Cardiovascular peripheral effector mechanism in postflight orthostatic intolerance: a simulation study.

Orthostatic intolerance (OI) following exposure to microgravity or head-down bed rest is frequently observed and is thought to be multifactorial origin. Although hypovolemia is considered as the primary cause of OI, the role played by other factors, such as the lowered vasoconstrictor responsiveness (VCR) of resistance vessels, the enhanced vasoconstriction response of cerebral vessels, and the depressed myocardial contractility need to be elucidated. It is difficult to assess experimentally how each of these changes would affect orthostatic tolerance and how these factors interact with each other. An alternative approach is to conduct simulation studies by use of mathematical models of cardiovascular system (CVS) capable of simulating the CVS response to orthostatic stress. This presentation describes the construction of the model used, and presents the preliminary simulation results illustrating the effects of varying individually the level of hypovolemia, VCR of the resistance vessels in lower limbs and abdominal viscera, VCR of the brain vessels or myocardial contractility on responses to orthostatic stress. The ultimate goal of our work was to integrate the new experimental findings and to simulate the complexity to get a thorough understanding of the mechanism of postflight cardiovascular dysfunction and orthostatic intolerance.