Effect of recruitment maneuver and tidal volume at post recruitment maneuver on endothelium-dependent relaxation of pulmonary arteries rings in rats with acute lung injury
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ZHONG-DA Hospital, Southeast Unibersity
Objective We sought to evaluate pulmonary arterial vasomotor functionmechanism at post recruitment maneuver with different tidal volume ventilation in rats with acute lung injury model., local inflammatory reaction and discuss the
Background Pulmonary hypertension is a clinical feature of ALI/ARDS, and it is an independent risk factor of mortality for ALI/ARDS. Pulmonary arteries vasomotor disfunction is a mainly key inducing pulmonary hypertension, and it is caused by impairing the function of pulmonary arterial endothelium in ALI patients. Recruitment maneuver (RM) could recruit collapsing alveoli, and regain functional residual volume, so RM could decrease pulmonary arteries pressure. Low tidal volume ventilation had been shown to ameliorate the prognosis of ALI/ARDS patients. However, effect of recruitment maneuver and tidal volume at post recruitment maneuver ventilation on the pulmonary arterial vasomotor function is unknown.
Methods The ALI rat model was induced by intravenous infusion lipopolysaccharide (6mg/kg). Thirty-six rats were randomly divided into (1) control group; (2) ALI group; (3) low tidal volume (VT) group (LV group, VT 6ml/kg); (4) sustained inflation (SI) with low VT group (SI+LV group, VT 6ml/kg); (5) SI with moderate VT group(SI+MV group, VT 12ml/kg); (6) SI with very low VT group(SI+VLV group, VT 3ml/kg). RM was carried out by SI, airway pressure 30cmH2O for 30s, positive end-expiratory pressure (PEEP) was set to 5cmH2O. Mean arterial blood pressure(MAP) was monitored during the experiment process. Endothelin-1 (ET-1), endothelial nitricoxide synthase(eNOS), Ach-induced endothelium-dependent relaxation response of isolated pulmonary artery rings were investigated at 5h. Lung tissue was extracted after 5h mechanical ventilation, and inflammatory response at the overlapped region was assessed by histopathology. Endothelial-dependent vasomotor function was measured by tensiometry.
Results We demonstrated that LPS could increase ET-1 level in lung tissue, decrease the expression of eNOS in lung tissue, impair the Ach-induced endothelium-dependent relaxation response in pulmonary vascular. Compared with the other groups, SI+LV significantly reduced LPS-induced elevation of ET-1 level and increased the expression of eNOS and significantly improve endothelial dysfunction and ameliorate dysfunction of endothelium-dependent relaxation in pulmonary vascular.
Conclusions RM with low VT could decrease the lung vascular endothelial function injury and inflammation, and low VT at post-RM could protect the lung vascular endothelial diastole function from injury.
Methods The ALI rat model was induced by intravenous infusion lipopolysaccharide (6mg/kg). Thirty-six rats were randomly divided into (1) control group; (2) ALI group; (3) low tidal volume (VT) group (LV group, VT 6ml/kg); (4) sustained inflation (SI) with low VT group (SI+LV group, VT 6ml/kg); (5) SI with moderate VT group(SI+MV group, VT 12ml/kg); (6) SI with very low VT group(SI+VLV group, VT 3ml/kg). RM was carried out by SI, airway pressure 30cmH2O for 30s, positive end-expiratory pressure (PEEP) was set to 5cmH2O. Mean arterial blood pressure(MAP) was monitored during the experiment process. Endothelin-1 (ET-1), endothelial nitricoxide synthase(eNOS), Ach-induced endothelium-dependent relaxation response of isolated pulmonary artery rings were investigated at 5h. Lung tissue was extracted after 5h mechanical ventilation, and inflammatory response at the overlapped region was assessed by histopathology. Endothelial-dependent vasomotor function was measured by tensiometry.
Results We demonstrated that LPS could increase ET-1 level in lung tissue, decrease the expression of eNOS in lung tissue, impair the Ach-induced endothelium-dependent relaxation response in pulmonary vascular. Compared with the other groups, SI+LV significantly reduced LPS-induced elevation of ET-1 level and increased the expression of eNOS and significantly improve endothelial dysfunction and ameliorate dysfunction of endothelium-dependent relaxation in pulmonary vascular.
Conclusions RM with low VT could decrease the lung vascular endothelial function injury and inflammation, and low VT at post-RM could protect the lung vascular endothelial diastole function from injury.
