RESUMO
Objective To evaluate the effect of the pulmonary stretch reflex on the lung injury in acute respiratory distress syndrome (ARDS). Method ARDS models of rabbits were induced by intratracheal infusion hydrochloric acid and ventilated with neurally adjusted ventilatory assist (NAVA) with a tidal volume ( VT) of 6 mL/kg and the electrical activity of diaphragm ( Eadi)-determined PEEP level. The rabbits were randomly ( random number) divided into two groups: ( 1 ) sham operation (Sham) group ( n = 5 ),(2) bilateral vagotom (VAG) group( n = 5 ). Gas exchange and pulmonary mechanics were determined at baseline, after lung injury and ventilation 1, 2, 3 h respectively. Indices about pulmonary permeability,pathological changes and inflammatory response were also measured. Results Compared with Sham group,the PaO2/FiO2in VAG group decreased significantly at ventilation 2 h, 3 h (P ＜0.05). There was no significant difference on PaCO2 between Sham and VAG group (P ＞ 0.05 ), and VAG group had the higher VT,peak pressure ( Ppeak), mean pressure (Pm) compared with Sham group at the time point of ventilation 1 h, 2 h, 3 h (P＜0.05). Compared with Sham group, the dead space fraction (VD/VT) and the respiratory system elastance (Ers) in VAG group increased (P ＜ 0.05 ) and the static pulmonary compliance (Cst)decreased markedly (P ＜ 0.05 ) after 3 h ventilation. The wet/dry weight (W/D), lung injury score, tumor necrosis factor-α ( TNF-α), interleukin-8 ( IL-8 ), myeloperoxidase ( M PO ) and malondialdehyde ( M DA )in VAG group elevated significantly when compared with Sham group ( P ＜ 0.05 ). Conclusions The lung injury in ARDS was aggravated after bilateral vagotomy, which demonstrated that the pulmonary stretch reflex may have the lung protective effect.
RESUMO
BACKGROUND: Pulmonary stretch reflex plays an important role in regulation of respiratory movement. This study aimed to evaluate the effect of pulmonary stretch reflex on lung injury in rabbits with acute respiratory distress syndrome (ARDS). METHODS: ARDS rabbits were given intratracheal infusion of hydrochloric acid and ventilated with neurally adjusted ventilatory assistance (NAVA) with a tidal volume (VT) of 6 mL/kg and the electrical activity of diaphragm (EAdi)-determined positive end expiratory pressure. After isolation of the bilateral vagusnerve trunk, the rabbits were randomized into two groups: sham operation (SHAM) group (n=5) and bilateral vagotomy (VAG) group (n=5). Gas exchange and respiratory mechanics were detected at baseline, after lung injury and 1, 2, and 3 hours after ventilation respectively. Pulmonary permeability index, pathological changes and inflammatory response were also measured. RESULTS: Compared with the SHAM group, PaO2/FiO2 in the VAG group decreased significantly 2 and 3 hours after ventilation (P<0.05). There was no significant difference in PaCO2 between the SHAM and VAG groups (P>0.05), and the VAG group had a high VT, peak pressure (Ppeak), and mean pressure (Pm) compared with the SHAM group 1, 2, 3 hours after ventilation (P<0.05). Compared to the SHAM group, dead space fraction (VD/VT) and respiratory system elastance (Ers) in the VAG group increased (P<0.05) and static pulmonary compliance (Cst) decreased markedly (P<0.05) after ventilation for 3 hours. Lung wet/dry weight ratio (W/D) (8.4±1.2 vs. 6.6±1.0), lung injury score (6.3±1.8 vs. 3.8±1.3), tumor necrosis factor-α (TNF-α) (779±372 pg/mL vs. 355±130 pg/mL) and interleukin-8 (IL-8) (169±21 pg/mL vs. 118±17 pg/mL) increased significantly in the VAG group compared with the SHAM group (P<0.05). CONCLUSION: Lung injury is aggravated after bilateral vagotomy, demonstrating that pulmonary stretch reflex may have protective effect on the lung.