title: [The effect of mechanical ventilation, thoracotomy, and one-lung respiration on intrapulmonary perfusion distribution. An animal experimental study].
abstract: The physiological pattern of regional pulmonary blood flow is mainly determined by the relationship of pulmonary arterial, venous, and alveolar pressures. 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) weighing 2200-3900 g (mean = 2860 g) received 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 (2LVC) and open chest (2LVT) conditions, as well as during unilateral hypoxia of the nondependent lung induced by nitrogen inflation (1LVN) or atelectasis (1LVA). The method used for one-lung ventilation (1LV) has been previously described in detail. 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. The Friedman test followed by paired comparisons according to Conover 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 1LVA as compared to 1LVN (P < 0.01). Since inspiratory pressure was kept constant throughout the experiments, moderate respiratory acidosis developed during both phases of 1LV. Regional perfusion (Qr) of the nondependent lung was slightly reduced during 2LVC compared to SB and 2LVT. One-lung ventilation induced a significant decrease in perfusion of the hypoxic lung (P < 0.001 1LVN, 1LVA vs. SB,2LVC,2LVT). In accordance with the data obtained from blood gas analysis and oximetry, this effect was more pronounced during N2 insufflation than during atelectasis (P < 0.01 1LVN vs. 1LVA). Among the factors that may account for this effect, PaCO2 did not differ significantly between both phases of 1LV. During N2 insufflation PO2 at the hypoxia-sensitive site is lower than during atelectasis, where it equals mixed-versus PO2 (PvO2). The difference in local PO2 is unlikely, however, to have caused the changes in regional perfusion between 1LVN and 1LVA, since PvO2 was as low as 40 mmHg during 1LVA 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 1LVN as compared to 1LVA 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 2LVC and 2LVT, no isogravitational Qr gradients were observed. CONCLUSION. We conclude that controlled mechanical ventilation in the lateral decubitus position causes only minor changes in vertical blood flow distribution.
authors.affiliation: Institut für Anaesthesiologie, Ludwig-Maximilians-Universität München.
authors.forename: J
authors.initials: J
authors.lastname: Groh
authors.forename: G E
authors.initials: GE
authors.lastname: Kuhnle
authors.forename: L
authors.initials: L
authors.lastname: Ney
authors.forename: A
authors.initials: A
authors.lastname: Sckell
authors.forename: A E
authors.initials: AE
authors.lastname: Goetz
mesh_terms: D000818:Animals; D006439:Hemodynamics / Q000502:physiology; D000860:Hypoxia / Q000503:physiopathology; D008168:Lung / Q000033:anatomy & histology / Q000502:physiology; D011652:Pulmonary Circulation / Q000502:physiology*; D011817:Rabbits; D012121:Respiration, Artificial; D015656:Respiratory Mechanics / Q000502:physiology*; D013908:Thoracotomy