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2007, Piran, Slovenia

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Invited presentation<br />

Gravitational Physiology<br />

EFFECTS OF GRAVITY ON VASCULAR WALL STIFFNESS<br />

Ola Eiken 1 , Igor B. Mekjavic 2 , Roger Kölegård 1<br />

1 Swedish Defence Research Agency, Berzelius väg 13, Karolinska Institutet, SE-171<br />

77 Stockholm, Sweden<br />

2 <strong>Slovenia</strong>, Institute of Josef Stefan, Ljubljana, <strong>Slovenia</strong><br />

Contact person: ola.eiken@ki.se<br />

INTRODUCTION<br />

In erect posture, gravitational pull causes great hydrostatic pressure differences in<br />

blood vessels oriented longitudinally in the body. It is commonly assumed that the<br />

stiffness of dependent blood vessels increases as a result of the long-term exposure to<br />

high transmural pressures that follows with ambulatory life in erect posture. It appears<br />

that this notion is primarily based on findings from cross-sectional studies showing<br />

that the vascular walls are thicker in leg veins than in arm veins. Until recently,<br />

information has, however, been scarce as regards the influence of hydrostatic pressure<br />

differences on the in vivo pressure-distension relationships of various vascular<br />

segments in humans. Accordingly, we addressed the following questions:<br />

Does the in vivo pressure-distension relationship of arteries, arterioles and veins<br />

differ between the leg and the arm?<br />

Will removal of the gravity-dependent pressure gradients that act along the vessels<br />

affect such pressure-distension relationships?<br />

Is it possible to increase vascular wall stiffness by repeatedly exposing the vessels to<br />

increased transmural pressure?<br />

If so, what mechanism might underlie such pressure habituation?<br />

METHODS<br />

Several series of experiments were performed in healthy male subjects. In all series,<br />

vascular pressure-distension relationships were determined by positioning the subject<br />

in a pressure chamber with an arm or a lower leg extended through a hole in the<br />

chamber door. Intravascular pressure in the arm/lower leg was increased by stepwise<br />

increasing chamber pressure to +180 mmHg and +240 mmHg, respectively.<br />

Diameters of blood vessels and arterial flow were measured using ultrasonographic<br />

techniques.<br />

Removal of gravity-dependent pressure gradients in blood vessels oriented<br />

longitudinally in the body was achieved by exposing the subjects to 5 weeks of<br />

sustained horizontal bedrest.<br />

A vascular pressure-habituation regimen was accomplished by use of the<br />

aforementioned pressure-chamber model. Subject’s arm vessels were exposed to<br />

moderately increased intravascular pressures (+ 65 to +105 mmHg) 3 x 40 min/week<br />

during a 5-week period.<br />

Mechanisms underlying local vascular pressure habituation/deconditioning was<br />

studied by determining changes in the intima-media thickness of the vessel walls in<br />

response to prolonged bedrest and pressure habituation. Furthermore, local release of<br />

several vasoactive substances, including endothelin-1 (ET-1) and angiotensin II was<br />

studied in response to increase transmural pressure.<br />

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