHI before, 1 hr and 24 hr after transfusion of fresh pRBCs ( 2.45±0.23, 2.26±0.08 and 2.26±0.21) showed no significant changes, p=0.87 or stored pRBCs ( 2.25±0.67, 2.27±0.53 and 2.22±0.26, p=0.42). Conclusions: Vascular NO activity and microvascular dilatory capacity are not impaired by transfusion of fresh or storage-aged autologous pRBC in healthy individuals, unlike findings with allogeneic transfusions in patients. These differences suggest that the risks of aged blood transfusions are likely to be greater in patients with vascular disease who have underlying endothelial dysfunction.

Arterial Stiffness and Endothelial Function Are Related To Brain Aging and Episodic Memory In Community-Dwelling Middle-Aged and Older Adults

Evaluation of: Tsao CW, Seshadri S, Beiser AS et al. Relations of arterial stiffness and endothelial function to brain aging in the community. Neurology 81, 1–8 (2013). This study reports the association between arterial stiffness and pressure pulsatility in middle-aged and older community-dwelling adults. As part of the Stroke- and Dementia-free Framingham Offspiring Study, 1587 participants were studied for tonometric arterial stiffness and endothelial function (years 1998–2001), and had MRI brain scans and cognitive assessments (1990–2002). The measures of the central aortic hemodynamics (e.g., carotid–femoral pulse wave velocity and mean arterial and central pulse pressure) were associated with greater white matter hyperintensity volumes and lower total cerebral brain volumes; this association was stronger for participants aged 65 years or older. The mean arterial and central pulse pressure were also associated with reduced verbal memory (p &lt; 0.05) but not executive function. The brachial artery endothelial function was not associated with cerebral changes. These findings indicate that peripheral vascular changes are related not only to distal cerebral microvascular pathology, but may also be used as a surrogate marker for subclinical stages of cognitive dysfunction.