The physiological pattern of regional pulmonary blood flow is mainly determined by the relationship of pulmonary arterial, venous, and alveolar pressures [12, 32]. Changes in alveolar pressure and pulmonary geometry may therefore be expected to influence regional perfusion, which is a key determinant of pulmonary gas exchange. Unilateral thoracotomy is usually performed with the patient in the lateral decubitus position. The present study examined the influence of mechanical factors on regional pulmonary blood flow distribution in rabbits in the lateral decubitus position during normoxia and unilateral hypoxia. Methods. Anaesthetised white New Zealand rabbits (n=8) 2200-3900g (($) over bar x = 2860g) central venous injections of radioactive microspheres while in the left lateral decubitus position during spontaneous breathing (SB) and during mechanical ventilation (two-lung ventilation, 2LV), under closed (2LV(C)) and open chest (2LV(T)) conditions, as well as during unilateral hypoxia of the nondependent lung induced by nitrogen inflation (1LV(N)) or atelectasis (1LV(A)). The method used for one-lung ventilation (1LV) has been previously described in detail [13]. Arterial, central venous, and pulmonary arterial pressures were recorded continuously. Lungs were excised, dried in the inflated state, and cut into 16 sagittal slices, which were further divided into lobar components, the lower lobes into center and periphery. The radioactivity of each specimen was measured in a gamma-counter; perfusion of the individual tissue specimens was quantified using the software program MIC III [14]. The Friedman test followed by paired comparisons according to Conover [33] was used for statistical analysis of differences between the experimental phases. Perfusion of central and peripheral parts of isogravitational slices was compared by use of the Wilcoxon matched pairs test. Values are given as means +/- SE; the level of significance was P<0.05 unless otherwise indicated. Results and discussion. Haemodynamic parameters did not differ significantly between the experimental phases (Table 1). Compared to 2LV, a significant increase in venous admixture (P<0.05) and a corresponding decrease in PaO2 (P<0.01) were observed during 1LV. This effect was significantly more pronounced during 1LV(A) as compared to ILV(N) (P<0.01). Since inspiratory pressure was kept constant thoughout the experiments, moderate respiratory acidosis developed during both phases of 1LV. Regional perfusion (Q(r)) of the nondependent lung was slightly reduced during 2LV(C) compared to SE and 2LV(T). One-lung ventilation induced a significant decrease in perfusion of the hypoxic lung (P<0.001 1LV(N), 1LV(A) vs. SB,2LV(C),2LV(T)). In accordance with the data obtained from blood gas analysis and oximetry, this affect was more pronounced during N-2 insufflation than during atelectasis (P< 0.01 LV(N) vs. 1LV(A)). Among the factors that may account for this effect, Pa-CO2 did not differ significantly between both phases of 1LV. During N-2 insufflation PO2 at the hypoxia-sensitive site is lower than during atelectasis, where it equals mixed-versus PO2 (P ($) over bar v(o2)). The difference in local PO2 is unlikely, however, to have caused the changes in regional perfusion between 1LV(N) and 1LV(A), since P ($) over bar vO(2) was as low as 40 mmHg during 1LV(A) and the pulmonary vascular response to hypoxia has been found to reach its maximum in this PO2 range [2, 11], Enhanced redistribution of regional perfusion during 1LV(N) as compared to 1LV(A) is therefore most likely attributed to differences in alveolar pressure and pulmonary geometry. Apart from a radial perfusion gradient in the right lower lobe during 2LV(c) and 3-LV(T), no isogravitational Q(r) gradients were observed. Conclusion. We conclude that controlled mechanical ventilation in the lateral decubitus position causes only minor changes in vertical blood flow distribution. During 1LV inflation of the hypoxic lung by positive airway pressure enhances hypoxia-induced blood flow redistribution, thereby improving arterial oxygenation. Differences in alveolar pressure and lung geometry are the most important factors to account for this effect.
