AN EXPERIMENTAL-MODEL FOR SIMULTANEOUS QUANTITATIVE-ANALYSIS OF PULMONARY MICROCIRCULATION AND MACROCIRCULATION DURING UNILATERAL HYPOXIA INVIVO

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 mum. 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 mum (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.