Levofloxacin decreased chest wall mechanical inhomogeneities and airway and vascular remodeling in rats with induced hepatopulmonary syndrome.

The administration of antibiotics decreases bacterial translocation, reduces the activity of nitric oxide synthase and improves the gas exchange of hepatopulmonary syndrome (HPS) in rats. We hypothesized that levofloxacin could reduce HPS-induced respiratory mechanical inhomogeneities and airway and pulmonary vascular remodeling. We assessed the respiratory mechanical properties and lung tissue structure in 24 rats assigned to the control, HPS (eHPS) and HPS+levofloxacin (eHPS+L) groups. The administration of levofloxacin reduced the HPS-induced chest wall but not the lung mechanical inhomogeneities. The eHPS airway proportion of elastic fibers increased 20% but was similar between the control and eHPS+L groups. The eHPS vascular collagen increased 25% in eHPS but was similar between the control and eHPS+L groups. Compared to the control group, the vascular proportion of elastic fibers of the eHPS and eHPS+L groups increased by 60% and 16%, respectively. The administration of levofloxacin decreased the HPS-induced chest wall mechanical inhomogeneities and airway and vascular remodeling.

Stability of the animal model of oleic acid-induced acute lung injury.

OBJECTIVE: To evaluate the stability of hemodynamic, respiratory and gas exchange variables in an animal model of oleic acid-induced acute lung injury. METHODS: This was an experimental study involving 10 mongrel dogs. The variables were measured at baseline, as well as at 30, 60, 90 and 120 min after the administration of oleic acid. In order to analyze repeated measurements, linear and quadratic effects were tested. Mixed linear models with diversified variance and covariance structures were used, depending on the variable studied. RESULTS: We found that mean arterial blood pressure stabilized at 30 min, as did heart rate, pulmonary arterial pressure and pulmonary capillary pressure at 60 min. Respiratory rate, tidal volume, minute volume and respiratory work stabilized at 30 min. Regarding gas exchange variables, PaO2, PaO2/FiO2 ratio and pulmonary shunt fraction stabilized at 30 min. The remaining variables maintained a continuous rise or fall. CONCLUSIONS: This oleic acid-induced acute lung injury model is stable for some of the variables tested, although stabilization occurs at different times. The respiratory and gas exchange variables stabilized at 30 min, whereas the hemodynamic variables stabilized at 60 min.

Estabilidade do modelo animal de lesão pulmonar aguda induzida por ácido oleico / Stability of the animal model of oleic acid-induced acute lung injury

OBJETIVO: Avaliar a estabilidade das variáveis hemodinâmicas, da mecânica respiratória e de troca gasosa do modelo animal de lesão pulmonar aguda induzida por ácido oleico. MÉTODOS: Trata-se de um estudo experimental no qual foram utilizados 10 cães de raça indeterminada. As variáveis foram aferidas inicialmente e em 30, 60, 90 e 120 min após a administração do ácido oleico. Para analisar as medidas repetidas, foram testados efeitos lineares e quadráticos e foram utilizados ajustes de modelos lineares mistos com estruturas de variâncias e covariâncias diversificadas, dependendo da variável analisada. RESULTADOS: Observamos estabilidade da pressão arterial média aos 30 min, assim como da frequência cardíaca, da pressão arterial pulmonar e da pressão de capilar pulmonar aos 60 min. Frequência respiratória, volume corrente, volume minuto e trabalho respiratório estabilizaram aos 30 min. Quanto às variáveis de troca gasosa, PaO2, relação PaO2/FiO2 e fração de shunt pulmonar estabilizaram-se aos 30 min. As demais variáveis mantiveram-se em ascensão ou queda contínuas. CONCLUSÕES: O modelo de lesão pulmonar aguda induzida por ácido oleico é estável para algumas das variáveis testadas; porém, a estabilização se dá em momentos diferentes. As variáveis da mecânica respiratória e de troca gasosa estabilizaram em 30 min, e as hemodinâmicas, em 60 min.

OBJECTIVE: To evaluate the stability of hemodynamic, respiratory and gas exchange variables in an animal model of oleic acid-induced acute lung injury. METHODS: This was an experimental study involving 10 mongrel dogs. The variables were measured at baseline, as well as at 30, 60, 90 and 120 min after the administration of oleic acid. In order to analyze repeated measurements, linear and quadratic effects were tested. Mixed linear models with diversified variance and covariance structures were used, depending on the variable studied. RESULTS: We found that mean arterial blood pressure stabilized at 30 min, as did heart rate, pulmonary arterial pressure and pulmonary capillary pressure at 60 min. Respiratory rate, tidal volume, minute volume and respiratory work stabilized at 30 min. Regarding gas exchange variables, PaO2, PaO2/FiO2 ratio and pulmonary shunt fraction stabilized at 30 min. The remaining variables maintained a continuous rise or fall. CONCLUSIONS: This oleic acid-induced acute lung injury model is stable for some of the variables tested, although stabilization occurs at different times. The respiratory and gas exchange variables stabilized at 30 min, whereas the hemodynamic variables stabilized at 60 min.