Research in Experimental Medicine

, Volume 192, Issue 1, pp 431–441

An experimental model for simultaneous quantitative analysis of pulmonary micro- and macrocirculation during unilateral hypoxia in vivo

Authors

  • Joachim Groh
    • Institut für AnaesthesiologieLudwig-Maximilians-Universität, Klinikum Großhadern
  • Gerhard E. H. Kuhnle
    • Institut für Chirurgische ForschungLudwig-Maximilians-Universität, Klinikum Großhadern
  • Wolfgang M. Kuebler
    • Institut für Chirurgische ForschungLudwig-Maximilians-Universität, Klinikum Großhadern
  • Alwin E. Goetz
    • Institut für AnaesthesiologieLudwig-Maximilians-Universität, Klinikum Großhadern
Article

DOI: 10.1007/BF02576301

Cite this article as:
Groh, J., Kuhnle, G.E.H., Kuebler, W.M. et al. Res. Exp. Med. (1992) 192: 431. doi:10.1007/BF02576301

Summary

An experimental model was developed for quantitative analysis of pulmonary microcirculation using in vivo fluorescence videomicroscopy during unilateral hypoxia induced by one-lung ventilation (1 LV). In five white New Zealand rabbits, pulmonary arterioles on the surface of the right lung were visualized by means of intra-arterial injection of FITC-labeled erythrocytes and FITC-Dextran. During 1 LV of the left lung, the mean airway pressure in the right lung was kept at the level of two-lung ventilation (2 LV) by means of N2-CPAP. Arteriolar diameters as well as parameters of macrocirculation (AP, CVP, PAP, LAP, CO) and gas exchange (paO2, Qs/Qt) were measured simultaneously during 2 LV and 1 LV. FiO2 was kept constant at 1.0 during both experimental phases. Macrohemodynamic parameters during 1 LV did not differ from those measured during 2 LV. 1 LV induced a significant decrease in paO2 (213±105 versus 427±22 mm Hg,P<0.05) and a significant increase in Qs/Qt (22±7 versus 13±2%,P<0.05). During 2 LV (baseline), the pulmonary arteriolar diameters ranged from 15–120 μm. 1 LV resulted in a significant decrease of arteriolar diameters to 89.0±9.3% of baseline (P<0.05). Relative changes in arteriolar diameters were similar for vessels with baseline diameters of 0–40, 40–60, and 60–120 μm (88.4±9.9%, 89.6±9.4%, and 88.4±8.7%, respectively). The present model is the first one allowing in-vivo, investigation of HPV during 1 LV and 2 LV on the basis of simultaneous measurement of pulmonary arteriolar diameters and macrocirculatory parameters in vivo. Although PAP and PVR did not change significantly, a reduction, of pulmonary arteriolar diameters was proven in response to alveolar hypoxia during 1 LV. We suggest the model to be useful in studying the physiological effects of HPV on macro- and microcirculation as well as investigating pathophysiological and pharmacological influences on HPV.

Key words

Pulmonary circulationIntravital fluorescence microscopyHypoxic pulmonary vasoconstrictionOne-lung ventilationRabbit

Copyright information

© Springer-Verlag 1992