The objectives of this project will be to: 1. Determine how active vasomotion and passive mechanical factors interact to determine the longitudinal distribution of pulmonary vascular resistance and compliance. We will be particularly concerned with the influence of vascular transmural pressures and the interdependence between the vessels and lung parenchyma on pulmonary hemodynamics in normal lungs and those in which vasoconstriction is induced by hypoxia, sympathetic nerve stimulation and vasoactive drugs. 2. Determine the effect of the size of the obstructed vessels on the pulmonary hemodynamic response to pulmonary embolism. The influence of embolus size on purely mechanical and on reflex and/or humorally mediated responses will be examined using multiple indicator dilution, vascular occlusion and low viscosity bolus techniques to determine the changes in pulmonary hemodynamics and the size of the perfused microvascular bed. 3. Continue to develop and improve mathematical models which we use to extract information about pulmonary hemodynamics from vascular occlusion and low viscosity bolus data. The experiments will be carried out using dog lung lobes which are either isolated from the dog, allowing for control over a number of experimental variables, or pump perfused in situ, allowing for reflex and humoral effects to be revealed. The results of the studies will provide a more detailed description of normal pulmonary hemodynamics and microvascular function, and they will reveal how active pulmonary vasoconstriction and passive mechanical obstruction interact to determine the overall hemodynamic response to emboli of different sizes. In addition, the modeling effort should help us to learn as much as possible from simple perturbations of the vascular bed, both to increase our knowledge of pulmonary hemodynamics and to provide tools for further investigation.
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