Venous Occlusion Strain Gauge Plethysmography Research Articles

Graduated Compression Stockings

The mechanisms by which graduated compression stockings prevent deep venous thrombosis are not completely understood. In the current study the physiologic effect of low-pressure graduated compression stockings on the venous blood flow in the lower limb and the practical aspects of their use were assessed. Patients having elective orthopaedic surgery at a university orthopaedic department were randomized into five groups to wear two different types of graduated compression stockings in thigh and knee lengths. Patients in the fifth control group did not wear graduated compression stockings. Venous occlusion strain gauge plethysmography was used to measure venous flow. After 20-minutes bed rest there was a highly significant increase in venous capacitance and venous outflow in patients in all of the four groups wearing stockings. There was no difference in the mean of the percentage change of venous capacitance in patients in the four groups wearing stockings. The knee length Brevet stockings were less efficient in increasing the venous outflow. There was no significant change in the venous capacitance and venous outflow in patients in the control group. Visual assessment of the fit and use of stockings was done, and patients' subjective opinion of comfort was sought. The knee length graduated compression stockings wrinkled significantly less, and significantly fewer patients reported discomfort with them. All stockings were reported to be difficult to use. Thigh and knee length stockings have a significant effect on decreasing venous stasis of the lower limb. Knee length graduated compression stockings are similarly efficient in decreasing venous stasis, but they are more comfortable to wear, and they wrinkle less.

ENDOTHELIAL FUNCTION OF CONDUIT AND RESISTANCE ARTERIES IN NEPHROTIC RANGE PROTEINURIA

OBJECTIVE: To test the hypothesis that endothelial dysfunction occurs in nephrotic range proteinuria primarily as a consequence of dyslipidaemia. METHODS: Brachial artery and forearm microcirculatory endothelial function was compared among patients with nephrotic range proteinuria (NRP, n = 14 ), primary hyperlipidaemia (HL, n = 15) and normal controls (NC, n = 16). Endothelial function was studied by measuring post-ischaemic flow-mediated dilatation (FMD) of the brachial artery using high resolution ultrasonography. Endothelium-independent, glyceryl trinitrate (GTN) mediated brachial artery vasodilatation was also measured. Basal and post-ischaemic blood flow of the forearm microcirculation was measured using venous-occlusion strain gauge plethysmography. RESULTS: Serum creatinine was similar among groups. The proteinuric group had a mean albumin of 27.6g/L(1.8) and 24-hour urinary protein excretion of 6.3g(1.3). Plasma lipids and lipoproteins were not statistically different between the NRP and HL groups. Brachial artery FMD was significantly lower in the NRP and HL groups compared with the controls (NRP 4.7%(1.3)*, HL 4.9%(0.7)* and NC 8.3%(0.6), *p = 0.012 vs. NC); GTN mediated dilatation and basal and post-ischaemic forearm blood flow were not statistically different among the three groups. CONCLUSION: Patients with nephrotic range proteinuria have endothelial dysfunction of conduit arteries in the peripheral circulation, similar to that observed in patients with primary hyperlipidaemia. This suggests dyslipoproteinaemia is the principal cause of endothelial dysfunction of conduit arteries in nephrotic range proteinuria. Confirmation of this should be sought with an intervention trial of lipid-regulating therapy.

Enhanced peripheral vasodilation in humans after a fatty meal

OBJECTIVESWe sought to study the effects of a fatty meal on vascular reactivity, including endothelial function and maximal vasodilation.BACKGROUNDRecent reports regarding the physiological changes in peripheral vasculature after eating a fatty meal have been controversial.METHODSTwelve volunteers were studied before, 3 h after, and 6 h after a high-fat meal (1030 kcal, 61 g fat) rich in saturated fatty acids, and 10 were restudied after a similar meal rich in monounsaturated fatty acids. Endothelial function was assessed as flow-mediated dilatation (FMD) in the brachial artery using ultrasound. Resting and postischemic forearm blood flow (FBF) were recorded using venous occlusion strain-gauge plethysmography, before, and every 10 to 15 s after, 5 min upper arm ischemia.RESULTSBrachial artery basal diameter, resting FBF and postischemic hyperemia increased after high-fat meals (all p < 0.001), whereas FMD did not change. The increase in resting FBF correlated with increases in postprandial insulin (r = 0.80, p < 0.002) and triglyceride (r = 0.77, p < 0.005) levels.CONCLUSIONSWe concluded that eating a fatty meal induces vasodilation and increases resting and stimulated FBF and that these observations are probably mediated by postprandial changes in insulin and/or triglyceride levels. The metabolic changes that occur after meals are not associated with impaired endothelial nitric oxide release in the conduit arteries.

Endothelial function of conduit and resistance arteries in nephrotic range proteinuria

OBJECTIVE: To test the hypothesis that endothelial dysfunction occurs in nephrotic range proteinuria primarily as a consequence of dyslipidaemia. METHODS: Brachial artery and forearm microcirculatory endothelial function was compared among patients with nephrotic range proteinuria (NRP, n = 14 ), primary hyperlipidaemia (HL, n = 15) and normal controls (NC, n = 16). Endothelial function was studied by measuring post-ischaemic flow-mediated dilatation (FMD) of the brachial artery using high resolution ultrasonography. Endothelium-independent, glyceryl trinitrate (GTN) mediated brachial artery vasodilatation was also measured. Basal and post-ischaemic blood flow of the forearm microcirculation was measured using venous-occlusion strain gauge plethysmography. RESULTS: Serum creatinine was similar among groups. The proteinuric group had a mean albumin of 27.6g/L(1.8) and 24-hour urinary protein excretion of 6.3g(1.3). Plasma lipids and lipoproteins were not statistically different between the NRP and HL groups. Brachial artery FMD was significantly lower in the NRP and HL groups compared with the controls (NRP 4.7%(1.3)*, HL 4.9%(0.7)* and NC 8.3%(0.6), *p = 0.012 vs. NC); GTN mediated dilatation and basal and post-ischaemic forearm blood flow were not statistically different among the three groups. CONCLUSION: Patients with nephrotic range proteinuria have endothelial dysfunction of conduit arteries in the peripheral circulation, similar to that observed in patients with primary hyperlipidaemia. This suggests dyslipoproteinaemia is the principal cause of endothelial dysfunction of conduit arteries in nephrotic range proteinuria. Confirmation of this should be sought with an intervention trial of lipid-regulating therapy.

No Evidence of Endothelial Dysfunction in Patients with Alzheimer’s Disease

In view of accumulating evidence of vascular pathology in Alzheimer’s disease (AD), we tested the hypothesis that AD patients have impaired endothelial function. This was assessed using the technique of strain-gauge venous occlusion plethysmography, which measures forearm blood flow (FBF). Intra-arterial (brachial) infusion of acetylcholine (ACh) and sodium nitroprusside (SNP) was used to assess local endothelial dependent and independent responses, respectively. There was no difference in the basal FBF of patients and controls. ACh and SNP caused dose-related increases in FBF from baseline, but no difference was recorded between the AD and control group. This study provides no evidence of endothelial dysfunction in the systemic circulation of patients with AD.

Numerical model of deep venous thrombosis detection using venous occlusion strain gauge plethysmography.

Strain gauge plethysmography (SGP) is a non-invasive method used in the detection of deep venous thrombosis (DVT). The technique is based on the measurement of calf volume changes in response to venous occlusion by a thigh cuff, the volume changes reflecting the rates of arterial inflow and venous outflow. A numerical model of the blood circulation within the limb and the response of this to a SGP test has been derived, based on treating the different parts of the circulatory system in the leg as resistance and capacitance elements. The simulation results were compared with clinical studies and support the ability of SGP to detect non-occlusive clots of more than 50-60% of the lumen, as well detecting calf vein occlusion. The non-linear behaviour of the venous compliance with intra-luminal pressure appears to be a particularly important factor within the model. In addition, increases in venous tone due to post-operative venospasm were shown to be a potential source of false positive results.

Calf and forearm blood flow in hypercholesterolemic patients.

Patients with hypercholesterolemia without vascular disease have an impaired endothelium-dependent (nitric oxide-mediated) vasodilation in coronary and peripheral vascular beds. This study was designed to establish whether hypercholesterolemia (and its reduction) affects also the microcirculation vasomotion during postischemic hyperemia in both calf and forearm. Thirteen male patients, aged 36.2+/-8.5 years, mean +/-SD, with heterozygous familial hypercholesterolemia and 10 male control subjects, aged 32.2+/-3.6 years free from vascular lesions were studied. Plasma lipids, hematologic parameters, and limb vasoreactivity were evaluated while the patients were treated only with diet and during therapy with simvastatin. Calf and forearm blood flows were determined by venous occlusion strain gauge plethysmography at rest, during reactive hyperemia, and after sublingual isosorbide dinitrate administration. Calf resting flow rate of the hypercholesterolemic patients during and without treatment was similar to that of the controls. Calf resting vascular resistance was greater in the untreated hypercholesterolemic subjects than in the normal controls, but during treatment this difference was abolished. Peak flow during reactive hyperemia and flow debt repayment were lower in the untreated hypercholesterolemic subjects as compared to the controls, but they were normalized following hypocholesterolemic therapy. No differences were observed in forearm blood flow measurements between hypercholesterolemic subjects (without and during therapy) and control subjects. The blood flow and vascular resistance after isosorbide dinitrate were modified in a similar manner in the hypercholesterolemic (without and during therapy) and control subjects at both calf and forearm. Hypercholesterolemia does not affect vasodilation in the forearm as determined by postocclusive reactive hyperemia, while in the calf hypercholesterolemia is associated with higher resting vascular resistance, lower peak flow during reactive hyperemia, and lower flow debt repayment. These abnormalities are corrected by the hypocholesterolemic treatment.

Angiotensin-(1-7) attenuates vasoconstriction evoked by angiotensin II but not by noradrenaline in man.

Angiotensin-(1-7) has been suggested to be a novel vasodilating peptide. We investigated the direct vascular effect of angiotensin-(1-7) in human forearm resistant vessels, particularly with regard to the interaction with angiotensin II, in healthy normotensive men by strain-gauge venous occlusion plethysmography with intra-arterial infusions of peptides. Intra-arterial infusion of angiotensin-(1-7) at 0.1 to 2000 pmol/min did not cause vasodilatation but rather reduced forearm blood flow by approximately 10% at the highest dose. A placebo-controlled study showed that angiotensin-(1-7) at 0.5 to 40 nmol/min caused weak but significant vasoconstriction (P=0.0016 by ANOVA). Angiotensin-(1-7) at 100 pmol/min, but not at 10 pmol/min, significantly shifted the angiotensin II dose-response curve toward the right (mean+/-SD of percent changes in forearm blood flow: -19+/-17%, -33+/-22%, -55+/-12%, -63+/-10%, and -68+/-5% at 5, 10, 25, 50, and 100 pmol/min of angiotensin II, respectively, with saline; 5+/-13%, 0. 9+/-18%, -40+/-16%, -54+/-9%, and -61+/-6% with angiotensin-(1-7), P=0.0021 by ANOVA). Angiotensin-(1-7) did not affect the dose-response curve of noradrenaline [3+/-12%, 5+/-16%, -20+/-22%, -31+/-18%, and -40+/-12% at 25, 50, 100, 300, and 600 pmol/min of noradrenaline, respectively, with saline; -4+/-15%, -2+/-23%, -29+/-22%, -34+/-16%, and -42+/-9% with angiotensin-(1-7)]. Our results suggest that angiotensin-(1-7) antagonizes vasoconstriction by angiotensin II in human resistant vessels and might act as an endogenous angiotensin II antagonist.

Effects of autonomic disruption and inactivity on venous vascular function.

The effects of autonomic disruption and inactivity were studied on the venous vascular system. Forty-eight subjects, 24 with spinal cord injury (SCI) and 12 sedentary and 12 active able-bodied controls, participated in this study. Peripheral autonomic data were obtained to estimate sympathetic vasomotor control [low-frequency component of systolic blood pressure (LF(SBP))]. Vascular parameters were determined using strain-gauge venous occlusion plethysmography: venous capacitance (VC), venous emptying rate (VER), and total venous outflow (VO(t)). An additional vascular parameter was calculated: venous compliance [(VC/occlusion pressure) x 100]. VC and VO(t) were significantly different (SCI < sedentary < active). VER adjusted for VC was not different for any group comparison, whereas venous compliance was significantly lower in the SCI group than in the able-bodied groups and in the sedentary group compared with the active group. Regression analysis for the total group revealed a significant relationship between LF(SBP) and venous compliance (r = 0.64, P < 0.0001). After controlling for LF(SBP) through analysis of covariance, we found that mean differences for all venous vascular parameters did not change from unadjusted mean values. Our findings suggest that in subjects with SCI, the loss of sympathetic vasomotor tone contributes more than inactivity to reductions in venous vascular function. Heightened VC, VO(t), vasomotor tone, and venous compliance in the active group compared with the sedentary group imply that regular endurance training contributes to optimal venous vascular function and peripheral autonomic integrity.

Venous function and delayed leg swelling following saphenectomy in coronary artery bypass grafting.

Some patients are troubled by leg swelling following saphenectomy long after CABG. Postsaphenectomy venous function in the leg has not, however, been well clarified. To determine whether venous dysfunction caused postsaphenectomy swelling, we measured the maximum venous outflow and time constant (tau) in the leg by venous occlusion strain-gauge plethysmography in 45 patients; a venous Doppler test was also conducted in 33 of the 45 at a mean 57.6 +/- 21.3 months after CABG. The saphenous vein was harvested unilaterally from the lower leg or from both the thigh and lower leg in all patients. Edema was seen in 4 patients (8.9%) and 8 reported leg swelling after saphenous vein harvest (17.8%). Legs were classified into three groups: group 1 consisted of 12 with edema or reports of swelling ipsilateral to the saphenous vein harvest site, group 2 consisted of 33 ipsilateral to the saphenous vein harvest without edema, and group 3 consisted of the 45 nonoperated-on, contralateral legs of the same patients as controls. No significant differences were seen in maximum venous outflow, tau, or the incidence of deep vein reflux among groups. No significant relationship was found between venous function and leg swelling occurring delayed after saphenectomy.

Effects of acute administration of natural progesterone on peripheral vascular responsiveness in healthy postmenopausal women

Peripheral vascular responses to acute administration of natural progesterone were studied in 12 postmenopausal women (mean ± SD age 50.3 ± 4.8 years) with no evidence of cardiovascular disease. According to a randomized, double-blind protocol, all subjects were given natural progesterone as a vaginal cream, able to produce a rapid peak and decay of plasma hormone concentrations, or matched placebo, with crossover after a 1-week washout period. Forearm blood flow and peak flow after ischemic stress (ml/100 ml/min), local vascular resistance (mm Hg/ml/100 ml/min), venous volume (ml/100 ml), and venous compliance (ml/100 ml/mm Hg) were measured by strain-gauge venous occlusion plethysmography at baseline and after progesterone or placebo administration. Plasma norepinephrine concentrations were determined by high-performance liquid chromatography with electrochemical detection. Progesterone sharply decreased forearm blood flow (p <0.01) through an increase in local vascular resistance (p <0.01). Measures of venous function remained unchanged. Although the hormone increased circulating norepinephrine concentrations (p <0.05), there were no significant changes in mean arterial pressure or heart rate. Furthermore, progesterone reduced the local vasodilator capacity, shown by a decrease in forearm Δ flow (difference between peak flow and basal flow, p <0.05). Compared with the well-known effect of estrogen, progesterone exerted an opposite action on peripheral vascular responsiveness. Peripheral circulatory changes may be attributed to a direct activity of progesterone on the arterial wall and may in part reflect a modulation of the hormone on peripheral sympathetic tone. Consideration must be given to the hypothesis that the addition of progestin may attenuate the beneficial effects of unopposed estrogen replacement therapy in postmenopausal women.

Replacement of Angiotensin-Converting Enzyme Inhibitors by Angiotensin-II-Receptor Antagonists in Hypertensive Patients with Type II Diabetes Mellitus

The main pharmacodynamic difference between angiotensin-converting enzyme-inhibitors (ACE-i) and angiotensin-II-receptor antagonists (AII-r) is that ACE-i increase levels of bradykinin, which, in addition to vasodilation, may cause a decrease in insulin resistance. Hypertensive patients with diabetes type II suffering from side effects from ACE-i are frequently changed over to AII-r. The objectives of this study were (1) to study whether this procedure reduces metabolic control, (2) to study effects on blood pressure and forearm blood flow (FLOW), and (3) to study possible associations between the variables hemoglobin A (1c) (HbA(1c)) and FLOW. A self-controlled sequential comparison is required to address such questions. Sixteen patients were treated with 10 mg enalapril or equipotent doses of other ACE-i for 6 months and subsequently with the AII-r losartan at 50 mg daily for 6 more months. Patients were examined at the outpatient clinic every 4 to 8 weeks during the trial. FLOW was measured by iridium strain gauge venous occlusion plethysmography. Mean arterial pressure (MAP) increased by 4 +/- 5 mm Hg (P <.05) after 6 months of losartan treatment as compared with the point of withdrawal of ACE-i. FLOW decreased by 5.4 +/- 5.0 mL/100 mL tissue/min (P <.001), and HbA (1c) increased by 0.6 +/- 0.8 mmol/L (P <.05). Other metabolic variables, including cholesterol, high-density lipoprotein cholesterol, and triglycerides, were not significantly influenced by the change in therapy. Multiple regression analysis revealed that after adjustment for difference in HbA (1c), the correlation between FLOW and MAP was unchanged, and after adjustment for difference in FLOW, the correlation between HbA (1c) and MAP was no longer significant. Replacement of ACE-i by AII-r in hypertensive patients with type II diabetes mellitus induced a significant increase in HbA (1c) and MAP and a decrease in FLOW. The associations of HbA (1c) and FLOW with MAP were at least partly independent of each other, suggesting that mechanisms other than the bradykinin system (eg, the angiotensin (2) -receptor system) are involved. Our study design did not control for placebo and time effects, and so the data are of a preliminary nature.

Impaired forearm blood flow and vasodilator reserve in healthy postmenopausal women

Background The natural process of cessation of ovarian estrogen production is associated with an increasing incidence of cardiovascular disease. Objective We aimed to determine whether postmenopausal women had menopause-associated vasomotor disturbances develop. Methods We studied the vascular forearm function using strain-gauge venous occlusion plethysmography in 12 healthy postmenopausal women (mean age ± SD, 47 ± 3 years; time-lapse from menopause >1 year). Twelve premenopausal subjects matched for age and biophysical characteristics were used as a control group. Results No differences were observed in heart rate or mean blood pressure between the 2 groups of women. Forearm blood flow at supine resting was lower in postmenopausal than in premenopausal women (2.4 ± 0.8 vs 3.1 ± 0.5 mL/100 mL/min; P < .05). Local vascular resistance was higher in postmenopausal than in premenopausal women (43.5 ± 17.5 vs 31.1 ± 4.3 mm Hg/mL/100 mL/min; P < .05). Moreover, peak forearm flow in response to forearm ischemia was 20.8 ± 7.9 mL/100 mL/min in postmenopausal women and 26.6 ± 9.7 mL/100 mL/min in premenopausal women ( P < .01). Plasma concentration of noradrenaline in the supine position was significantly higher in postmenopausal than in premenopausal women (286 ± 22 pg/mL vs 195 ± 33 pg/mL; P < .01). Finally, a significant positive relation was revealed in postmenopausal women between the amount of vasodilator reserve (D flow) in local peripheral circulation and levels of circulating estradiol-17β. Conclusions Abnormalities observed in forearm blood flow and vasodilator capacity in postmenopausal women may be attributed to a critical loss of the vasodilating property of physiologic estrogen. Our data support the possibility that reduction in dilator capacity of the vasculature may contribute to the increase of cardiovascular disease after menopause. (Am Heart J 1999;137:692-7.)

Effect of endothelin-1 on endothelium-derived vascular responsiveness in man

1. Endothelium-dependent vasodilatation via nitric oxide in response to muscarinic stimulation is decreased in chronic heart failure while basal release of nitric oxide may be increased. As production of the endothelium-derived vasoconstrictor endothelin-1 is increased in chronic heart failure, endothelin-1 may act in an autocrine manner to modulate these effects. 2. To test this, we determined whether prolonged endothelin infusion in normal subjects would reproduce the alterations in basal and stimulated nitric oxide release observed in patients with chronic heart failure. Basal nitric oxide production was determined by measurement of forearm blood flow using strain gauge venous occlusion plethysmography before and after brachial artery infusion of a nitric oxide synthase inhibitor (NG-monomethyl-L-arginine). Stimulated nitric oxide production was determined by brachial artery infusion of acetylcholine. As metabolic vasodilatation is thought to be mediated in part via nitric oxide and is decreased in chronic heart failure, forearm blood flow during peak reactive hyperaemia was also measured. Studies were then repeated during brachial artery infusion of endothelin-1 and a non-specific vasoconstrictor, noradrenaline. 3. Neither basal nor stimulated nitric oxide production was altered by endothelin-1 and noradrenaline infusion. However, absolute forearm blood flow responses to peak reactive hyperaemia were decreased during infusion of endothelin-1 in comparison to noradrenaline. These data suggest that increased endothelin-1 may not contribute greatly to altered basal and stimulated nitric oxide production in patients with chronic heart failure but may contribute to impaired metabolic vasodilatation, by mechanisms presumably unrelated to altered nitric oxide production.

Forearm vasorelaxation in hypertensive renal transplant patients

To determine whether cyclosporine A-induced hypertension in renal transplant recipients is accompanied by impairment of endothelium-dependent vasodilatation, which has been suggested by in-vitro and in-vivo animal experiments. In-vivo endothelium-dependent and endothelium-independent vasodilatation, and plasma concentrations of vasoactive hormones in 16 renal transplant patients were determined while they were being treated with cyclosporine A, and 16 weeks later, after their treatment had been changed to azathioprine therapy. The vasodilator response of the forearm vascular bed was measured by strain gauge venous occlusion plethysmography during intra-arterial infusion of acetylcholine (endothelium-dependent vasodilatation) and nitroprusside (endothelium-independent vasodilatation). Postischemic reactive flow was measured after 10 min of arterial occlusion. In addition, plasma concentrations of norepinephrine, and the prostanoids prostaglandin E2 and thromboxane B2, and also concentration of cyclosporine A in blood, were measured. Glomerular filtration rate and renal blood flow were estimated 1 day before the plethysmography study during each treatment period. Upon changing from cyclosporine A to azathioprine treatment, mean arterial pressure fell significantly by 12+/-3% (P< 0.05). Glomerular filtration rate and renal blood flow increased by 13+/-5 and 19+/-8%, respectively (both P< 0.05), while renal vascular resistance fell by 48+/-11% (P< 0.01). Both baseline forearm blood flow and baseline forearm resistance did not change after conversion (5.7+/-0.7 versus 4.9+/-0.6 ml/100 ml/min, and 27.3+/-4.2 versus 26.2+/-3.2 arbitrary units). The absolute and relative forearm blood flow responses, and forearm vascular resistance responses to infusions of acetylcholine and nitroprusside were similar during treatments with cyclosporine A and azathioprine. Peak postischaemic forearm blood flow was 42+/-12% higher during cyclosporine A treatment than it was during azathioprine treatment (P< 0.05), but the minimal postischaemic forearm vascular resistance did not differ for these treatments. Plasma prostaglandin E2 and thromboxane B2 levels decreased by 34+/-7 and 45+/-8%, respectively, after changing treatment, but norepinephrine levels did not change. Our data indicate that cyclosporine A-induced hypertension in renal transplant recipients is not accompanied by an increase in forearm vascular resistance. In addition, changing from cyclosporine A to azathioprine treatment did not cause changes in endothelial vasodilator functioning, although mean arterial pressure decreased significantly. Our results do not support the hypothesis that attenuation of endothelial vasodilator functioning contributes to the development of cyclosporine A-induced hypertension.

Effect of Endothelin-1 on Exercise-Induced Vasodilation in Normal Subjects and in Patients With Heart Failure

Forearm blood flow (ml/min/100 ml) was determined with strain-gauge venous occlusion plethysmography at rest and in response to handgrip exercise in 7 patients with congestive heart failure and in 9 normal subjects before and after regional administration of endothelin-1 in the brachial artery. Administration of endothelin-1 significantly decreased forearm blood flow at rest and during exercise in normal subjects but did not change it at rest or during exercise in patients with congestive heart failure.

Effects of Transdermal Estrogen Administration on Peripheral Vascular Responsiveness in Menopausal Women

This study was designed to evaluate the peripheral vascular responses to acute estrogen replacement. According to a cross-over, double-blind study design, we randomized nine healthy postmenopausal women (time lapse from menopause to >1 year; mean age ± SD 45.4 ± 11.7 years) to treatment with transdermal patches of estradiol-17β or matched placebo. The estrogen patch was rated to assure a plasma concentration of substance of more than 100 pg/ml after 8–10 hours of treatment. Forearm blood flow (ml/100 ml/minute), local vascular resistance (mmHg/ml/100 ml/minute), venous volume (ml/100 ml), and venous compliance (ml/100 ml/mmHg) were measured in supine resting subjects by the straingauge venous occlusion plethysmography. Plasma concentration of norepinephrine (pg/ml) was quantified by HPLC-ED. Estradiol-17β produced increase in forearm blood flow and decrease in local vascular resistance. The drug reduced circulating norepinephrine concentrations. There were no significant changes in mean arterial pressure or heart rate. Venous volume and venous compliance were both enhanced by estrogen administration. The peripheral circulatory changes are attributed to a direct activity of estradiol-17β on arterial and venous wall and may in part reflect a modulation of estrogen on peripheral sympathetic tone.

The Effect of Active Movement of the Foot on Venous Blood Flow after Total Hip Replacement*

Surgeons often encourage patients to move their feet in an attempt to prevent venous stasis, but there is little evidence that this measure is beneficial. We investigated the effect of active movement of one foot on the venous blood flow four days after total hip replacement. The actual venous outflow at rest was measured with use of venous occlusion strain-gauge plethysmography in thirty-eight patients. The patients were randomly allocated to the control group (eighteen patients) or the exercise group (twenty patients). A baseline measurement was followed by a one-minute period of rest (control group) or of maximum plantar flexion and dorsiflexion of the foot, ankle, and toes at a rate of thirty cycles per minute (exercise group). The venous outflow was measured again at two, seven, twelve, and thirty minutes in both groups. Movement of the foot for one minute produced a significant and sustained increase (p < 0.002) in the venous outflow (mean maximum increase, 22 per cent). The value remained greater than the baseline level for thirty minutes (mean increase, 6.5 per cent) (p < 0.2). The increase was gradual, reaching a maximum twelve minutes after the completion of exercise. Our results confirm the beneficial hemodynamic effects of active movement of the foot in the postoperative period and suggest that patients should move the feet and ankles postoperatively as part of a prophylactic regimen directed at decreasing the risk of venous thrombosis.

Relation between serum uric acid and lower limb blood flow in patients with chronic heart failure.

OBJECTIVE: To determine whether lower limb blood flow is related to serum uric acid concentrations in patients with chronic heart failure, taking into account the hyperuricaemic effects of diuretic treatment...

Training improves endothelium-dependent vasodilation in resistance vessels of patients with heart failure.

The effects of physical training on endothelium-dependent vasodilation in skeletal muscle resistance vessels were investigated in patients with heart failure. Forearm blood flows (ml.min-1.100 ml-1) in response to brachial arterial administration of acetylcholine (5 x 10(-5) and 5 x 10(-4) M at 1 ml/min) and nitroglycerin (5 x 10(-6) and 5 x 10(-5) M at 1 ml/min) were determined by strain-gauge venous occlusion plethysmography before and after 8 wk of daily handgrip exercise in 12 patients with chronic heart failure. After 8 wk of daily handgrip exercise, the vasodilatory responses to acetylcholine significantly increased from pretraining values, i.e., 16.6 +/- 2.0 vs. 8.6 +/- 1.3 ml.min-1.100 ml-1 (P < 0.05) and 27.5 +/- 1.5 vs. 14.6 +/- 1.7 ml.min-1.100 ml-1 (P < 0.05), respectively, whereas the vasodilatory responses to nitroglycerin did not change. Handgrip exercise training appears to specifically enhance endothelium-dependent vasodilation in the forearm skeletal muscle circulation of patients with heart failure.