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DOI 10.1152/ajpheart.00576.2008

Медицинская библиотека · American journal of physiology. Heart and circulatory physiology · 2008

Pressure-distension relationship in arteries and arterioles in response to 5 wk of horizontal bedrest.

Eiken Ola, Kölegård Roger, Mekjavic Igor B

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Аннотация

We hypothesized that exposure to prolonged recumbency (bedrest), and thus reductions of intravascular pressure gradients, increases pressure distension in arteries/arterioles in the legs. Ten subjects underwent 5 wk of horizontal bedrest. Pressure distension was investigated in arteries and arterioles before and after the bedrest, with the subject seated or supine in a hyperbaric chamber with either one arm or a lower leg protruding through a hole in the chamber door. Increased pressure in the vessels of the arm/leg was accomplished by increasing chamber pressure. Vessel diameter and flow were measured in the brachial and posterior tibial arteries using Doppler ultrasonography. Electrical tissue impedance was measured in the test limb. Bedrest increased (P < 0.01) pressure distension threefold in the tibial artery (from 8 +/- 7% to 24 +/- 11%) and by a third (P < 0.05) in the brachial artery (from 15 +/- 9% to 20 +/- 10%). The pressure-induced increase in tibial artery flow was more pronounced (P < 0.01) after (50 +/- 39 ml/min) than before (13 +/- 23 ml/min) bedrest, whereas the brachial artery flow response was unaffected by bedrest. The pressure-induced decrease in tissue impedance in the leg was more pronounced (P < 0.01) after (16 +/- 7%) than before (10 +/- 6%) bedrest, whereas bedrest did not affect the impedance response in the arm. Thus, withdrawal of the hydrostatic pressure gradients that act along the blood vessels in erect posture markedly increases pressure distension in dependent arteries and arterioles.

Для цитирования: Eiken Ola, Kölegård Roger, Mekjavic Igor B. Pressure-distension relationship in arteries and arterioles in response to 5 wk of horizontal bedrest.. American journal of physiology. Heart and circulatory physiology. 2008. DOI: 10.1152/ajpheart.00576.2008.

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