Wilcoxon Signed Rank Test was used to compare mechanical parameters between TLV and OLV PRE and between OLV PRE and OLV POST. In all instances the significance level was set at 5%. After stabilization of two-lung ventilation (TLV), V5P5 showed higher mechanical parameters (driving and viscoelastic pressures, and specific compliance) than V5P2 while V10P2 displayed greater driving pressure and
Csp than V5P2. Csp was higher in V5P5 and V10P2 than in V5P2 right after one-lung ventilation (OLV PRE) and at 1 h (OLV POST, Fig. 2). In the three groups OLV worsened all mechanical parameters in relation to TLV. Additionally, 1-h OLV (OLV POST, Fig. 2) deteriorated the mechanical parameters in relation to OLV selleck inhibitor PRE Vorinostat purchase in V5P2. With the exception of V5P5, end-expiratory lung volume (EELV) was lower in all groups compared to Non-Vent rats. EELV was higher in V5P5 than in V5P2. EELV did not differ between V5P2 and V10P2. The median EELV (1st to 3rd quartiles) measured in Non-Vent, V5P2, V5P5 and V10P2 groups amounted to 1.57 (1.25–1.73), 0.63 (0.53–0.72), 0.77 (0.68–0.93) and 0.65 (0.57–0.87) ml, respectively. The fractional area of alveolar collapse was higher in V5P2 than in Non-Vent, V5P5 and
V10P2 groups. V10P2 animals presented an inhomogeneous lung parenchyma characterized by a higher fraction area of the lung occupied by large-volume gas-exchanging air spaces than Non-Vent and V5P2 (Table 1). Total cell content was higher in V5P2 and V5P5, while the percentage of PMN was higher in V5P2 and V10P2 than in Non-Vent group. The amount of PMN cell was smaller in V5P5 than in V5P2 (Table 1). At the beginning of
the study all animals presented normal arterial oxygenation. The mean PaO2PaO2 (±SEM) of all groups was 94.0 ± 3.3 mmHg. At the end of 1-h ventilation with 5 ml/kg VT (V5P2) hypoxemia was established, which was avoided by 5 cm H2O PEEP (V5P5). High tidal volume (10 ml/kg) did not cause hypoxemia ( Table 1). PCIII ifenprodil mRNA expression was increased only when one-lung ventilation with high tidal volume (10 ml/kg, V10P2 group) was used (Fig. 4). In relation to low V T associated with physiological PEEP, OLV with higher PEEP or V T prevented deterioration of lung mechanics and alveolar collapse and maintained arterial blood gas oxygenation at the end of 1-h ventilation. We also demonstrated that in the face of normal PaO2PaO2 and stable Csp, high VT and physiological PEEP induced alveolar hyperinflation and expressed PCIII mRNA in lung homogenate. In order to analyze the effects of OLV, the animals underwent 1-h volume-controlled ventilation (VCV). Although pressure-controlled ventilation (PCV) allows a more homogeneous distribution of lung ventilation (Prella et al., 2002) and also reduces peak airway pressure (Unzueta et al.
Related posts: