| In this study, we explored whether conventional mechanical ventilation under pneumoperitoneum resulted in lung injury of rats and declared protective effects on pulmonary function of lower tidal volume combined with permissive hypercapnia in ventilation with pneumoperitoneum.1 Conventional mechanical ventilation induced lung injury under pneumoperitoneum in ratsMethods 30 Wistar rats were involved in this experiment.After anesthetized with an intraperitoneal injection of 2% phenobarbital (40 mg/kg), an endotracheal tube was inserted via a tracheostomy. The femoral artery was cannulated with a catheter to monitor systemic arterial pressure and collect blood, when the venous catheter was used for continuous infusion of 0.9% saline (10 ml/kg/h). Mechanical ventilation was initiated using a infant ventilator with tidal volume (VT) of 12 ml/kg, fresh gas flw rate of 2.0 L/min, (FIO2) of 0.50. The rate was adjusted to obtain a PaCO2 in the target range (35-45 mmHg). These rats were assigned into 3 groups(n=10) randomly:Group A, rats had no mechanical ventilation; The control group(group C), ventilated with VT of 12 mL/kg for 4h;The experimental group(group P), (pneumoperitoneum pressure of 12 mmHg) rats were ventilated with VT of 12 mL/kg for 4h and subjected to pneumoperitoneum (pneumoperitoneum pressure of 15 mmHg)for 4h. After 4 h ventilation the animals were sacrified by exsanguinations. Arterial blood gases were measured at every one hour. Specimens of lung tissues were harvested. Lung pathological changes were observed with optical microscope,and lung wet/dry weight ratio was measured. Bronchoalveolar lavage fluid was collected and TNF-a, IL-6 and IL-8 in it were measured.Results No substantial changes in morphology of group A were observed. Lung volume increased slightly in group C, but the appearance is normal. But in experimental group, the alveolar congestion, hemorrhage, infiltration of neutrophils in airspace, vessel wall and the thickness of alveolar wall were observed; the interstitial pulmonary edema and pneumorrhagia were observed, too. The W/D ratio in experimental group was significantly higher compared with the group A and the group C.The expression of TNF-a, IL-6 and IL-8 in group A and group C was no significant change (P>0.05), but those in group P were higher than group A and group C(P<0.05).Conclusion The study results suggest that when the pneumoperitoneum pressure was 15 mmHg, conventional mechanical ventilation can result in lung injury.2 The relationship between conventional mechanical ventilation induced lung injury under pneumoperitoneum and TLR4-TRIF-Inflammatory factor pathway.Methods Rats were treated the same as the first portion, and then divided into 3 groups. Control group(groupC):rats were ventilated with VT of 12 mL/kg and adjusted RR to maintain ETCO2 35-45 mmHg;The experimental group(group P):were ventilated with 12 mL/kg tidal volume and subjected to pneumoperitoneum for 4h; TLR4 blocker+ pneumoperitoneum mechanical ventilation group(group B):the rats were injected TLR4 blocker (TAK242,0.3mg/kg), and then ventilated with 12 mL/kg tidal volume and subjected to pneumoperitoneum for 4h. All rats were adjusted RR to maintain ETCO2 35-45 mmHg.Results BALF concentrations of TNF-a, IL-6, IL-8 in group P and group B were significant higher than groupC (P<0.05), and these cytokines in group B were lower than group P(P<0.05). The expression of TLR4 mRNA in group P and group B were significantly higher than group C (P>0.05), but it in group B was lower than group P (P＜0.05). The expression of TRIF protein showed a same tendency. Lung volume increased slightly in group P, the alveolar congestion, hemorrhage, infiltration of neutrophils in airspace, vessel wall and the thickness of alveolar wall were observed; the interstitial pulmonary edema and pneumorrhagia were observed, too. In group B, these changes were less than group P.Conclusion TLR4-TRIF-inflammatory factor pathway was closely related to conventional mechanical ventilation induced lung injury under pneumoperitoneum.3 The realationship between oxidative stress and lung injury induced by conventional mechanical ventilation under pneumoperitoneum.Methods Rats were treated the same as the first portion, and then divided into 3 groups. Control group(groupC):rats were ventilated with VT of 12 mL/kg and adjusted RR to maintain ETCO2 35-45 mmHg;The experimental group(group P):were ventilated with 12 mL/kg tidal volume and subjected to pneumoperitoneum for 4h; TLR4 blocker+ pneumoperitoneum mechanical ventilation group(group B):the rats were injected TLR4 blocker (TAK242, 0.3mg/kg), and then ventilated with 12 mL/kg tidal volume and subjected to pneumoperitoneum for 4h. All rats were adjusted RR to maintain ETCO235-45 mmHg.Results MPO and MDA levels in group P and group B was significantly higher than group C (P<0.05), but these in group B were lower than group P (P＜0.05). SOD levels showed an opposite tendency(P<0.05). The expression of iNOS and TLR4 mRNA in group P and group B was significantly higher than group C (P>0.05), but these in group B were lower than group P (P＜0.05).Conclusion These results suggest that conventional mechanical ventilation induced lung injury under pneumoperitoneum was related to oxidative stress.4 The influence of lower tidal volume with permissive hypercapnia on lung injury induced by mechanical ventilation under pneumoperitoneum.Methods Rats were treated the same as the first portion, and randomly divided into 3 groups. Group A:rats were ventilated with VT of 12 mL/kg and adjusted RR to maintain ETCO2 35-45 mmHg; The control group(group C):Rats were ventilated to establishment of pneumoperitoneum (pneumoperitoneum pressure was 15 mmHg), then with 12 mL/kg tidal volume and subjected to pneumoperitoneum for 4h, and adjusted RR to maintain ETCO2 35-45 mmHg;The experimental group (group L): Rats were ventilated to establishment of pneumoperitoneum (pneumoperitoneum pressure was 15 mmHg), and then with 6 mL/kg tidal volume and subjected to pneumoperitoneum for 4h，adjusted RR to maintain ETCO26O mmHg.Results BALF concentrations of TNF-a, IL-6, IL-8 in group C and group L were significant higher than group A (P＜0.05), and these cytokines in group L were lower than group C(P＜0.05). The expression of TLR4 mRNA in group C and group L were significantly higher than group A (P>0.05), but it in group L was lower than group C (P＜0.05). The expression of TRIF protein showed a same tendency. MPO and MDA levels in group C and group L was significantly higher than group A (P＜0.05), but these in group L were lower than group C (P＜0.05). SOD levels showed an opposite tendency(P＜0.05).Conclision Lower tidal volume with permissive hypercapnia ameliorated lung injury induced by mechanical ventilation under pneumoperitoneum.In conclusion, conventional mechanical ventilation under pneumoperitoneum may induce lung injury in rats and the lung injury was not only related to TLR4-TRIF-Inflammatory factor pathway, but also oxidative stress reaction. Lower tidal volume combined with permissive hypercapnia can ameliorate lung injury induced by mechanical ventilation under pneumoperitoneum. |
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