Only a small portion of available pulmonary gas exchange surface area is required to oxygenate blood completely during rest. However, when demands for oxygen become high, gas exchange capacity can be taxed. This challenge occurs in normal individuals during exercise or in diseased lungs at Test in which enough gas exchange units have been destroyed so that the flow load on the remaining normal units is very high. In both cases, the normally functioning gas exchange units must utilize all of their reserves to oxygenate blood effectively as flow increases. Understanding the mechanisms by which the normal pulmonary microcirculation responds to high flow, therefore, is physiologically important in both health and disease. Our working hypothesis is that there are three components of gas exchange reserve: (1) capillary recruitment which adds directly to surface area, (2) distension of capillaries which expands their cross sectional shape and permits more red cells to traverse the capillary bed per unit time, and (3) decreased capillary transit time which forces more red cells per unit time through the capillaries. Detailed information about these aspects of gas exchange reserve at the alveolar level are sparse, because of the technical difficulty in making direct measurements. During the last 25 years, we have developed the in vivo videomicroscopy techniques necessary for directly studying capillary recruitment, transit time, and distension. In this application we propose investigations of the mechanisms that control intra-alveolar capillary recruitment and transit times by applying our videomicroscopy technique not only to intact animals but also to an isolated, perfused lobe model in which flow and pressure are rigorously controlled and capillary pressures are measured exactly by the double occlusion technique. These preparations permit a wide range of novel experiments to investigate pulmonary capillary perfusion at the alveolar and capillary segmental level.
Our first aim i s to determine the factors that control pulmonary capillary recruitment in single alveolar walls by altering pressure and flow independently and observing the effect on: (a) the temporal stability of perfusion patterns, (b) the distribution of capillary segment opening pressures and resistances, and (c) the effects of microtheologic alterations by changing hematocrit, white blood cell count, and red cell deformability using fixed or sickled cells.
Our second aim i s to determine the interactive effects of vascular pressure and flow on the distribution f capillary transit times for red blood cells in single capillary nets. By independently altering pulmonary blood flow, transmural pressure, pressure waveform, and hematocrit, we can determine the effect of these variables on the distribution of transit times. These studies will provide important information on the transit of the fastest red cells, the ones most likely to leave the capillaries in a desaturated state during high flow, and on how recruitment and distension interact to keep transit times from becoming too short for complete red cell oxygenation.
| Baumgartner Jr, William A; Peterson, Amanda J; Presson Jr, Robert G et al. (2004) Blood flow switching among pulmonary capillaries is decreased during high hematocrit. J Appl Physiol 97:522-6 |
| Baumgartner Jr, William A; Jaryszak, Eric M; Peterson, Amanda J et al. (2003) Heterogeneous capillary recruitment among adjoining alveoli. J Appl Physiol 95:469-76 |
| Presson Jr, Robert G; Baumgartner Jr, William A; Peterson, Amanda J et al. (2002) Pulmonary capillaries are recruited during pulsatile flow. J Appl Physiol 92:1183-90 |
| Tanabe, N; Todoran, T M; Zenk, G M et al. (2000) Role of positive airway pressure on pulmonary acinar perfusion heterogeneity. J Appl Physiol 89:1943-8 |
| Jaryszak, E M; Baumgartner Jr, W A; Peterson, A J et al. (2000) Selected contribution: measuring the response time of pulmonary capillary recruitment to sudden flow changes. J Appl Physiol 89:1233-8 |
| Hanson, W L; Boggs, D F; Kay, J M et al. (2000) Pulmonary vascular response of the coati to chronic hypoxia. J Appl Physiol 88:981-6 |
| Wagner Jr, W W; Todoran, T M; Tanabe, N et al. (1999) Pulmonary capillary perfusion: intra-alveolar fractal patterns and interalveolar independence. J Appl Physiol 86:825-31 |
| Tanabe, N; Todoran, T M; Zenk, G M et al. (1998) Perfusion heterogeneity in the pulmonary acinus. J Appl Physiol 84:933-8 |
| Presson Jr, R G; Audi, S H; Hanger, C C et al. (1998) Anatomic distribution of pulmonary vascular compliance. J Appl Physiol 84:303-10 |
| Hillier, S C; Graham, J A; Hanger, C C et al. (1997) Hypoxic vasoconstriction in pulmonary arterioles and venules. J Appl Physiol 82:1084-90 |
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