Simulation Study of Mechanism of Postflight Orthostatic Intolerance.

摘要

The aim of this study was to investigate the role played by the factors, such as altered vasoreactivity of resistance vessels in different body regions, and depressed cardiac contractility in the genesis of postflight cardiovascular dysfunction. The model we used is based on the model developed by Mechior et al. (1994) with modification by incorporating into the model, some more detailed sub-models to describe blood redistribution, cardiac contractility, local vascular tone changes, and baroreflex control mechanism. The simulated cardiovascular response to LBNP, HUT, and +Gz(low level) stresses have been shown to compare well with the relevant experimental data. Further computer simulation studies were performed to assess the contributions of each factor on cardiovascular dysfunction postflight. The simulation demonstrated that both the hypovolemia and depressed cardiac contractility elicit obvious changes in cardiovascular responses to orthostatic stress. Although an increase in vasoconstrictor responsiveness of brain vessels does not elicit significant changes for the main hemodynamic variables, the cerebral blood flow is decreased dramatically. However, if the vasoreactivity of brain vessels kept unchanged, the decrease in vascular tone of vessels in lower body does not cause significant changes in cerebral blood flow.