Reactive Hyperemic Response Research Articles

Prolonged postocclusive hyperemia response in patients with normal-tension glaucoma.

BackgroundIt is believed that endothelial dysfunction may be a link between systemic and ocular dysregulation in glaucoma. The aim of this study was to evaluate peripheral vascular reactive hyperemia in response to occlusion test and to correlate peripheral vascular findings with retrobulbar hemodynamics parameters in patients with normal-tension glaucoma.Material/MethodsForty-eight patients with normal-tension glaucoma (mean age 58.1 years, 38 women) and 40 control subjects (mean age 54.1 years, 36 women) were subjected to a brachial arterial occlusion test and color Doppler imaging (LOGIQ 9, GE Medical Systems) of the retrobulbar arteries. Finger hyperemia was assessed by using a 2-channel laser Doppler flowmeter (MBF-3D, Moor Instruments, Ltd.). Time parameters (time to peak flow, half-time of hyperemia, time of recovery) and amplitude parameters (maximum hyperemia response, biological zero) of the post-occlusive reactive hyperemia signal pattern as well as velocities and resistance index of the ophthalmic, central retinal, and short posterior ciliary arteries were evaluated and compared between study groups.ResultsIn glaucoma patients, time to peak flow and half-time of hyperemia were significantly longer (21.4 vs. 12.0 s, p=0.02 and 74.1 vs. 44.2 s, p=0.03, respectively) and biological zero was significantly lower (2.4 vs. 3.2, p=0.01) comparing with healthy subjects. In glaucoma patients, peak-systolic and end-diastolic velocities of central retinal artery were significantly lower (12.8 vs.14.1, p=0.03 and 3.9 vs. 4.7, p=0.01, respectively) and resistance index of this artery was significantly higher (0.69 vs. 0.67, p=0.03) compared to controls. In the glaucoma group, maximum hyperemic response was negatively correlated with the resistance index of temporal short posterior ciliary arteries (r=−0.4, p=0.01), whereas in the control group half-time of hyperemia was negatively correlated with end-diastolic velocity of the central retinal artery (r=−0.3, p=0.03).ConclusionsArterial occlusion test elicited a prolonged systemic hyperemia response in patients with glaucoma as compared with healthy subjects. Retrobulbar blood flow alterations in glaucoma patients may be related to systemic vascular dysregulation.

Influence of Cardiac Decentralization on Cardioprotection

The role of cardiac nerves on development of myocardial tissue injury after acute coronary occlusion remains controversial. We investigated whether acute cardiac decentralization (surgical) modulates coronary flow reserve and myocardial protection in preconditioned dogs subject to ischemia-reperfusion. Experiments were conducted on four groups of anesthetised, open-chest dogs (n = 32): 1- controls (CTR, intact cardiac nerves), 2- ischemic preconditioning (PC; 4 cycles of 5-min IR), 3- cardiac decentralization (CD) and 4- CD+PC; all dogs underwent 60-min coronary occlusion and 180-min reperfusion. Coronary blood flow and reactive hyperemic responses were assessed using a blood volume flow probe. Infarct size (tetrazolium staining) was related to anatomic area at risk and coronary collateral blood flow (microspheres) in the anatomic area at risk. Post-ischemic reactive hyperemia and repayment-to-debt ratio responses were significantly reduced for all experimental groups; however, arterial perfusion pressure was not affected. Infarct size was reduced in CD dogs (18.6±4.3; p = 0.001, data are mean±1SD) compared to 25.2±5.5% in CTR dogs and was less in PC dogs as expected (13.5±3.2 vs. 25.2±5.5%; p = 0.001); after acute CD, PC protection was conserved (11.6±3.4 vs. 18.6±4.3%; p = 0.02). In conclusion, our findings provide strong evidence that myocardial protection against ischemic injury can be preserved independent of extrinsic cardiac nerve inputs.

Relationship between brachial artery blood flow and total [hemoglobin + myoglobin] during post-occlusive reactive hyperemia

The associations between macrovascular and microvascular responses reported previously during post-occlusive reactive hyperemia have been inconsistent. The purpose of this study was therefore to determine the temporal relationship between the reactive hyperemic responses within a conduit artery and the downstream microvessels. Conduit artery blood flow was measured in the brachial artery with pulsed Doppler ultrasound. A potential analog of microvascular flow, changes in skeletal muscle total[hemoglobin+myoglobin] (T[Hb+Mb]), was assessed with near-infrared spectroscopy (NIRS). We found a high degree of correlation between these two measures (r=0.91). Cross-correlation analysis revealed two distinct response patterns. In 10 of our 15 subjects there was time displacement between peak brachial artery blood flow (BABF) and T[Hb+Mb] responses; in the remaining 5 the peaks were coincident. Granger causality testing suggested that reactive hyperemia in the macrovessel determined hyperemia in the downstream microvessels in all 15 study subjects. Time constants for the on (τ1) and off (τ2) kinetics of each response were calculated; our initial hypothesis was that τ1 and τ2 for T[Hb+Mb] would correlate with τ1 and τ2 for BABF, respectively. However, only for τ2 was this observed (r=0.52; p<0.05). No similar relationship was observed for τ1. Adipose tissue thickness did not influence either time constant for T[Hb+Mb]. Taken together, our results show that the temporal characteristics of the hyperemic response in the conduit artery are qualitatively reflected in the downstream microvasculature, but mechanisms for quantitative differences remain to be identified.

Endothelium Dependent Vasomotion and In Vitro Markers of Endothelial Repair in Patients with Severe Sepsis: An Observational Study

BackgroundOutcome in sepsis is mainly defined by the degree of organ failure, for which endothelial dysfunction at the macro- and microvascular level is an important determinant. In this study we evaluated endothelial function in patients with severe sepsis using cellular endothelial markers and in vivo assessment of reactive hyperaemia.Materials and MethodsPatients with severe sepsis (n = 30) and 15 age- and gender- matched healthy volunteers were included in this study. Using flow cytometry, CD34+/KDR+ endothelial progenitor cells (EPC), CD31+ T-cells, and CD31+/CD42b- endothelial microparticles (EMP) were enumerated. Migratory capacity of cultured circulating angiogenic cells (CAC) was assessed in vitro. Endothelial function was determined using peripheral arterial tonometry at the fingertip.ResultsIn patients with severe sepsis, a lower number of EPC, CD31+ T-cells and a decreased migratory capacity of CAC coincided with a blunted reactive hyperaemia response compared to healthy subjects. The number of EMP, on the other hand, did not differ. The presence of organ failure at admission (SOFA score) was inversely related with the number of CD31+ T-cells. Furthermore, the number of EPC at admission was decreased in patients with progressive organ failure within the first week.ConclusionIn patients with severe sepsis, in vivo measured endothelial dysfunction coincides with lower numbers and reduced function of circulating cells implicated in endothelial repair. Our results suggest that cellular markers of endothelial repair might be valuable in the assessment and evolution of organ dysfunction.

Postocclusive Reactive Hyperemia Occurs in the Rat Retinal Circulation but Not in the Choroid

We tested the hypothesis that retinal blood flow has a postocclusive reactive hyperemia response modulated by occlusion duration and metabolic activity, and that choroidal blood flow does not. Anesthetized and paralyzed rats (n = 34) were studied. Retinal and choroidal blood flow was measured by laser speckle imaging and laser Doppler flowmetry, respectively. Blood oxygenation level-dependent functional magnetic resonance imaging (BOLD fMRI) was used to measure changes in relative blood oxygenation of the retinal and choroidal circulations. Transient carotid occlusion was elicited with a hydraulic occluder on the common carotid artery. Several occlusion durations were tested during dark, constant light, and flicker light conditions to modulate metabolic demand. The hyperemia response magnitude was quantified by integrating the area above the blood flow baseline for the 3 minutes after release of the occlusion. Systemic arterial pressure (108.2 ± 1.4 mm Hg) was unaffected by the carotid occlusions, and was similar among animals and conditions. Retinal blood flow had a reactive hyperemia, but choroidal blood flow did not (e.g., 14 ± 2%.sec versus 0.5 ± 4%. sec after 60-second occlusion). The hyperemia magnitude increased as a nonlinear function of occlusion duration and reached a plateau at occlusion durations < 60 second. The hyperemia magnitude was not altered by different lighting conditions at occlusion durations of 15 and 60 seconds. BOLD fMRI results were similar to the laser-based blood flow measurements. The results indicate that metabolic local control has a negligible role in choroidal blood flow regulation and only partially accounts for the blood flow behavior in the retinal circulation.

Hybrid Equation/Agent-Based Model of Ischemia-Induced Hyperemia and Pressure Ulcer Formation Predicts Greater Propensity to Ulcerate in Subjects with Spinal Cord Injury

Pressure ulcers are costly and life-threatening complications for people with spinal cord injury (SCI). People with SCI also exhibit differential blood flow properties in non-ulcerated skin. We hypothesized that a computer simulation of the pressure ulcer formation process, informed by data regarding skin blood flow and reactive hyperemia in response to pressure, could provide insights into the pathogenesis and effective treatment of post-SCI pressure ulcers. Agent-Based Models (ABM) are useful in settings such as pressure ulcers, in which spatial realism is important. Ordinary Differential Equation-based (ODE) models are useful when modeling physiological phenomena such as reactive hyperemia. Accordingly, we constructed a hybrid model that combines ODEs related to blood flow along with an ABM of skin injury, inflammation, and ulcer formation. The relationship between pressure and the course of ulcer formation, as well as several other important characteristic patterns of pressure ulcer formation, was demonstrated in this model. The ODE portion of this model was calibrated to data related to blood flow following experimental pressure responses in non-injured human subjects or to data from people with SCI. This model predicted a higher propensity to form ulcers in response to pressure in people with SCI vs. non-injured control subjects, and thus may serve as novel diagnostic platform for post-SCI ulcer formation.

Using Reactive Hyperemia to Assess the Efficacy of Local Cooling on Reducing Sacral Skin Ischemia Under Surface Pressure in People With Spinal Cord Injury: A Preliminary Report

ObjectivesTo investigate the efficacy of local cooling on reducing sacral skin ischemia in a weight-bearing position, and to identify the underlying physiological mechanisms using wavelet-based spectrum analysis of reactive hyperemia in people with spinal cord injury (SCI). DesignRepeated-measures and before-after trial design. SettingUniversity research laboratory. ParticipantsWheelchair users with SCI with injury level between C4 and T5 (n=10) and able-bodied controls (n=10). InterventionsThree protocols consisting of pressure without temperature changes, pressure with local cooling (Δt=−10°C), and pressure with local heating (Δt=+10°C) were tested. Each protocol consisted of a 10-minute baseline period, a 20-minute loading period at 60mmHg, and a 20-minute recovery period (reactive hyperemia). A 30-minute washout period was allowed between protocols. Main Outcome MeasuresA compound sensor head consisting of laser Doppler and heating and cooling probes was used to measure sacral skin blood flow and control skin temperature. Reactive hyperemic response to pressure and temperature stimuli was characterized in the time and frequency (metabolic [.0095–.02Hz], neurogenic [.02–.05Hz], and myogenic [.05–.15Hz] components) domains. ResultsPressure with local cooling resulted in a smaller reactive hyperemic response in both people with SCI and able-bodied controls as compared with pressure with local heating (P<.017) and pressure without temperature changes (P<.017), and the smaller hyperemia was attributed to reduced metabolic and neurogenic activities. People with SCI showed an attenuated response in reactive hyperemia (P<.017). ConclusionsThis study supports the concept of using local cooling to reduce skin ischemia under surface pressure in people with SCI.

P69: Analysis of acute and chronic effects of (−)-epicatechin on NO bioavailability and organ redox state in the cardiovascular system in vivo

Background and Hypothesis Consumption of cocoa flavanols may have beneficial effects on cardiovascular health. (−)-Epicatechin, the major flavanol monomer present in cocoa, has been shown to positively affect endothelial function and a (−)-epicatechin-rich cocoa drink increased the circulating nitric oxide (NO) metabolites in humans. There is also evidence that flavanols and flavonoids may activate the expression and the activity of Nrf2-dependent phase II genes in cultured non-endothelial cells. We hypothesized that (−)-epicatechin may induce a systemic Nrf2-dependent antioxidant response, thereby contributing to maintain the redox state, NO bioavailability, and the functionality of the vasculature. Methods In vivo effects of acute and chronic oral administration of (−)-epicatechin were analyzed in C57/Bl6 mice. (−)-Epicatechin was administrated at 1–10 mg/kg body weight (BW) intragastrically and the effects analyzed after 1 h. Chronic effects were assessed after 5 days (−)-epicatechin administration of 2 and 10 mg/kg BW in drinking water. Vascular function was assessed by measuring reactive hyperemic response of the hindlimb by laser Doppler perfusion imaging (LDPI). Chronic inhibition of nitric oxide synthase (NOS) was achieved by administration of the specific inhibitor l -NNA in drinking water for 6 days. Circulating levels of (−)-epicatechin metabolites were determined with HPLC. In vitro effects of (−)-epicatechin and its main plasma metabolites present in humans were analyzed in human umbilical vein endothelial cells (HUVECs). The H 2 O 2 concentration in media was measured by a peroxide assay. The activation of Nrf2 by epicatechin was measured by immunohistochemistry and confocal microscopy of cells cultured on cover slips, Western blot analysis of nuclear and cytoplasmic extracts, as well as by ARE (antioxidant responsive element)-binding assay (TransAM). The expression of eNOS and of phase II genes was assessed in cells and organs by real time RT-PCR and Western blot analysis. Phosphorylation of eNOS was assessed by Western blot analysis. The concentration of reduced glutathione in mouse organs were assessed by the glutathione reductase recycling assay. Results Acute administration of (−)-epicatechin dose-dependently increased the circulating levels of epicatechin metabolites along with improved vascular response to reactive hyperemia of the hindlimb. This was paralleled by an increase in eNOS phosphorylation in the aorta of the mice, indicating that (−)-epicatechin application induces NOS activation. Chronic treatment with (−)-epicatechin improved vascular response in a NOS-dependent fashion, and increased cGMP levels in aorta and plasma of the mice, demonstrating enhanced NO bioavailability. Interestingly, we observed a parallel increase in the expression of Nrf2-dependent phase II genes, including glutamate cysteine ligase (Gclc), and GSH levels in the heart and lung of the mice. In vitro we found that (−)-epicatechin induced the translocation of Nrf2 into the nucleus of the cells and the binding to the ARE. Moreover,(−)-epicatechin and its main plasma metabolites increased expression of GCL (mRNA and protein), as well as eNOS expression and phosphorylation. Conclusions Taken together, our findings demonstrate that administration of (−)-epicatechin leads to an increase of systemic NO bioavailability and vascular response in vivo and activates eNOS and Nrf2-dependent pathways. Disclosure Nothing to disclose.

Real-time RT-PCR threshold cycles value for Kir6.1 from the blood correlates with parameters of vascular function: a potential for the vascular function biomarker?

We examined the presence of KATP channel subunits, Kir6.1 and SUR2B, mRNAs in the blood and vascular function in healthy volunteers (41 males, 34 females). Real-time reverse transcriptase (RT)-PCR threshold cycles (Ct) was used as an indicator of mRNA levels. Baseline skin perfusion and the post-occlusion reactive hyperemia response exhibited a significant positive correlation with Ct for Kir6.1. There was no correlation between Kir6.1 Ct and brachial artery flow-mediated dilatation. Gender had no influence on relationships between blood Kir6.1 Ct and vascular function. We conclude that blood Kir6.1 mRNA levels could be potentially used as a biomarker of the vascular function.

Association of Venous Function and Post-Exercise Oxygen Consumption

Excess post-exercise oxygen consumption (EPOC) has been attributed to metabolic, hemodynamic, neuroendocrine, and pulmonary factors. Interestingly, few studies have examined the role of venous system on EPOC. The purpose of this study was to examine the relationship between measures of vascular function and EPOC. Measures of vascular function and VO2 recovery kinetics were examined in 20 individuals [age=22+2.41 yrs]. Nondominant forearm arterial inflow, venous capacitance and venous outflow were evaluated at rest and after 5 minutes of upper arm occlusion, using strain gauge plethysmography. VO2 recovery kinetics was assessed using gas exchange analysis following a six-minute constant work rate protocol at 60 percent of VO2peak (VO2@60%), on a cycle ergometer. The average VO2peak was 33.48±8.22 ml×kg-1×min-1 (Range: 18.7 to 46.1 ml×kg-1×min-1). Following the six-minute constant work rate protocol, recovery half-time (T1/2VO2) and Tau were 17.01±3.51 seconds and 54.45±11.28 seconds, respectively. Arterial resting inflow was 2.77±1.51 ml×100ml-1×min-1, reactive hyperemic blood flow was 17.72±3.65 ml×100ml-1×min-1, venous capacitance was 2.86±0.72 percent, and venous outflow was 34.19±10.03 ml×100ml-1×min-1. Bivariate correlations revealed significant inverse associations between T1/2VO2 and the reactive hyperemic response (r=-0.48, p=0.03) and T1/2VO2 and venous outflow post-occlusion (r=-0.50, p=0.02). In conclusion, these findings suggest an important role of both the arterial and venous circulation on EPOC.

Cardiometabolic Diseases and Related Complications: Current Status and Future Perspective

Cardiometabolic Diseases and Related Complications: Current Status and Future Perspective

Ascorbic acid blocks hyperglycemic impairment of endothelial function in adolescents with type 1 diabetes

To determine whether acute ascorbic acid infusions alter the effect of hyperglycemia on endothelial function in adolescents with type 1 diabetes. The forearm blood flow (FBF) reactive hyperemic response to 5 min of upper arm occlusion was studied in eight adolescents with type 1 diabetes during euglycemic and hyperglycemic insulin clamp (40 mU/m2/min) with and without ascorbic acid infusion (3 mg/min). The ratio of post- to preocclusion FBF decreased during hyperglycemia without ascorbic acid (p = 0.013), but did not change during hyperglycemia with ascorbic acid. The changes during hyperglycemia were different between the two studies (p = 0.038). Similar results were found when the percent change in forearm vascular resistance following occlusion was assessed. These results indicate that antioxidant treatment with ascorbic acid blocks acute hyperglycemic impairment of endothelial function in adolescents with type 1 diabetes.

Habitual Flavonoid Intake and Endothelial Function in Healthy Humans

Objective: Endothelial function, as measured by noninvasive techniques, is known to vary widely within populations. Our study was designed to test the hypothesis that this variation is determined in large part by a person's habitual dietary intake of flavonoids.Methods: This was an analytical study examining the relationship between endothelial function and dietary flavonoids in 19 healthy older adults (mean age 72 years). The study took place in the inpatient Clinical Research Center of the Brigham and Women's Hospital. Habitual flavonoid intake was assessed via a focused food frequency questionnaire. Endothelial function, measured as the reactive hyperemia response to 1 dose of flavonoid-rich cocoa, was recorded with a plethysmographic device via peripheral arterial tonometry (PAT).Results: Background flavonoid intake and the reactive hyperemia PAT (RH-PAT) response were significantly correlated (r = 0.7, p = 0.001); subjects with higher habitual flavonoid intake showed a significantly greater RH-PAT response than did lower consumers. PAT response to cocoa was also significantly correlated with simultaneous flavanol concentration in the blood (r = 0.5, p = 0.03).Conclusion: Individual variation in endothelial function among healthy older people, measured as PAT response to flavonoid-rich cocoa, is highly dependent upon usual daily flavonoid consumption. These data raise the possibility that the consumption of fruits and vegetables dictates basal endothelial function, likely related to their flavonoid content and influence on nitric oxide.

Commentary on high flow, non-ischemic, priapism.

High-flow, non-ischemic priapism is a rare condition, with which many urologists and andrologists are unfamiliar. There are three types of high-flow priapism: traumatic, neurogenic and post-shunting. Traumatic high-flow priapism may arise from penetrating or blunt trauma to the penis resulting in rupture of the cavernous artery or its branches. Despite the unregulated large arterial flow, this does not result in rigid and painful erections, as seen in low-flow, ischemic priapism, because the venous channels are still competent. The neurogenic type is seen after irritation or injury to the central nervous system, and this is typically self-limiting. If this type persists, then it may change to ischemic priapism, and should be treated accordingly. Post-shunting high-flow priapism is a result of reactive hyperemia in response to the hypoxic and acidotic state of ischemicpriapism that lasts more than 24 hours. This condition will continue only if the shunt remains open. Once the hyperemic state subsides, the minimal flow in the flaccid penis will not be able to keep the shunt open leading to its spontaneous closure in most cases. In general, since blood circulation into and out of the corpora cavernosa is not impeded in cases of high-flow priapism, the condition is not painful, the penis is not completely rigid, and the prognosis is excellent if it is treated properly.

Reactive hyperemia is not responsible for stimulating muscle protein synthesis following blood flow restriction exercise

Blood flow restriction (BFR) to contracting skeletal muscle during low-intensity resistance exercise training increases muscle strength and size in humans. However, the mechanism(s) underlying these effects are largely unknown. We have previously shown that mammalian target of rapamycin complex 1 (mTORC1) signaling and muscle protein synthesis (MPS) are stimulated following an acute bout of BFR exercise. The purpose of this study was to test the hypothesis that reactive hyperemia is the mechanism responsible for stimulating mTORC1 signaling and MPS following BFR exercise. Six young men (24 ± 2 yr) were used in a randomized crossover study consisting of two exercise trials: low-intensity resistance exercise with BFR (BFR trial) and low-intensity resistance exercise with sodium nitroprusside (SNP), a pharmacological vasodilator infusion into the femoral artery immediately after exercise to simulate the reactive hyperemia response after BFR exercise (SNP trial). Postexercise mixed-muscle fractional synthetic rate from the vastus lateralis increased by 49% in the BFR trial (P < 0.05) with no change in the SNP trial (P > 0.05). BFR exercise increased the phosphorylation of mTOR, S6 kinase 1, ribosomal protein S6, ERK1/2, and Mnk1-interacting kinase 1 (P < 0.05) with no changes in mTORC1 signaling in the SNP trial (P > 0.05). We conclude that reactive hyperemia is not a primary mechanism for BFR exercise-induced mTORC1 signaling and MPS. Further research is necessary to elucidate the cellular mechanism(s) responsible for the increase in mTOR signaling, MPS, and hypertrophy following acute and chronic BFR exercise.

Peripheral endothelial function and arterial stiffness in women with migraine with aura: a case-control study

Vascular dysfunction may be involved in migraine pathophysiology and contribute to the increased risk of ischemic stroke in migraine, particularly in women with migraine with aura (MA). However, data on endothelial function in MA are controversial. Here, we investigated whether systemic endothelial function and arterial stiffness are altered in women with MA, using a novel peripheral arterial tonometry device for the first time. Twenty-nine female MA patients without comorbidities and 30 healthy women were included, and carotid intima-media thickness was assessed by a standardized procedure. Endothelial function was assessed using peripheral arterial tonometry. Reactive hyperaemic response of digital pulse amplitude was measured following 5 minutes of forearm occlusion of the brachial artery. Arterial stiffness was assessed by fingertip tonometry derived and heart-rate-adjusted augmentation index. No differences were found in peripheral arterial tonometry ratio (2.3 ± 0.6 vs 2.2 ± 0.8; p = 0.58) and left carotid intima-media thickness (in µm: 484 ± 119 vs 508 ± 60; p = 0.37). Women with MA had higher heart-rate-averaged augmentation index [median (interquartile range, IQR) of 5 (IQR 0.5 to 18) vs -5 (IQR -16.8 to 8.3), p = 0.005] and heart-rate-adjusted augmentation index [1 (IQR -6 to 12.5) vs -8 (IQR -20.3 to 2.5), p = 0.008] than healthy controls. Peripheral endothelial function is not impaired in women with MA, but they have greater arterial stiffness. This may contribute to the increased stroke risk in women with MA.

Daño arterial asociado a la enfermedad renal crónica: evaluación mediante técnicas de laboratorio no invasivo en pacientes hemodializados

Hemodialysis patients (HD) display high rates of cardiac disease and mortality. The cardiovascular morbidity and mortality of HD patients is attributable in a significant proportion to endothelial dysfunction, arterial stiffness, and vascular calcifications. To measure vascular reactivity in HD subjects and compare them with healthy volunteers. Forty eight non diabetic patients aged 58 ± 4.6 years (29 males) on hemodialysis for a mean lapse of 4.8 years were studied. Arterial stiffness was measured in the radial artery. Pulse wave velocity was measured by noninvasive peripheral arterial tonometry in carotid and femoral arteries. Endothelial function was assessed, measuring reactive hyperemia response after a 5 min period of ischemia. As a control, all values were also measured in age and gender-matched healthy volunteers. Arterial stiffness was significantly higher in HD patients than controls (23.9 ± 3.3 and 18.4 ± 3.4% respectively, p < 0.05). HD subjects had an increased pulse wave velocity (10.0 ± 0.8 and 7.6 ± 0.9 m/s respectively, p < 0.05). A reduction in the change in pulse amplitude pressure, as a measure of arterial dysfunction, was only observed in male patients (1.7 ± 0.4 and 2.7 ± 0.4 respectively p < 0.01). Noninvasive assessment of peripheral vascular function may be useful for the identification of patients at risk for late cardiac events.

Age- and sex-related differences in vascular function and vascular response to mental stress: Longitudinal and cross-sectional studies in a cohort of healthy children and adolescents

ObjectiveLimited data, especially from longitudinal studies, are available regarding vascular health assessment in childhood. In this study, we performed longitudinal and cross-sectional studies in healthy children and adolescents to investigate age- and sex-related differences in vascular functions and vascular response to mental stress. MethodsPulse wave velocity (PWV) was measured by tonometry. Endothelial function and vascular response to mental arithmetic test were assessed using a peripheral artery tonometry device. Data were obtained in 162 adolescents (mean age of 17 years, 94 girls) in a 3-year follow-up study and 241 children (mean age of 10 years, 115 girls) in a first-time investigation. Physical activity was assessed in adolescents by a self-report questionnaire. ResultsOur 3-year follow-up study revealed that the increased PWV was greater in male adolescents (0.79±0.79m/s) than in females (0.27±0.89m/s, p<0.001). Adolescents who reported decreased physical activity over the 3-year period had increased arterial stiffness. Comparing the cross-sectional data, we found that sex-related differences in reactive hyperemic response was more apparent by evaluating the overall response curve than measuring the reactive hyperemic index from one arbitrary time point, with lower peak response and smaller area-under-curve found in boys. Moreover, we found that, in response to mental stress, male adolescents had a more vasoconstrictive response, followed by a less vasodilatory response, and needed longer time to return to baseline level than the females. ConclusionThese findings suggest that boys are likely to have adverse changes in vascular health earlier than the age-matched girls.

Skin microdialysis coupled with Laser Speckle Contrast Imaging to assess microvascular reactivity

ObjectiveLaser Speckle Contrast Imaging (LSCI) can be used to assess real-time responses of skin microcirculation to pharmacological interventions. The main objective of this study was to determine whether intradermal or subdermal microdialysis fiber insertion, coupled with skin flux recording using LSCI, can be used to assess baseline cutaneous flux and the post-occlusive reactive hyperemic response. The microdialysis sites were compared to control area without microdialysis fibers. MethodsOne dermal and two subdermal microdialysis fibers were randomly inserted in the right forearm skin of six healthy volunteers. We performed consecutively tests of post-occlusive hyperemia, infusion of 29mM sodium nitroprusside (SNP), local thermal hyperemia at 43°C and a second 29mM SNP infusion at the end of the experiment. ResultsTwo hours after fiber insertion, cutaneous vascular conductances (CVC) at the subdermal fiber sites were not different from their respective control regions of interest, while at the dermal site CVC remained higher (0.48+/−0.15 versus 0.37+/−0.1PU.mm Hg−1, P=0.003). The peak CVC and area under the curve observed during post-occlusive reactive hyperemia were similar at all fiber sites and their respective controls. We observed a similar increase in CVC using 29mM SNP infusion, 40min local heating at 43°C, and their combination. Finally, physiological and pharmacological responses of the subdermal sites were reproducible in terms of amplitude, whether expressed as raw CVC or as %CVCmax. ConclusionsWe showed that studying skin microvascular physiological or pharmacological responses using inserted subdermal microdialysis fibers coupled with LSCI is feasible and reproducible, and provides two-dimensional information. This technique will be useful for future mechanistic studies of skin microcirculation.

Journal-related Activities and Other Special Activities at the 2011 American Society of Anesthesiologists Annual Meeting

Journal-related Activities and Other Special Activities at the 2011 American Society of Anesthesiologists Annual Meeting