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      Evaluation of the Time Course of Vascular Responses to Venous Congestion in the Human Lower Limb


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          This study examined the time course of changes in blood flow to the lower leg in response to venous distension – the veni-arteriolar vasoconstrictor response – in 31 healthy males. During a 5-min period of venous distension (thigh cuff pressure 50 mm Hg), calf blood flow (venous occlusion plethysmography) decreased more rapidly (within 30 s) compared to skin perfusion (after 2 min, Laser Doppler flowmetry), consistent with disparate filling times of superficial and deeper veins and a greater increase in deep vein volume. On completion of venous filling, vascular resistance in the skin was unchanged from baseline, implying that the reduction in perfusion was solely the result of reduced perfusion pressure. For the whole calf, vascular resistance was unchanged after 1 min but decreased thereafter by 35–45% from baseline, indicating adjustment of pre- or post-capillary resistances to maintain flow. Repeated plethysmographic flow measurements assisted the decrease in resistance, most likely by intermittent compression of the thigh cuff acting to displace blood volume centrally and alleviate congestion. These findings do not support an active veni-arteriolar vasoconstrictor mechanism in response to venous distension alone in the lower leg, and provide evidence of dynamic flow adjustments that should be acknowledged during procedures that involve prolonged periods of venous congestion.

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          Most cited references 13

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          Local reflex in microcirculation in human skeletal muscle.

          The effect of venous stasis of 40 mmHg upon blood flow in human skeletal muscle was studied in four normal subjects and in two chronically sympathectomized patients. Blood flow in skeletal muscle was measured by the local 133Xenon washout technique. Blood flow decreased about 30 per cent during venous stasis of 40 mmHg. In a "passive vascular bed" induced by means of histamine, blood flow decreased only by 16 per cent, indicating that the decrease in blood flow is due to a vasoconstrictor response to increase in vascular transmural pressure. The vasoconstrictor response was unaffected by a spinal sympathetic blockade, but was blocked in areas infiltrated with lidocaine or with phentolamine. The vasoconstrictor response was present in the nonoperated limbs used as a control, but abolished in the denervated arms in the two chronically sympathectomized patients. The findings strongly suggest that the vasoconstrictor response in skeletal muscle is due to a local nervous mechanism involving adrenergic fibres. Thus a local reflex mechanism, most likely a sympathetic axon reflex, seems to be present in human skeletal muscle as in cutaneous and subcutaneous tissue. This indicates that about 45 per cent of the change in total vascular conductance, when a person changes from supine to upright position, is due to this local reflex mechanism operating independently of the central nervous system.
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            Local reflex in microcirculation in human subcutaneous tissue.

            The effect of changes in transmural pressure in the vessles of the extremities on blood flow in subcutaneous adipose tissue were investigated in three healthy subjects. Changes in transmural pressure were obtained either by postural changes of a limb, by locally induced subatmospheric pressure, or be venous stasis. Blood flow in subcutaneous tissue was measured 10 cm distal to the fibular head and at the lateral malleolus in the leg, or in the distal part of the forearm by the local 133Xenon washout technique. When transmural pressure increased 25 mmHg or more, blood flow decreased about 50 per cent due to an increase in vascular resconstrictor response to increase in transmural pressure could be blocked by infiltrating the area under study with phentolamine or lidocaine or by induced counterpressure. In these cases blood flow remained constant. The findings indicate that the vasoconstrictor response to increase in transmural pressure of 25 mmHg or more is due to a local nervous mechanism involving adrenergic nerves. The receptors are presumably stretch receptors placed in the small veins. The effector site is probably the arterioles. When the vasoconstrictor response is blocked, autoregulation of blood flow in subcutaneous tissue, i.e. maintenance of constant blood flow during changes in perfusion pressure head or during changes in transmural pressure, is revealed. The vasoconstrictor response to increase in transmural pressure will counteract an increase in transmural pressure in the exchange vessles and thereby act as an edema protecting factor.
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              Assessment of venous capacitance. Radionuclide plethysmography: methodology and research applications.


                Author and article information

                J Vasc Res
                Journal of Vascular Research
                S. Karger AG
                February 2006
                16 February 2006
                : 43
                : 2
                : 166-174
                School of Sport and Exercise Sciences, University of Birmingham, Birmingham, UK
                90946 J Vasc Res 2006;43:166–174
                © 2006 S. Karger AG, Basel

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                Page count
                Figures: 5, Tables: 1, References: 35, Pages: 9
                Research Paper


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