9 research outputs found

    EDRF coordinates the behaviour of vascular resistance vessels

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    Constriction of vascular smooth muscle in response to the stimulus of raised intravascular pressure—the myogenic response1,2— represents a positive feedback mechanism which, if unopposed, could theoretically lead to instability in the intact circulation3,4. Dilation in response to increased intraluminal flow would provide an opposing feedback mechanism which could confer overall stability4. Flow-dependent dilation in conduit vessels5–7 is mediated by endothelium-derived relaxing factor (EDRF)8–14, but the relationship between flow and EDRF activity has not been studied in resistance vessels in situ. We here demonstrate that EDRF can coordinate the aggregate hydrodynamic properties of an intact network. Under control conditions, EDRF maintains a fourth-power relationship between diameter and flow so that the pressure gradient in each vessel asymptotically approaches a constant value at high flow rates. Basal EDRF release may also maintain a similar spatial distribution of flow at different flow rates, even under conditions of moderate pharmacological constriction

    Mathematical methods for modeling the microcirculation

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    Alterations in the rheological artery during rhythmic thigh flow profile in conduit femoral muscle contractions in humans

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    The present study examined the rheological blood velocity profile in the conduit femoral artery during rhythmic muscle contractions at different muscle forces. Eight healthy volunteers performed one-legged, dynamic knee-extensor exercise at work rates of 5, 10, 20, 30, and 40 W at 60 contractions per minute. The time and space-averaged, amplitude-weighted mean ( V-mean) and maximum (V-max) blood flow velocities in the common femoral artery were measured during the cardiosystolic phase (CSP) and cardiodiastolic phase (CDP) by the Doppler ultrasound technique. The V-max /V-mean ratio was used as a flow profile index, in which a ratio of similar to 1 indicates a m m "flat velocity flow profile" and a ratio significantly > 1 indicates a "parabolic velocity flow profile ' " At rest, the V-max / V-mean ratio was similar to 1.3 and similar to 1.8 during the CSP and CDP, respectively. The V-max/V-mean ratio was higher (p < 0.01) during the CDP than during the CSP, both at rest and at all work rates. The V-max/V-mean ratio during the CSP was higher Max (p < 0.01) at 30 and 40 W compared to at rest. The V-max/V-mean ratio during the CDP was lower (p < 0.05) at 5 and 10 W compared to at rest. There was a positive linear correlation between blood flow and incremental work rates during both the CSP and CDP, respectively. Thus under resting conditions, the findings indicate a "steeper" parabolic velocity profile during the CDP than during the CSR The velocity profile during the CDP furthermore shifts to being less "steep" during rhythmic muscle contractions at lower intensities, but to being reelevated and normalized as at rest during higher intensities. The "steepness" of the parabolic velocity profile observed during the CSP at rest increased during muscle contraction at higher intensities. In conclusion, the blood velocity in the common femoral artery is parabolic both at rest and during exercise for both the CSP and CDP, indicating the persistence of laminar flow. The occurrence of any temporary slight disturbance or turbulence in the flow at the sight of measurement in the common femoral artery does consequently not induce a persisting "disturbed" and fully flat "plug-like" velocity profile. Instead, the "steepness" of the parabolic velocity profile is only slightly modified, whereby blood flow is not impaired. Thus the blood velocity profile, besides being influenced by the muscle contraction-relaxation induced mechanical "impedance," seems also to be modulated by the cardiac- and blood pressure-phases, consequently influencing the exercise blood flow response

    Functional Adaptation and Remodeling of Arteries to Hemodynamic Forces: Role of Reactive Oxygen Species and the Vascular Renin-Angiotensin System

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    Skeletal Muscle Circulation

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    Shock

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