Conduit Artery Diameter Research Articles

Length as a Determinant of the Longitudinal Stress and Diameter of Different Conduit Arteries

Article Length as a Determinant of the Longitudinal Stress and Diameter of Different Conduit Arteries was published on January 1, 1992 in the journal Biomedical Engineering / Biomedizinische Technik (volume 37, issue s1).

Evidence for a Greater Elevation in Vascular Shear Stress after Morning Exercise

The vascular endothelium plays an important role in the maintenance of vascular health and the modulation of vascular tone and blood pressure. Recently, it has been demonstrated that blood pressure reactivity to physical activity is greater in the morning, and possibly, diurnal variation in vascular function may also be evident. The aim of this study was to assess vascular responses after exercise at different times of day. After 45 min of supine rest, 12 male normotensives completed a 30-min bout of cycling at 70% peak oxygen uptake beginning on separate days at 0800 and 1600 h. Edge detection and wall tracking of high-resolution arterial B-mode ultrasound images combined with synchronized Doppler waveform analysis were used to measure brachial and femoral conduit artery diameter and to calculate blood flow and shear rate. Measurements were recorded before and 20 min after exercise. At 5 min after exercise, the mean +/- SE brachial shear rate was 72 +/- 21 arbitrary unit (AU) higher in the morning compared with the afternoon (P = 0.05), but this was not compensated for by enlargement of arterial diameter (P = 0.59). No diurnal variation was observed in the femoral artery measurements. Diurnal difference in conduit artery regulatory control manifests as an elevated intravascular shear stress after morning exercise. Potentially, higher postexercise shear rate in the morning in at-risk individuals could contribute to the elevated cardiovascular risk evident in the postwaking hours.

Brachial Artery Blood Flow Responses to Different Modalities of Lower Limb Exercise

Cycling is associated with a reproducible systolic anterograde and diastolic retrograde flow pattern in the brachial artery (BA) of the inactive upper limb, which results in endothelial nitric oxide (NO) release. The purpose of this study was to examine the impact of different types and intensities of lower limb exercise on the BA flow pattern. We examined BA blood flow and shear rate patterns during cycling, leg kicking, and walking exercise in 12 young subjects (24 +/- 3 yr). BA diameter, blood flow, and shear rate were assessed at baseline (1 min) and at three incremental intensity levels of cycling (60, 80, and 120 W), bilateral leg kicking (5, 7.5, and 10 kg), and walking (3, 4, and 5 km x h(-1)), performed for 3 min each. Edge detection and wall tracking of high-resolution B-mode arterial ultrasound images, combined with synchronized Doppler waveform envelope analysis, were used to calculate conduit artery diameter and anterograde/retrograde blood flow and shear rate continuously across the cardiac cycle. BA mean blood flow and shear rate increased significantly throughout each exercise protocol (P < 0.001), and BA anterograde blood flow and shear rate showed comparable increases throughout each protocol (P < 0.001). Retrograde blood flow and shear rate, however, demonstrated a significant increase during cycling and walking (P < 0.001) but not during leg kicking. Rhythmic lower limb exercise (cycling and walking) results in an increase in BA systolic anterograde blood flow and shear rate, directly followed by a large retrograde flow and shear rate. This typical pattern, previously linked with endothelial NO release, is not present during a different type of exercise such as leg kicking.

I018 Short and long lasting action of shear stress changes on diameter of conduit arteries in patients with arterial hypertension

Aim of the study was to investigate short and long lasting actions of shear stress changes on vascular diameter of brachial artery in patients with arterial hypertension. 57 patients with arterial hypertension (mean age±SD, 51.26±1.94; 30 men and 27 women) and 17 healthy controls (mean age±SD, 51±5.41 ; 9 men and 8 women) were included in the study. All the subjects underwent to the investigation of vascular characteristics via high resolution vascular dopplerechography and clinical blood pressure investigations. Patients with cardiovascular, peripheral and cerebrovascular diseases, diabetes mellitus, smokers, pregnant, obese as well as those with secondary forms of hypertension, ischemic heart disease and heart failure were excluded from the study. Compared with normotensive control subjects, initial vascular diameter (D0), was higher in hypertensive subjects (3.76±0.28 vs. 4.32±0.14, P<0.01). Initial shear stress was not significantly different between the two groups. Therefore, after reactive hyperemia test (RHtest) shear stress as well as changes of shear stress were higher in hypertensive population compared with healthy control subjects (5.86±0.32 vs. 5.15±0.32, P<0.05 and -0.35±0.09 vs. -0.71±0.09; P<0.001). Initial vascular diameter was in a negative correlation with initial shear stress, as well as with after RHtest shear stress, but there was appeared positive correlation between initial vascular diameter and changes of it. Arterial hypertension is associated with permanent changes of vascular wall diameter via neuro-humoral factors. Therefore, obtained results confirm an opinion that different from the short action of the changes of shear stress, vascular diameter of conduit arteries increases in response to the chronic increase of the shear stress.

Does arterial shear explain the magnitude of flow-mediated dilation?: a comparison between young and older humans

Flow-mediated dilatation (FMD) has become a commonly applied approach for the assessment of vascular function and health in humans. Recent studies emphasize the importance of normalizing the magnitude of FMD to its apparent eliciting stimulus, the postdeflation arterial shear. However, the relationship between shear stress and the magnitude of FMD may differ between groups. The aim of this study was to examine the relationship between the brachial FMD and four different indexes of postdeflation shear rate (SR) in healthy children (n = 51, 10 +/- 1 yr) and young (n = 57, 27 +/- 6 yr) and older (n = 27, 58 +/- 4 yr) adults. SR was calculated from deflation (time 0) until 9 s (peak), 30 s (0-30), 60 s (0-60), or until the time-to-peak diameter in each individual (0-ttp). Edge detection and wall tracking of high resolution B-mode arterial ultrasound images were used to calculate the conduit artery diameter. In young adults, the brachial artery FMD demonstrated a significant correlation with the area under the SR curve (SR(AUC)) 0-30 s (r(2) = 0.12, P = 0.009), 0-60 s (r(2) = 0.14, P = 0.005), and 0-ttp (r(2) = 0.14, P = 0.005) but not for the peak SR(AUC) 0-9 s (r(2) = 0.04, P = 0.12). In children and older adults, the magnitude of the brachial artery FMD did not correlate with any of the four SR(AUC) stimuli. These findings suggest that in young subjects, postdeflation SR(AUC) correlates moderately with the magnitude of the FMD response. However, the relationship between FMD and postdeflation shear appears to be age dependent, with less evidence for an association in younger and older subjects. Therefore, we support presenting SR(AUC) stimuli but not normalizing FMD responses for the SR(AUC) when using this technique.

Heterogeneity in conduit artery function in humans: impact of arterial size

To determine whether conduit artery size affects functional responses, we compared the magnitude, time course, and eliciting shear rate stimulus for flow-mediated dilation (FMD) in healthy men (n = 20; 31 +/- 7 yr). Upper limb (brachial and radial) and lower limb (common and superficial femoral) FMD responses were simultaneously assessed, whereas popliteal responses were measured in the same subjects during a separate visit. Glyceryl trinitrate (GTN)-mediated responses were similarly examined. Edge detection and wall tracking of high-resolution B-mode arterial ultrasound images, combined with synchronized Doppler waveform envelope analysis, were used to calculate conduit artery diameter, blood flow, and shear rate continuously across the cardiac cycle. Baseline artery size correlated inversely with the FMD response (r = -0.57, P < 0.001). Within-artery comparisons revealed a significant inverse correlation between artery size and FMD% for the radial (r = -0.66, P = 0.001), brachial (r = -0.55, P = 0.01), and popliteal artery (r = -0.48, P = 0.03), but not for the superficial and common femoral artery. Normalization of FMD responses for differences in eliciting shear rate did not abolish the between-artery relationship for artery function and size (r = -0.48, P < 0.001), suggesting that differences between artery function responses were not entirely due to size-related differences in shear rate. This was reinforced by a significant between-artery correlation for GTN responses and baseline artery size (r = -0.74, P < 0.001). In summary, systematic differences exist in vascular function responses of conduit arteries that differ in size. This raises the possibility that differences in artery size within or between individuals may influence functional responses.

The impact of baseline diameter on flow-mediated dilation differs in young and older humans

Flow-mediated dilation (FMD) has become a commonly applied approach for the assessment of vascular function and health, but methods used to calculate FMD differ between studies. For example, the baseline diameter used as a benchmark is sometimes assessed before cuff inflation, whereas others use the diameter during cuff inflation. Therefore, we compared the brachial artery diameter before and during cuff inflation and calculated the resulting FMD in healthy children (n=45; 10+/-1 yr), adults (n=31; 28+/-6 yr), and older subjects (n=22; 58+/-5 yr). Brachial artery FMD was examined after 5 min of distal ischemia. Diameter was determined from either 30 s before cuff inflation or from the last 30 s during cuff inflation. Edge detection and wall tracking of high resolution B-mode arterial ultrasound images was used to calculate conduit artery diameter. Brachial artery diameter during cuff inflation was significantly larger than before inflation in children (P=0.02) and adults (P<0.001) but not in older subjects (P=0.59). Accordingly, FMD values significantly differed in children (11.2+/-5.1% vs. 9.4+/-5.2%; P=0.02) and adults (7.3+/-3.2% vs. 4.6+/-3.3%; P<0.001) but not in older subjects (6.3+/-3.4% vs. 6.0+/-4.2%; P=0.77). When the diameter before cuff inflation was used, an age-dependent decline was evident in FMD, whereas FMD calculated using the diameter during inflation was associated with higher FMD values in older than younger adults. In summary, the inflation of the cuff significantly increases brachial artery diameter, which results in a lower FMD response. This effect was found to be age dependent, which emphasizes the importance of using appropriate methodology to calculate the FMD.

Assessment Of Peak Peripheral Artery Conduit And Resistance Artery Structure In Humans: Does Occluding Cuff Position Matter?

PURPOSE: To determine whether the position of an occluding cuff on the lower and upper limbs modifies conduit artery diameter and blood flow responses to peak vasodilator stimuli. Edge-detection and wall tracking of high resolution B-mode arterial ultrasound images, combined with synchronized Doppler waveform envelope analysis, was used to calculate conduit artery blood flow (BF) and diameter responses continuously across the cardiac cycle. METHODS: Thirty-six healthy subjects (47.4±3 yrs; 42.2±2 ml.kg-1.min-1) underwent assessment of popliteal and brachial artery blood flow and diameter responses to periods of ischemic exercise and glyceryl trinitrate (GTN) administration. Ischemia was induced with occluding cuff placement both proximal and distal to the imaged artery. RESULTS: The peak popliteal artery diameter response (PADpeak) was observed following a 5 minute period of ischemic combined with 3 minutes of exercise, with the occluding cuff placed above the imaged artery (12.8±1.1% vs 9.7±0.9%, thigh vs calf cuff placement, P<0.05). Peak brachial artery diameter response (BADpeak) was observed following a similar ischemic handgrip exercise stimulus with upper arm cuff placement (17.9±1.3% vs 11.2±0.9%, arm vs forearm cuff placement, P<0.0001). No significant effect of cuff placement was evident for either peak brachial (BAFpeak) or popliteal artery flow (PAFpeak) or conductance responses. CONCLUSIONS: These data indicate that cuff position modifies peak diameter responses through both the popliteal and brachial arteries. Future studies should utilize proximal cuff placement if the aim is to determine peak arterial vasodilation responses as an index of conduit arteriogenic adaptation.

Differences In The Characteristics Of Flow-Mediated Dilatation (FMD) In Brachial and Popliteal Arteries Of Humans.

PURPOSE: To compare the change in arterial diameter and shear rate in the upper and lower limbs following a 5 minute period of ischemia, and to examine the impact of ageing. METHODS: Twelve young healthy (Y: 6F/6M; 26±1yrs,VO2max: 51±3ml.kg-1.min-1), 12 fitness matched older trained (OT: 6F/6M; 57±1 yrs, 47±3ml.kg-1.min-1) and 12 older sedentary (OS: 6F/6M; 59±2yrs, 29±2ml.kg-1.min-1) subjects. Edge-detection and wall tracking of high resolution B-mode popliteal and brachial arterial ultrasound images, combined with synchronized Doppler waveform envelope analysis, was used to calculate conduit artery diameter, blood flow and shear rate continuously across the cardiac cycle. RESULTS: Brachial artery FMD was significantly higher in Y (7.8±3.2%) compared with OS (5.2±2.8%, P<0.05), but not OT (6.4±2.3%). Popliteal artery FMD was not different between groups (Y:7.6±2.2%,OS:6.6±4.0%,OT: 6.4±3.4%) and these values did not differ from those in the brachial artery. A significant difference existed in the brachial artery time-to-peak diameter between young (50±11 seconds) and both older groups (OT:80±21 seconds, P<0.001; OS:83±36 seconds, P<0.001), whereas no differences were evident in the popliteal artery (Y:103±34 seconds, OT:96±56 seconds, OS:96±40 seconds). However, popliteal artery time-to-peak diameter was significantly longer than that in the brachial artery in all groups (P=0.007). After correction for area-under- the-curve for shear rate, calculated to each individual's time to peak diameter, brachial FMD data revealed no differences between groups, whilst the popliteal artery exhibited an enhanced vascular responsiveness compared with the brachial artery. CONCLUSIONS: The impact of ageing and exercise on FMD characteristics were limb-dependent and, more importantly, influenced by the methods used to establish time-to-peak diameter and corrected FMD.

ROLE OF ENDOTHELIUM‐DERIVED HYPERPOLARIZING FACTOR IN THE REGULATION OF RADIAL ARTERY BASAL DIAMETER AND ENDOTHELIUM‐DEPENDENT DILATATION IN VIVO

1. The role of the balance between nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF), synthesized by cytochrome epoxygenase and acting through calcium-activated potassium channels, in the regulation of basal diameter and endothelium-dependent flow-mediated dilatation of conduit arteries has been poorly assessed in humans. 2. Radial artery diameter and flow (echotracking coupled to Doppler) were measured in healthy volunteers under basal conditions and during flow-mediated dilatation induced by hand skin heating, in the presence of saline and inhibitors of NO-synthase, N(G)-monomethyl-L-arginine (L-NMMA), calcium-activated potassium channels, tetraethylammonium (TEA) and cytochrome epoxygenases, fluconazole, infused alone and in combination. Mean wall shear stress, the flow-mediated dilatation stimulus, was calculated and taken as cofactor into statistical analysis. 3. Under basal conditions, the radial artery diameter was not affected by L-NMMA and fluconazole infused alone but was decreased by TEA, the combinations of L-NMMA + fluconazole and, to a greater extent, L-NMMA + TEA. During heating, radial artery diameter increased with temperature in all cases. This increase in diameter, compared with saline, was reduced by L-NMMA, TEA, fluconazole and to a greater extent, by L-NMMA + TEA and L-NMMA + fluconazole. 4. These data show that EDHF is involved in balance with NO in the regulation of basal diameter and endothelium-dependent dilatation of human peripheral conduit arteries. The alteration of this balance could play a major role in the physiopathology of the endothelial dysfunction, in particular during essential hypertension.

In vivo measurement of flow-mediated vasodilation in living rats using high-resolution ultrasound

In humans, endothelial vasodilator function serves as a surrogate marker for cardiovascular health and is measured as changes in conduit artery diameter after temporary ischemia [flow-mediated dilation (FMD)]. Here we present an FMD-related approach to study femoral artery (FA) vasodilation in anesthetized rats. Diameter and Doppler flow were monitored in the FA. Using high-resolution ultrasound (35 MHz) and automated analysis software, we detected dose-dependent vasodilation using established endothelium-independent [intravenous nitroglycerin EC(50) = 3.3 x 10(-6) mol/l, peak 21Delta% (SD 4)] and endothelium-dependent [intra-arterial acetylcholine EC(50) = 1.3 x 10(-6) mol/l, peak 27Delta% (SD 4)] pharmacological vasodilators. Wall shear stress induced by intra-aortic injection of adenosine and infusion of saline at increasing rates (1.5-4.5 ml/min) led to vasodilation at 1 to 2 min. Transient hindlimb ischemia by common iliac occlusion (5 min) led to reactive hyperemia with flow velocity and wall shear stress increase and was followed by FA dilation [16Delta% (SD 2)], the latter of which was completely abolished by nitric oxide synthase (NOS) inhibition with N(G)-monomethyl-L-arginine [1Delta% (SD 2)]. FMD was significantly reduced in adult 20-24-wk-old animals compared with 9- to 10-wk-old animals, consistent with age-dependent endothelial dysfunction [16Delta% (SD 3) vs. 10Delta% (SD 3), P < 0.05]. Whereas FMD was completely NOS dependent in 9- to 10-wk-old animals, NOS-dependent mechanisms accounted for only half of the FMD in 20-24-wk-old animals, with the remainder being blocked by charybdotoxin and apamin, suggesting a contribution of endothelium-derived hyperpolarizing factor. To our knowledge, this is the first integrative physiological model to reproducibly study FMD of conduit arteries in living rats.

Evidence for a basal release of a cytochrome-related endothelium-derived hyperpolarizing factor in the radial artery in humans

Whether a cytochrome P-450 (CYP)-related endothelium-derived hyperpolarizing factor (EDHF), acting through calcium-activated potassium (K(Ca)) channels, interacts with nitric oxide (NO) to regulate the basal diameter of human peripheral conduit arteries is unexplored in vivo. Radial artery diameter (echo tracking) and blood flow (Doppler) were measured, after oral aspirin (500 mg), in eight healthy volunteers during local infusion for 8 min of tetraethylammonium chloride (TEA; 9 micromol/min), as K(Ca) channel inhibitor, and fluconazole (0.4 micromol/min), as CYP inhibitor, alone and in combination with N(G)-monomethyl-L-arginine (L-NMMA; 8 micromol/min), as endothelial NO synthase inhibitor. Endothelium-independent dilatation was assessed by using sodium nitroprusside (SNP). Radial diameter was unaffected by L-NMMA (0.4 +/- 0.9%) and fluconazole (-1.6 +/- 0.8%) but was decreased by TEA (-5.0 +/- 1.0%), L-NMMA + fluconazole (-5.3 +/- 0.5%), and L-NMMA + TEA (-9.9 +/- 1.3%). These effects are still significant even when the concomitant decreases in blood flow induced by L-NMMA (-24 +/- 4%), TEA (-21 +/- 3%), L-NMMA + fluconazole (-26 +/- 5%), and L-NMMA + TEA (-35 +/- 4%) were taken as covariate into analysis. Conversely, fluconazole alone slightly but not significantly increased radial flow (13 +/- 6%). L-NMMA alone or with TEA and with fluconazole enhanced radial artery dilatation to SNP, whereas TEA and fluconazole alone did not modify this response. These results confirm in humans the involvement of NO and K(Ca) channels in the regulation of basal conduit artery diameter. Moreover, the synergistic effect of combined inhibition of NO synthesis and CYP on the decrease in radial diameter in the absence of such effect after L-NMMA and fluconazole alone unmasks the role of CYP in this regulation and shows the presence of an interaction between NO and a CYP-related EDHF to maintain peripheral conduit artery diameter in vivo. Furthermore, the higher vasoconstrictor effect of TEA compared with fluconazole suggests that different K(Ca) channel-dependent hyperpolarizing mechanisms could exist in conduit arteries.

Flow-mediated changes in pulse wave velocity: a new clinical measure of endothelial function

To test whether measuring hyperaemic changes in pulse wave velocity (PWV) could be used as a new method of assessing endothelial function for use in clinical practice. Flow-mediated changes in vascular tone may be used to assess endothelial function and may be induced by distal hyperaemia, while endothelium-mediated changes in vascular tone can influence PWV. These three known principles were combined to provide and test a novel method of measuring endothelial function by the acute effects of distal hyperaemia on upper and lower limb PWV (measured by a recently developed method). Flow-mediated changes in upper and lower limb PWV were compared in 17 healthy subjects and seven patients with stable chronic heart failure (CHF), as a condition where endothelial function is impaired but endothelium-independent dilator responses are retained. Corroborative measurements of PWV and brachial artery diameter responses to endothelium-dependent and -independent pharmacological stimuli were performed in a further eight healthy subjects. Flow-mediated reduction of PWV (by 14% with no change in blood pressure) was found in normal subjects but was almost abolished in patients with CHF. PWV responses appear to be inversely related to and relatively greater than brachial artery diameter responses. The method may offer potential advantages of practical use and sensitivity over conduit artery diameter responses to measure endothelial dysfunction.

Role of vascular calcium-activated potassium channels in the regulation of human peripheral conduit artery diameter

Role of vascular calcium-activated potassium channels in the regulation of human peripheral conduit artery diameter

Calcium-Activated Potassium Channels and NO Regulate Human Peripheral Conduit Artery Mechanics

The role of NO in the regulation of the mechanical properties of conduit arteries is controversial in humans, and the involvement of an endothelium-derived hyperpolarizing factor (EDHF), acting through calcium-activated potassium (KCa) channels, has never been investigated at this level in vivo. We assessed in healthy volunteers, after oral administration of aspirin (500 mg), the effect of local infusion of NG-monomethyl-L-arginine (L-NMMA; 8 mumol/min for 8 minutes), an NO synthase inhibitor, tetraethylammonium chloride (TEA; 9 mumol/min for 8 minutes), a KCa channels inhibitor, and the combination of both on radial artery internal diameter, wall thickness (echo tracking), blood flow (Doppler), and pressure. The incremental elastic modulus and compliance were fitted as functions of midwall stress. L-NMMA decreased modulus and increased compliance at high levels of midwall stress (all P<0.05) without affecting radial diameter. TEA reduced radial diameter from 2.68+/-0.07 to 2.50+/-0.08 10(-3) m, increased the modulus, and decreased the compliance at all levels of stress (all P<0.05). Combination of both inhibitors synergistically enhanced the increase in modulus, the decrease in diameter (from 2.71+/-0.10 to 2.42+/-0.09 10(-3) m), and compliance compared with TEA alone (all P<0.05). These results confirm that inhibition of NO synthesis is associated with a paradoxical isometric smooth muscle relaxation of the radial artery. They demonstrate the involvement of KCa channels in the regulation of the mechanical properties of peripheral conduit arteries, supporting a role for EDHF at this level in vivo. Moreover, the synergistic effect of l-NMMA and TEA shows that KCa channels compensate for the loss of NO synthesis to maintain peripheral conduit artery diameter and mechanics.

Measuring peripheral resistance and conduit arterial structure in humans using Doppler ultrasound

The purpose of this study was to establish valid indexes of conduit and resistance vessel structure in humans by using edge detection and wall tracking of high-resolution B-mode arterial ultrasound images, combined with synchronized Doppler waveform envelope analysis, to calculate conduit artery blood flow and diameter continuously across the cardiac cycle. Nine subjects aged 36.7 (9.2) yr underwent, on separate days, assessment of brachial artery blood flow and diameter response to 5-, 10-, and 15-min periods of forearm ischemia in the presence and absence of combined sublingual glyceryl trinitrate (GTN) administration. Two further sessions examined responses to ischemic exercise, one in combination with GTN. The peak brachial artery diameter was observed in response to the combination of ischemic exercise and GTN; a significant difference existed between resting brachial artery diameter and peak brachial artery diameter, indicating that resting diameter may be a poor measure of conduit vessel structure in vivo. Peak brachial artery flow was also observed in response to a combination of forearm ischemia exercise and GTN administration, the response being greater than that induced by periods of ischemia, GTN, or ischemic exercise alone. These data indicate that noninvasive indexes of conduit and resistance vessel structure can be simultaneously determined in vivo in response to a single, brief, stimulus and that caution should be applied in using resting arterial diameter as a surrogate measure of conduit artery structure in vivo.

運動時の筋血流量

The recent development of non-invasive ultrasound for studying blood flow has contributed to knowledge about changes in blood flow to exercising muscle. Using this method, the vessel diameter of conduit arteries, such as the femoral artery and brachial artery, was measured. The diameter of the brachial artery tncreased as handgrip exercise was prolonged, though no changes in diameter were observed in the femoral artery during knee extension exercise. Blood flow to the muscle was impeded mechanically by muscle contraction due to the increased intramuscular pressure even at low intensity (10% MVC). A greater reduction of muscle blood flow was demonstrated during the concentric phase, and it recovered toward the baseline during the eccentric phase. The effect of geometrical changes in muscle fibers on muscle circulation remained to be studied. The Doppler ultrasound method with good time resolution allowed us to investigate the time course of blood flow changes during exercise. The results of previous studies indicated a faster adaptation of muscle blood flow at the onset of exercise, followed by a steady state or gradual increase toward the end of exercise, depending on the exercise intensity. Redistribution of blood flow between active muscles has been an issue of interest; several studies indicated blood flow reduction during combined exercise and others did not. Further studies should be conducted focusing on the combination of the exercise intensity of individual muscle recruited during exercise. Muscle blood flow plays a key role in determining muscle endurance capacity. However, it is still unknown how high muscle blood flow increases during exercise. Accumulation of knowledge about exercise-induced maximal blood flow is needed in relation to training, exercise mode, exercise intensity, exercise frequency and contraction/relaxation schedule during the duty cycle.

Human femoral artery diameter in relation to knee extensor muscle mass, peak blood flow, and oxygen uptake.

It is not known whether the diameter of peripheral conduit arteries may impose a limitation on muscle blood flow and oxygen uptake at peak effort in humans, and it is not clear whether these arteries are dimensioned in relation to the tissue volume they supply or, rather, to the type and intensity of muscular activity. In this study, eight humans, with a peak pulmonary oxygen uptake of 3.90 +/- 0.31 (range 2.29-5.03) l/min during ergometer cycle exercise, performed one-legged dynamic knee extensor exercise up to peak effort at 68 +/- 7 W (range 55-100 W). Peak values for knee extensor blood flow (thermodilution) and oxygen uptake of 6.06 +/- 0.74 (range 4.75-9.52) l/min and 874 +/- 124 (range 590-1,521) ml/min, respectively, were achieved. Pulmonary oxygen uptake reached a peak of 1.72 +/- 0.19 (range 1.54-2.33) l/min. Diameters of common and profunda femoral arteries determined by ultrasound Doppler were 10.6 +/- 0.4 (range 8.2-12.7) and 6.0 +/- 0.4 (range 4.5-8.0) mm, respectively. Thigh and quadriceps muscle volume measured by computer tomography were 10.06 +/- 0.66 (range 6.18-10.95) and 2.36 +/- 0.19 (range 1.31-3.27) liters, respectively. The common femoral artery diameter, but not that of the profunda branch, correlated with the thigh volume and quadriceps muscle mass. There were no relationships between either of the diameters and the absolute or muscle mass-related resting and peak values of blood flow and oxygen uptake, peak pulmonary oxygen uptake, or peak power output during knee extensor exercise. However, common femoral artery diameter correlated to peak pulmonary oxygen uptake during ergometer cycle exercise. In conclusion, common and profunda femoral artery diameters are sufficient to ensure delivery to the quadriceps muscle. However, the common branch may impose a limitation during ergometer cycle exercise.

Biomechanical signals in the coronary artery triggering the metabolic processes during cardiac overload.

Peculiarities in structure and deformability of epicardial conduit coronary arteries are described. The thin wall of animal coronary artery contrasts the human coronary artery in which the remarkable wall thickness is due namely by the intima thickness. Deformation in length and diameter of conduit coronary arteries, due to the left and right ventricle volume increase, has been defined in non-beating canine heart. Ramus interventricularis anterior being firmly tethered to the myocardium undergoes about 3 times larger deformation than ramus circumflexus. In anaesthetized dogs a 30% increase in blood pressure, elicited by aortic constriction, induces an increase in diameter of coronary artery, in segment length, in blood flow and consequently in shear stress which represents a load for circumferentially running smooth muscle bundles, longitudinally running smooth muscle bundles, as well as for the endothelium. The above load lasting 4 h is already reflected by an increase in total RNA content and [14C] leucin incorporation in the left ventricle myocardium in the wall of ramus interventricularis anterior, not in ramus circumflexus. The findings fit completely with the different range of deformation of both the above coronary branches and indicates an increase in proteosynthesis not only in myocardium, but in ramus interventricularis anterior as well. An increase in ornithindecarboxylase activity in coronary wall leading to an increase in biogenic polyamines, is present in the case only, when blood pressure increase is induced by infusion of noradrenaline.

Vibration-induced inhibition of vascular smooth muscle contraction.

Vascular smooth muscle is known to be exposed to an oscillating strain under physiological and patho-physiological conditions as well as in different occupational and environmental situations. The effect of vibrations of smooth muscle seems to be largly unknown. In the present experiments on isolated preparations of the rat portal vein and the rabbit thoracic aorta, imposed sinusoidal changes in length were found to cause prompt reduction in active force, the extent of which was dependent on amplitude (1-10% of tissue length, peak to peak, i.e. approximately plus or minus 50-500 mum) and frequency of vibration (1-400 Hz) as well as on the prevailing level of active and passive forces. Vibration caused only small and inconsistant reductions of passive force of vascular smooth muscle. The results are in accordance with the hypothesis that vibrations exert a direct action on the contractile process by causing an increased rate of detachment of actin-myosin cross-links. It is suggested that, in vivo, vibrations may affect the diameter of conduit arteries locally in the case of turbulent blood flow as seen in post-stenotic dilation and arterio-venous anastomosis. Possibly, even the normal pulse pressure oscillations may sometimes tend to inhibit the smooth muscle activity in such arteries and thereby influence their diameters.