Calf Blood Flow Research Articles

Testing the Fundamental Assumption of Choice Experiments: Are Values Absolute or Relative?

Fifty-one men with atherosclerotic intermittent claudication and haemorheological abnormalities completed a double-blind, one-year randomised trial of Ticlopidine (500 mg/day), a new antiplatelet agent. Ticlopidine caused significant inhibition of platelet aggregation but did not fully correct abnormalities of coagulation, viscosity, and fibrinolysis. There was no significant improvement in walking ability, Doppler ankle-pressure indices, or calf blood flow. Sustained platelet inhibition for 12 months was insufficient to correct the prothrombotic abnormality of extensive atherosclerosis.

Effects of moxonidine on sympathetic nerve activity in patients with end-stage renal disease

End-stage renal disease (ESRD) is characterized by markedly increased sympathetic outflow that contributes to increased cardiovascular mortality in these patients. The central sympatholytic drug moxonidine (MOX) has been shown to reduce muscle sympathetic nerve activity (MSNA) in initial stages of chronic kidney disease; however, the effects in ESRD are not known. The aim of this study was to test the hypothesis that low-dose MOX causes sustained decreases in sympathetic outflow in ESRD patients. Twenty-three ESRD patients (mean age 46.4 +/- 16 years, 14 men, seven women, no diabetic patients) were randomized to a daily treatment of 0.3 mg MOX or placebo (PLA) in addition to pre-existing antihypertensive therapy. At baseline and after 1 and 6 months of treatment, heart rate (HR, ECG), blood pressure (mean arterial pressure, automatic sphygmanometer), calf blood flow (CBF, venous occlusion plethysmography), muscle sympathetic nerve activity (MSNA) (microneurography at the peroneal nerve) were measured. Data are mean +/- SEM. MOX acutely decreased MSNA within 2 h after oral intake (from 45 +/- 3.7 to 35 +/- 3.9 bursts/min, P < 0.05). This decrease was sustained over 6 months (MSNA 45 +/- 3.7, 35 +/- 4.6, 33 +/- 4.5 bursts/min at 0, 1 and 6 months, P < 0.05). PLA had no effect. Neither MOX nor PLA resulted in any significant acute or long-term changes in HR, MAP or CBF. In ESRD patients, low-dose MOX produced sustained and substantial reductions in sympathetic outflow without hemodynamically compromising them. We suggest that the inhibition of central sympathetic outflow may improve cardiovascular prognosis in ESRD.

14 nights of intermittent hypoxia elevate daytime blood pressure and sympathetic activity in healthy humans

Obstructive sleep apnoea syndrome (OSAS) causes nocturnal chronic intermittent hypoxia (IH) that contributes to excess cardiovascular morbidity. To explore the consequences of IH, we used our recently developed model of nocturnal IH in healthy humans to characterise the profile of this blood pressure increase, to determine if it is sustained and to explore potential physiological mechanisms. We performed 24-h ambulatory monitoring of blood pressure in 12 healthy subjects before and after 2 weeks of IH exposure. We also assessed systemic haemodynamics, muscle sympathetic nerve activity (MSNA), ischaemic calf blood flow responses and baroreflex gain. We obtained blood samples for inflammatory markers before, during and after exposure. IH significantly increased daytime ambulatory blood pressure after a single night of exposure (3 mmHg for mean and diastolic) and further increased daytime pressures after 2 weeks of exposure (8 mmHg systolic and 5 mmHg diastolic). Mean ± sd MSNA increased across the exposure (17.2 ± 5.1 versus 21.7 ± 7.3 bursts·min⁻¹; p < 0.01) and baroreflex control of sympathetic outflow declined from -965.3 ± 375.1 to -598.4 ± 162.6 AIU·min⁻¹ ·mmHg⁻¹ (p < 0.01). There were no evident changes in either vascular reactivity or systemic inflammatory markers. These data are the first to show that the arterial pressure rise is sustained throughout the waking hours beyond the acute phase immediately after exposure. Moreover, they may suggest that sympathoactivation induced by IH likely contributes to blood pressure elevation and may derive from reduced baroreflex inhibition. These mechanisms may reflect those underlying the blood pressure elevation associated with OSAS.

The Effect of Exercise on Haemodynamics in Intermittent Claudication

Changes in lower limb haemodynamics such as arterial pressure and/or flow have often been, and continue to be, cited as possible mechanisms for the improvement in walking performance that occurs with exercise training in individuals with peripheral arterial disease (PAD), but data are conflicting in this regard. There are a small number of literature reviews examining the effects of exercise on PAD, however, there has been insufficient analysis synthesizing possible mechanisms of effect, overall benefits and limitations of these trials. Our objective was therefore to systematically review the evidence for the effect of exercise on lower limb haemodynamic measures of resting and post-exercise ankle brachial index (ABI), resting toe pressure, and resting and reactive hyperaemic calf blood flow in PAD. A systematic search of studies published between 1934 and March 2010 was conducted using MEDLINE, EMBASE, AMED, SportDiscus, CINAHL, PEDro, Premedline, Google Scholar and Web of Knowledge databases. Eligible studies included randomized controlled trials using an exercise intervention for the treatment of intermittent claudication with haemodynamic measures of disease severity as outcomes. Relative effect sizes (ESs) and 95% confidence intervals were calculated for outcomes. Correlation and regression analyses were performed to establish relationships between symptoms and haemodynamic outcomes. Thirty-three trials including 1237 subjects with mild to moderate claudication met the eligibility criteria. Exercise did not significantly change lower extremity haemodynamics in most trials; nor were clinical improvements related to changes in resting ABI (mean ES 0.09 +/- 0.26; r = 0.02; p = 0.94), post-exercise ABI (mean ES 0.18 +/- 0.3; r = -0.33; p = 0.52) or reactive hyperaemic calf blood flow (mean ES 0.38 +/- 0.67; r = 0.35; p = 0.26). A relationship may exist between a change in symptoms and changes in resting toe pressure (mean ES 0.22 +/- 0.22; r = 0.75; p = 0.25) and resting calf blood flow (mean ES 0.09 +/- 0.16; r = 0.59; p = 0.22). Changes in resting and post-exercise ABI and reactive hyperaemic calf blood flow do not appear to explain the clinical benefits of exercise in PAD. More study is required in the areas of resting toe pressure and resting calf blood flow.

Resting energy expenditure in patients with intermittent claudication and critical limb ischemia

The primary aim of this study was to compare the resting energy expenditure of patients with intermittent claudication and critical limb ischemia. A secondary aim was to identify predictors of resting energy expenditure. One hundred patients limited by intermittent claudication and 40 patients with critical limb ischemia participated in this study. Patients were assessed on resting energy expenditure, body composition, ankle brachial index (ABI), and calf blood flow. Patients with critical limb ischemia had a lower resting energy expenditure than patients with intermittent claudication (1429 +/- 190 kcal/day vs 1563 +/- 229 kcal/day; P = .004), and higher body fat percentage (34.8 +/- 7.8% vs 31.5 +/- 7.8%; P = .037), higher fat mass (30.0 +/- 9.3 kg vs 26.2 +/- 8.9 kg;P = .016), and lower ABI (0.31 +/- 0.11 vs 0.79 +/- 0.23; P < .001). Resting energy expenditure was predicted by fat free mass (P < .0001), age (P < .0001), ABI (P < .0001), ethnicity (P < .0001), calf blood flow (P = .005), and diabetes (P = .008). Resting energy expenditure remained lower in the patients with critical limb ischemia after adjusting for clinical characteristics plus fat free mass (1473 +/- 27.8 kcal/day [mean +/- SEM] vs 1527 +/- 19.3 kcal/day; P = .031), but it was no longer different between groups after further adjustment for ABI and calf blood flow (1494 +/- 25.2 kcal/day vs 1505 +/- 17.7 kcal/day; P = .269). Resting energy expenditure is decreased with a progression in peripheral arterial disease (PAD) symptoms from intermittent claudication to critical limb ischemia. Furthermore, patients with critical limb ischemia who are most susceptible for decline in resting energy expenditure are older, African American patients with diabetes. The lower resting energy expenditure of patients with critical limb ischemia, combined with their sedentary lifestyle, suggests that they are at high risk for long-term positive energy balance and weight gain.

Central, peripheral and resistance arterial reactivity: fluctuates during the phases of the menstrual cycle

The purpose of this study was to document the temporal changes in vascular reactivity occurring simultaneously in central, peripheral and microvascular resistance arteries in the same cohort of women during the normal menstrual cycle. Twenty-three (n = 23) women (mean age (+/-SD) = 19 +/- 1 y) were tested during four phases of a normal menstrual cycle. Delineation of the four phases occurred as follows: (1) the early follicular phase; (2) the late follicular (LF) phase; (3) the early luteal (EL) phase; and (4) the late luteal phase. Non-invasive measurement of central hemodynamics and peripheral artery pulse wave velocity (PWV) were performed using applanation tonometry. Measurement of peripheral endothelial function was determined by flow-mediated dilation (FMD) testing in the brachial artery and venous occlusion plethysmography in the forearm and calf resistance arteries. Additionally, plasma NOx and 17beta-estradiol (E) concentrations were measured. Both central (aortic) and peripheral blood pressure (BP) were lowest (P < 0.05) during the LF phase and BP reduction was sustained (P < 0.05) into the EL phase. The timing and amplitude of the reflected pressure wave were attenuated only during the LF phase (P < 0.05). No temporal changes were observed in either central (carotid-femoral) or peripheral PWV (femoral-dorsalis pedis, carotid-radial). Peak forearm and calf blood flow during reactive hyperemia were greatest in LF. Brachial FMD was greatest during the LF phase (P < 0.05). Plasma E and NOx concentrations were highest during the LF phase (P < 0.05). Young premenopausal women experienced an overwhelming pattern of reduced BP and increased systemic vascular reactivity during the LF phase prior to ovulation.

Menstrual cycle elicits divergent forearm vascular responses to vestibular activation in humans

The menstrual cycle has been reported to alter mean arterial pressure (MAP), but not muscle sympathetic nerve activity (MSNA), during vestibular activation. Specifically, MAP responses to head-down rotation (HDR) are augmented during the mid-luteal (ML) phase compared to the early follicular (EF) phase in young, eumenorrheic women. The purpose of the present study was to determine if the menstrual cycle influences vestibular-mediated changes in limb blood flow. MSNA, MAP, heart rate, and limb blood flow responses to HDR were measured in 12 healthy women. Resting MSNA, MAP, heart rate, forearm blood flow and calf blood flow were not altered by the menstrual cycle. HDR elicited similar increases in MSNA during the EF (Δ3 ± 1 bursts/min; P < 0.05) and ML (Δ2 ± 1 bursts/min; P < 0.05) phase, but only increased MAP during the ML phase (Δ4 ± 2 mm Hg; P < 0.05). HDR did not change heart rate during either the EF or ML phase. HDR elicited similar increases in calf vascular resistance during the EF (Δ6 ± 2 mm Hg/mL/100 mL/min; P < 0.05) and ML (Δ7 ± 2 mm Hg/mL/100 mL/min; P < 0.05) phases of the menstrual cycle. In contrast, HDR increased forearm vascular resistance during the ML phase (Δ4 ± 2 mm Hg/mL/100 mL/min; P < 0.05), but not the EF phase (Δ0 ± 2 mm Hg/mL/100 mL/min). These findings suggest an increased transduction of sympathetic nerve activity into forearm vascular resistance during the ML phase, and reveal the first recorded divergent vascular response to vestibular excitation in human limbs.

Determinants of Exercise Capacity in CKD Patients Treated With Hemodialysis

There are many ways to measure physical functioning. Oxygen uptake at peak exercise is considered to be the most objective or 'gold-standard' measure and is determined by the integrated functioning of multiple physiological systems. Renal failure can affect the functioning of several of these systems which results in low levels of peak oxygen uptake. This review examines the determinants of oxygen uptake as defined by the Fick Equation, and presents data from studies that have reported these physiological measures. It becomes clear that there are many factors that may limit peak oxygen uptake in these patients and any one mechanism may be difficult to identify.

Physiological Predictors of Maximum Treadmill Walking Performance in Patients with Intermittent Claudication

The purpose of this investigation was to identify physiological predictors of maximum treadmill walking performance (MWD) in patients with intermittent claudication. Forty-five claudicants performed a graded treadmill test to determine MWD, peak oxygen uptake, and gas exchange threshold. Calf muscle oxygenation (StO2) at 1 min and time to minimum StO2 were also measured using near-infrared spectroscopy. On other occasions, peak calf blood flow, resting ankle-brachial index, and pulmonary oxygen uptake kinetics during steady-state walking were assessed. A forward stepwise multiple regression analysis was performed to determine predictors of MWD. A regression model comprising time to minimum StO2, peak oxygen uptake, and StO2 at 1 min explained 64% of the variation in MWD. The results suggest that cardiopulmonary fitness and the ability to match oxygen delivery to metabolic demand are important determinants of walking performance in claudicants, and that certain near-infrared spectroscopy variables might be useful in studies that evaluate the mechanisms of clinical improvement with different treatment interventions.

Effects of short-term endurance exercise training on vascular function in young males

We investigated effects of 6 days of endurance exercise training [cycling at 65% of peak oxygen consumption (VO(2peak)) for 2 h a day on six consecutive days] on vascular function in young males. Measures of VO(2peak), arterial stiffness, calf vascular conductance and heart rate variability were obtained pre- and post-training. Indices of arterial stiffness were obtained by applanation tonometry to determine aortic augmentation index normalized to a heart rate of 75 bpm (AI(x) at 75 bpm), and central and peripheral pulse wave velocity (CPWV, PPWV). Resting and maximal calf vascular conductances were calculated from concurrent measures of blood pressure and calf blood flow using venous occlusion strain-gauge plethysmography. Time and frequency domain measures of heart rate variability were obtained from recording R-R intervals during supine and standing conditions. Both CPWV (5.9 +/- 0.8 vs. 5.4 +/- 0.8 m/s) and PPWV (9.7 +/- 0.8 vs. 8.9 +/- 1.3 m/s) were reduced following the training program. No significant changes were observed in AI(x) at 75 bpm, vascular conductance, heart rate variability or VO(2peak). These data indicate that changes in arterial stiffness independent of changes in heart rate variability or vascular conductance can be achieved in healthy young males following only 6 days of intense endurance exercise.

Resting energy expenditure in subjects with and without intermittent claudication

Subjects with peripheral arterial disease and intermittent claudication have ischemia of the lower extremities, but little is known how this influences resting energy expenditure. The objective of the study was to compare the resting energy expenditure of subjects with and without intermittent claudication. One hundred six subjects limited by intermittent claudication and 77 controls who did not have peripheral arterial disease and intermittent claudication participated in this study. Subjects were assessed on resting energy expenditure, body composition, ankle/brachial index (ABI), and calf blood flow. Subjects with intermittent claudication had a lower resting energy expenditure (1585 ± 251 vs 1716 ± 277 kcal/d, P = .019), higher body fat percentage (33.4% ± 10.7% vs 29.6% ± 7.7%, P = .016), higher fat mass (29.6 ± 10.6 vs 24.2 ± 8.9 kg, P = .011), and lower ABI (0.66 ± 0.20 vs 1.19 ± 0.12, P < .001). Resting energy expenditure was predicted by fat-free mass ( P < .001), ABI ( P = .027), and calf blood flow ( P = .040). Resting energy expenditure remained lower in the subjects with intermittent claudication after adjusting for clinical characteristics plus fat-free mass (1611 ± 171 vs 1685 ± 209 kcal/d, P = .035), but was no longer different between groups after further adjustment for ABI and calf blood flow (1622 ± 165 vs 1633 ± 185 kcal/d, P = .500). Subjects with intermittent claudication have lower resting energy expenditure than controls, which is partially explained by ABI and calf blood flow.

Beta Blockers for Peripheral Arterial Disease

To quantify the potential harm of beta blockers in patients with peripheral arterial disease. All randomised controlled trials (RCTs) comparing beta blockers with placebo for the outcomes of claudication and maximal walking distance and time, calf blood flow, vascular resistance and skin temperature were searched using the Cochrane Controlled Trials Register, PubMed and CINAHL. Trials comparing different types of beta blockers were excluded. Six RCTs fulfilling the above criteria, with a total of 119 patients, were included. The beta blockers studied were atenolol, propranolol, pindolol and metoprolol. None of the trials showed a statistically significant worsening effect of beta blockers on the outcomes measured. There were no reports of any adverse events with the beta blockers studied. Currently, there is no evidence to suggest that beta blockers adversely affect walking distance in people with intermittent claudication. Beta blockers should be used with caution if clinically indicated, especially in patients with critical ischaemia where acute lowering of blood pressure is contraindicated.

Physiological Predictors of Maximum Treadmill Walking Performance in Patients with Intermittent Claudication

The purpose of this investigation was to identify physiological predictors of maximum treadmill walking performance (MWD) in patients with intermittent claudication. Forty-five claudicants performed a graded treadmill test to determine MWD, peak oxygen uptake, and gas exchange threshold. Calf muscle oxygenation (StO (2)) at 1 min and time to minimum StO (2) were also measured using near-infrared spectroscopy. On other occasions, peak calf blood flow, resting ankle-brachial index, and pulmonary oxygen uptake kinetics during steady-state walking were assessed. A forward stepwise multiple regression analysis was performed to determine predictors of MWD. A regression model comprising time to minimum StO (2), peak oxygen uptake, and StO (2) at 1 min explained 64% of the variation in MWD. The results suggest that cardiopulmonary fitness and the ability to match oxygen delivery to metabolic demand are important determinants of walking performance in claudicants, and that certain near-infrared spectroscopy variables might be useful in studies that evaluate the mechanisms of clinical improvement with different treatment interventions.

Weight Loss May Reverse Blunted Sympathetic Neural Responsiveness to Glucose Ingestion in Obese Subjects With Metabolic Syndrome

OBJECTIVEThe purpose of this study was to examine the effects of weight loss on sympathetic nervous system responsiveness to glucose ingestion in obese subjects with metabolic syndrome, in whom such responses are reportedly blunted.RESEARCH DESIGN AND METHODSThirty four subjects, 19 insulin resistant and 15 insulin sensitive and aged 55 ± 1 years (mean ± SE) with BMI 31.6 ± 0.6 kg/m2, who fulfilled the Adult Treatment Panel III criteria for metabolic syndrome participated. Simultaneous measurements of whole-body norepinephrine spillover rate, calf blood flow, and intra-arterial blood pressure were made at times 0, 30, 60, 90, and 120 min postglucose (75 g). The experiment was repeated after a 3-month hypocaloric diet with or without an exercise program.RESULTSBody weight decreased by 8.1 ± 0.9 and 8.4 ± 1.1 kg and resting norepinephrine spillover by 94 ± 31 and 166 ± 58 ng/min (all P ≤ 0.01) in insulin-resistant and insulin-sensitive subjects, respectively. Weight loss was accompanied by a marked increase in sympathetic responsiveness after glucose but only in insulin-resistant subjects. In this subgroup, comparative increases in norepinephrine spillover rates at baseline and after weight loss averaged −3 ± 25 versus 73 ± 24 ng/min at 30 min (P = 0.039), 36 ± 21 versus 115 ± 28 ng/min at 60 min (P = 0.045), 9 ± 21 versus 179 ± 50 ng/min at 90 min (P < 0.001), and 40 ± 48 versus 106 ± 39 ng/min at 120 min (P = 0.24).CONCLUSIONSWeight loss reverses blunted sympathetic responsiveness to glucose ingestion in insulin-resistant subjects with metabolic syndrome, which is relevant to postprandial energy utilization and body weight homeostasis.

Pathophysiological aspects of lower limb oedema in patients with proximal femoral fractures

Objectives: To examine the changes in Starling components, regulating the transcapillary fluid transport, in patients with proximal femoral fractures (PFF). Material and methods: Twenty-eight patients with proximal femoral fracture were classified into femoral column fracture (FCF) and pertrochanteric fracture (PTF) groups. The following measurements were made in both groups of patients on the 7th post-operative day: colloid osmotic pressure of plasma and subcutaneous interstitial fluid (COPpl and COPif), capillary filtration coefficient (CFC) and interstitial fluid pressure (Pif) in the anterior muscle compartment of the leg and calf muscle blood flow, in both lower extremities. Results: The transcapillary colloid osmotic gradient was significantly reduced (p<0.02) in patients with PTF, and they also showed a significant increase in CFC values (p=0.038). Moreover, Pif was elevated (1.9 mmHg, SD 2.1, p=0.01) and calf muscle blood flow was significantly higher (p=0.02), than in the contralateral limb in patients with PTF. Conclusion: The transcapillary colloid osmotic gradient is significantly reduced in patients with PTF. This may partly explain why patients with PTF develop more oedema in the lower limb than those with FCF. CFC and calf blood flow are also significantly increased in the fractured limb, which allows increased transcapillary filtration.

Blunted sympathetic neural response to oral glucose in obese subjects with the insulin-resistant metabolic syndrome

BackgroundGlucose ingestion stimulates sympathetic nervous system (SNS) activity in lean subjects, whereas blunted responses have been reported in the obese. ObjectiveThe objective was to investigate the impact of insulin resistance on the SNS response to oral glucose. DesignNineteen insulin-resistant (IR) and 12 insulin-sensitive (IS) obese subjects with the metabolic syndrome and matched for age, sex, and blood pressure participated. Simultaneous measurements of muscle sympathetic nerve activity (MSNA) by microneurography, whole-body norepinephrine spillover rate, cardiac baroreflex sensitivity (BRS), calf blood flow, and arterial blood pressure were made at baseline and 30, 60, 90, and 120 min after a 75-g glucose load. ResultsIR subjects had a higher insulin area under the curve from 0 to 120 min (AUC0–120: 13,468 ± 677 compared with 6399 ± 612 mU/L · min; P < 0.001), glucose AUC0–120 (P < 0.05), and resting MSNA (41 ± 3 compared with 31 ± 3 bursts/min; P = 0.03) than did IS subjects. MSNA and the norepinephrine spillover rate increased from baseline (by 29 ± 7% and 40 ± 13%, respectively; P ≤ 0.001 for both) in IS subjects after the glucose load. In contrast, there was a blunted and delayed sympathetic response in IR subjects. Cardiac BRS and diastolic blood pressure decreased, whereas calf blood flow increased after the glucose load and by a similar magnitude in both groups (P < 0.01). Body mass index, abdominal fat, and insulin AUC0–120 were independent (inverse) predictors of the SNS response. ConclusionsIR subjects with the metabolic syndrome have a blunted SNS response to oral glucose compared with IS subjects with the metabolic syndrome, which is related to central adiposity and the insulin response but not to differences in skeletal muscle vasodilation or BRS.

Attenuated peripheral vasoconstriction during an orthostatic challenge in older men

orthostatic hypotension is common in older men and associated with morbidity and mortality. During orthostatic challenges, older men maintain their blood pressure by an augmented increase in total peripheral resistance. Changes in the leg vascular bed contribute importantly to blood pressure regulation during orthostatic challenges, partly because of blood pooling in the legs. Little is known about the contribution of the leg vascular bed to the augmented increase in total peripheral resistance. to examine tilt-induced peripheral vasoconstriction in the leg vascular bed of young and older men. we measured forearm and calf blood flow in 12 young and 12 older men, using venous occlusion plethysmography during 30 degrees head-up tilt (HUT). Forearm and calf vascular resistance were calculated as mean arterial blood pressure divided by blood flow. during HUT, calf and forearm vascular resistance increased in older and young men. The increase in forearm vascular resistance was similar between older (40 +/- 6%) and young men (51 +/- 12%). However, the increase in calf vascular resistance was lower in older (96 +/- 15%) than in young men (175 +/- 30%). advancing age leads to an attenuated tilt-induced increase in calf vascular resistance, which may contribute to age-related orthostatic hypotension.

Reply to Rennie, Phillips, and Smith

to the editor: Several points need to be made to allow the readers of the Journal of Applied Physiology to put the comments made by Drs. Rennie, Phillips, and Smith ([3][1]) into proper context. 1 ) We will begin by addressing the two specific points raised about methodology. First, the authors of

Effects of remifentanil-based general anaesthesia with propofol or sevoflurane on muscle microcirculation as assessed by near-infrared spectroscopy

BackgroundAlthough anaesthetics are known to alter microcirculation no study has, to our knowledge, documented changes in human skeletal microcirculatory function during general anaesthesia. MethodsForty-four patients undergoing maxillofacial surgery at a university hospital were prospectively randomized to receive general anaesthesia with remifentanil combined with propofol or sevoflurane. Muscle microcirculation was investigated with near-infrared spectroscopy (NIRS) before general anaesthesia was induced and 30 min later. An NIRS device (NIMO, Nirox) was used to quantify calf deoxyhaemoglobin [HHb], oxyhaemoglobin [HbO2], and total haemoglobin [HbT] concentrations, coupled to a series of venous and arterial occlusions to measure calf blood flow, muscle oxygen consumption, calf vascular resistance, microvascular compliance, and haemoglobin resaturation rate (RR). ResultsIn both the groups, general anaesthesia induced marked changes in muscle microcirculation: the tissue blood volume increased (+33% in remifentanil–sevoflurane and +45% with remifentanil–propofol groups), microvascular resistance decreased (−31% and −38%, respectively), and the post-ischaemic haemoglobin RR decreased (−48% and −36%, respectively). In the remifentanil–propofol group, the muscle blood flow increased (P<0.001), whereas in the remifentanil–sevoflurane group microvascular compliance and muscle oxygen consumption decreased (P<0.01). ConclusionsRemifentanil-based general anaesthesia with propofol or sevoflurane altered the muscle microcirculation in different ways. Quantitative NIRS, a technique that takes into account the optical tissue properties of the individual subject, can effectively measure these changes non-invasively.

Near‐infrared spectroscopy provides an index of blood flow and vasoconstriction in calf skeletal muscle during lower body negative pressure

Near-infrared spectroscopy (NIRS) has been used previously for forearm blood flow estimation at rest and during exercise. In this study we applied NIRS to selectively monitor deep calf oxygenated haemoglobin (Hb) responses in order to estimate blood flow changes in the calf muscle during lower body negative pressure (LBNP). The purpose of this study was to test the hypothesis that changes in calf skeletal muscle oxygenated-Hb, after the removal of superficial tissue responses, were related to blood flow changes during orthostatic stress, and to determine the efficacy of using NIRS measurements as an index of vasoconstriction. Twenty-nine subjects participated in this study. All attempted a graded LBNP trial from baseline (0 mmHg) to -60 mmHg LBNP in 10 mmHg steps at 5-min intervals. Calf blood flow changes were estimated by oxygenated-Hb responses in relation to changes in mercury strain gauge plethysmography and muscle sympathetic nerve activity (MSNA). Calf selective deep oxygenated-Hb decreased continuously from -10 mmHg LBNP. Regression analysis showed that oxygenated-Hb was significantly related to declines in plethysmography evaluations of blood flow [oxygenated-Hb = (-1.57 +/- 0.26) + (1.86 +/- 0.49) plethysmography, r(2) = 0.87 +/- 0.09]. Changes in MSNA (total activity) were also inversely related to oxygenated-Hb (slope < 0, P = 0.037; r(2) = 0.52 +/- 0.15). These results suggest that changes in selective deep calf oxygenated-Hb can be utilized to estimate calf muscle blood flow changes that are most likely caused by vasoconstriction during graded LBNP.