Objective To compare the effects of high frequency oscillatory ventilation (HFOV) and conventional mechanical ventilation (CMV) whith or without pulmonary surfactant(PS) supplement on water vapour inhalation injury.Methods New Zealand rabbits model of severe acute lung injury with acute respiratory failure caused by steam inhalation was established.Then the animals were treated by CMV，HFOV，CMV+PS or HFOV+PS，respectively while animals in control group did not ventilated and supplemented with PS.Femoral arterial blood samples were obtained at 1，2，3，4 h after treatment for blood gas analysis.4 h after treatment ,the lowest lobe of right lung was weighed for calculating wet-to-dry weight ratio (W/D).Four different parts including dependent areas and non-dependent areas of the middle lobe of right lung were excised for histological observation.Results (A) After ALI established PaO2 in the five groups decreased below 60mmHg (Plt;0.01) but intergroup differences were found.Meanwhile the change of PaCO2 showd no statistical significance(Pgt;0.05).(B) PaO2 in the four treatment groups had increased since one hour after treatmentand sustained at favorite levels during treatment period.PaO2 in the HFOV and HFOV+PS groups were higher than those in CMV and CMV+PS groups,respectively (Plt;0.01，Plt;0.05).PaO2 in the CMV+PS group at 2 h and HFOV+PS group at 2 h and 3 h were significantly higher than those in corresponding non-PS groups at the same timepoints (Plt;0.05).P（A-a）O2 in the HFOV and HFOV+PS groups were lower than those in CMV and CMV+PS groups (Plt;0.05).P（A-a）O2 in the two groups with PS at 2 h，3 h and 4 h t were statistically lower than those in the two corresponding groups without PS (Plt;0.05).The pH and PaCO2 as well as circulatory function in the four groups were not significantly different at different treatment timepoints (Pgt;0.05).(C) Lung W/D was not different between CMV and HFOV groups (Pgt;0.05)，or CMV+PS and HFOV+PS.But lung W/D in the two groups treated with PS showed statistically decrement than that in non-PS groups (Plt;0.05).(D) Histological injury score was lowest in HFOV+PS group and highest in CMV group.Conclusion HFOV combined with exogenous PS supplement can improve arterial oxygenation and alleviate pulmonary edema and injury，which may be a optimal method for the treatment of acute lung injury with acute respiratory failure caused by water vapour inhalation.
Objective To review the effects of pulmonary surfactant in adult patients with acute lung injury ( ALI) /acute respiratory distress syndrome ( ARDS) . Methods Randomized controlled trials ( RCTs) were recruited from PubMed ( 1966.1-2011.3) , ISI Web of Knowledge ( all the years) and Wanfang Database ( 1982-2011) . Related published data and attached references were hand searched. All the RCTs about pulmonary surfactant for the adult patients with ALI/ARDS were included, then a meta-analysis was performed. Results Eight eligible trials were enrolled. Pooled analysis showed that treatment with pulmonary surfactant was not associated with reduction in 28 or 30-day mortality compared with the control group [ OR 1.05, 95% CI ( 0.90, 1.22 ) , P = 0.55] , neither did subgroup analysis in the pneumoia/ aspiration, sepsis, and trauma/ surgery induced ALI/ARDS patients. Three RCTs showed the oxygenation was significantly improved in adult ALI/ARDS patients receiving pulmonary surfactant compared with the control group( Plt;0.05) . Shorter mechanical ventilation days was shown in the ALI/ARDS patients receiving pulmonary surfactant in one RCT(Plt;0.05) . Conclusions Meta-analysis showed pulmonary surfactant did not reduce the 28 or 30-day mortality of adult patients with ALI/ARDS, however, improved the oxygenation. Pulmonary surfactant can be considered a therapy in ALI/ARDS.
Objective To investigate the relationship of pulmonary surfactant protein D( SP-D) with chronic obstructive pulmonary disease ( COPD) by measuring SP-D level in serum and lung tissue of rats with COPD.Methods The rat COPD model was established by passive smoking as well as intratracheal instillation of lipopolysaccharide ( LPS) . Thirty male SD rats were randomly divided into a control group, a LPS group, and a COPD group( n =10 in each group) . The pathologic changes of lung tissue and airway were observed under light microscope by HE staining. Emphysema changes were evaluated by mean linear intercept ( MLI) of lung and mean alveolar number ( MAN) . The level of SP-D in serum was measured by enzymelinked immunosorbent assay ( ELISA) . The expression of SP-D in lung tissue was detected by Western-blot and immunohistochemistry.Results The MLI obviously increased, and MAN obviously decreased in the COPD group compared with the control group ( Plt;0.05) . There was no significant difference in the MLI and MAN between the LPS group and the control group ( Pgt;0.05) . The serum SP-D level was ( 49.59 ±2.81) ng/mL and ( 53.21±4.17) ng/mL in the LPS group and the COPD group, which was significantly higher than that in the control group [ ( 42.14±2.52) ng/mL] ( Plt;0.05) . The expression of SP-D in lung tissue was 0.56±0.01 and 0.63±0.01 in the LPS group and the COPD group, which was also obviously ber than that in the control group ( 0.39 ±0.01) ( Plt;0.05) .Meanwhile the SP-D levels in serumand lung tissue were higher in the COPD group than those in the LPS group ( Plt;0.05) . The levels of SP-D between serum and lung tissue were positively correlated in all three groups ( r=0.93, 0.94 and 0.93, respectively, Plt;0.01) .Conclusion Both the SP-D level in serum and in lung tissue increase significantly in COPD rats and correlate well each other, which suggests that SP-D may serve as a biomarker of COPD.
Objective To observe the effects of exogenous pulmonary surfactant (PS) on ventilation-induced lung injury (VILI) in rats, and to investigate its possible mechanisms. Methods A total of 40 Wistar rats were divided into 4 groups with randomized blocks method: control group, high tidal volume (HV) group, VILI group, and PS group, with 10 rats in each group. The control group was subjected to identical surgical procedure but was never ventilated. After 30 min of mechanical ventilation (MV) with Vt 45 ml/kg, the rats in HV group were killed immediately; rats in the VILI group were continually ventilated for up to 150 min with Vt 16 ml/kg; in the PS group, 100 mg/kg of PS administered intratracheally and with the same settings as VILI group. Mean artery pressure (MAP), blood gas analysis, lung wet to dry weight ratios (W/D), thorax-lung compliance, and cell counts in bronchoalveolar lavage fluid (BALF) were determined. Nuclear factor-κB(NF-κB) activity in lungs was measured by enzyme-linked immunosorbent assay (ELISA), interleukin-8(IL-8) in serum and BALF was determined by radioimmunoassay (RIA). Pathological examination of the lung was performed. Results Injurious ventilation significantly decreased MAP and PaO2/FiO2, but increased NF-κB activity and W/D. MAP and PaO2/FiO2 improved, but NF-κB activity, IL-8 in serum and BALF, and cell counts in BALF reduced significantly in PS group compared with those in VILI group. Histological studies showed reduced pulmonary edema and atelectasis in the PS group. Conclusion PS administered intratracheally can suppress the increased activity of NF-κB induced by VILI, exogenous PS can be used to treat VILI.
Objective To compare the changes between deep hypothermic circulatory arrest (DHCA) with deep hypothermic low flow (DHLF) cardiopulmonary bypass (CPB) on pulmonary surfactant (PS) activity in infants with congenital heart disease. Methods Twenty infants with ventricular septum defect and pulmonary hypertension were assigned to either DHCA group or DHLF group according to the CPB methods respectively. Measurements of saturated phosphatidylcholine /total phospholipids (SatPC /TPL), saturated phosphatidylcholine/ total protein (SatPC/TP) and static pulmonary compliance were performed before institution of CPB, 5 minutes after cessation of CPB and 2 hours. Results The length of ICU stay in DHLA group was significantly longer ( P lt;0 05) than that in DHCA group. SatPC/TPL, SatPC/TP and static pulmonary compliance in DHLF group were significantly lower compared with DHCA group ( P lt;0.01). Conclusion DHLF could lower the PS activity level significantly as compared with DHCA in infants with congenital heart disease.
Objective To evaluate the efficacy of pulmonary surfactant (PS) on severe acute respiratory distress syndrome (ARDS) in different age baby with congenital heart disease. Methods We divided 43 baby patients into two separate groups including a little baby group (12 patients with age less than 3 months) and an infants group (31 patients with age of 3 months to one year). Both groups of patients were treated with intratracheal PS at the same time. The clinical data were collected and analyzed. Results The little baby group had lower body weight. There was no statistical difference in the cardiopulmonary bypass (CPB) time, operation blocking time, mechanical ventilation time, ICU stay time between the two groups (P>0.05). Before treatment, arterial partial presurre of oxygen (PaO2), fractional oxygen concentration in inspire gas (FiO2), the ratio of arterial PO2 to the inspired oxygen fraction (P/F) and arterial-alveolar N2 difference or gradient (a/A) had no difference between the two groups (P>0.05). After treatment, PaO2 and P/F of both groups were significantly lower than before (P<0.05), and FiO2 and P/F were significantly higher than before (P<0.05). After 24 h of treatment, PaO2 and P/F of the little baby group was significantly higher than that of the infants group (P<0.05), and FiO2 and P/F were significantly lower than those of the infants group (P<0.05). Conclusion PS treating severe ARDS in little baby with congenital heart disease has better effect than infants.
ObjectiveTo investigate the effects of short-time hyperoxia ventilation on lung tissue and pulmonary surfactant proteins C and D (SP-C and SP-D) in rats.MethodsSixteen male Sprague-Dawley rats were randomly divided into two groups (n=8): hyperoxia group (FiO2=0.90), air group (FiO2=0.21). Tracheal intubations were administrated after anesthesia, and rats in two groups were exposed hyperoxia or air ventilation for 4 h. At the same time, carotid artery blood gas was analyzed after 2 h and 4 h of ventilation, then oxygenation index (OI) was calculated. Four hours later, the anterior lobe of right lung was taken to observe the pathological change and the injury level was scored. The middle lobe of right lung was prepared for making tissue homogenate, and the remaining part of the lung was used to measure the wet/dry weight (W/D) ratio. The bronchoalveolar lavage fluid (BALF) was prepared in left lung. The content of SP-C and SP-D were detected in lung tissue homogenate and BALF by ELISA.ResultsComparing with hyperoxia group, the arterial partial pressure of oxygen, lung histopathology score and lung W/D ratio in air group were significantly increased (P<0.05), but OI, the content of SP-C and SP-D in lung tissue homogenate and BALF were significantly decreased (P<0.05).ConclusionHyperoxia ventilation for 4 h in rats can cause lung injury histologically, and reduce the concentration of SP-C and SP-D apparently in the lungs.