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Long term peripheral arterial and venous alteration in relation to weightlessness (cerebral, splanchnic and lower limb vascular vasomotricity)

Summary

Vascular wall properties and regulation (artery, and vein) are very likely to be impaired by weightlessness contributing to orthostatic intolerance after space flight. We will combine non invasive measurements of major peripheral arterial and vein flows and vessel wall, and autonomic nervous system activity, at rest inflight and during pre inflight and post flight stand/LBNP tests.

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WISE LBNP Art
WISE LBNP Vein 
STBR AG
Otolith Zero G

The main objective will be to evaluate non-invasively the cardiovascular and autonomic regulation changes in territories not deeply investigated yet [Distal peripheral arterial hemodynamics, vessel wall reactivity, central (splanchnic) and distal (leg) venous return] in order to quantify the alteration of the cardiovascular regulation (deconditioning) at these levels.

  • On the arterial side the efficiency of the neural regulation in distal territories will be quantified and compared with data extracted from ECG and Cardiac output and blood pressure.

  • Arterial and cardiopulmonary baro-reflex contributions to the patterns of blood flow distribution will be evaluated by ECG, blood pressure, and cardiac output processing. 

  • The splanchnic vessels vasomotricity and venous return will be measured through Portal vein investigation.

  • The deep and muscular leg vein wall distensibitlity and flow will be quantified.

  • Non-cardiovascular organs and systems (e.g: otolith, muscle proprioceptors, muscle tissue filtration) interfering with cardiovascular regulation will be considered.

Background

One of the most serious symptoms in relation with cardiovascular deconditioning is represented by a decrease in orthostatic tolerance, along with a significantly reduced capacity for exercise and an increase of heart rate. A large number of hypotheses have been forwarded and well reviewed (Pavy-Le Traon et al., 1999; Zhang, 2001). Many of those hypotheses are focussing on the alteration of the arterial, the microcirculation and the vein properties. Vascular impairment is likely to be an important factor of the cardiovascular deconditioning. This vascular alteration concerns large and distal arteries and veins and also tissue surrounding the vessels, and other non cardiovascular factors. 

In general the cerebral flow reduction is not significantly different between finishers and non finishers but the cumulated reduction of this flow over the duration of the test is higher than 8% in the non finishers and lower than 8% for the finishers. 

On the other hand previous short and long term bed rest (4d, 42 days) and spaceflight (15 days, 6 months) studies reported a lack of lower limb arterial vasoconstriction during lower body negative pressure (LBNP) and stand tests (Arbeille et al, 1995, 1998, 2008) with similar observations using pharmacological tests with human and animal models (Ma et al 1998; Purdy et al 1998; Sangha et al 2000, Piwinsky et al 1994, Vernikos et al 1991). Moreover the ratio of the cerebral to lower limb flow as measured by Doppler ultrasound, increases significantly (40% to 60%) in tolerant subjects or cosmonauts (Herault et al, 2000; Tobal et al, 2001) whereas it increases significantly less in non tolerant ones. Changes in this ratio are highly correlated to the existence of cardiovascular deconditioning preceding orthostatic intolerance as it becomes abnormal long before (several minutes) blood pressure drop and before the test has to be stopped. Also it recovers with appropriate counter measure against cardiovascular deconditioning (LBNP + exercise) (Arbeille et al 1995).

The cerebral/femoral flow ratio is the cardiovascular parameter that cumulates the effect of the various cardiovascular and non cardiovascular organs contributing to a reduction in brain blood supply leading to Orthostatic intolerance.

Thus our main objective is to identify and quantify those parameters like peripheral arteries, veins (Belin et al 2004), otoliths (Herault et al 2002), muscle... that could contribute to impair the cardiac output redistribution towards the brain, and validate them as early predictors of cardiovascular deconditioning inflight or postflight.