Objective To observe the effects of penehyclidine hydrochloride ( PHCD) combined with mechanical ventilation ( MV) on inflammatory response in rats with ARDS induced by oleic acid ( OA) .Methods The rat ARDS model was established by OA via intravenous injection ( iv) . 32 adult healthy male SD rats were randomly divided into four groups, ie. a normal control group( group C: intra-peritoneal injection of a same amount of normal saline and intravenous injection of a same amount of normal saline respectively rather than PHCD) , a model group( group A1) , a PHCD group ( group A2: intra-peritoneal injection of 0. 5 mg/kg PHCD30 minutes before OA iv) and a PHCD+MV group ( group A3: VT = 4 mL/kg,respiratory rate =70 beats /min, I∶E =1∶2, FiO2 =21%) . Four hours after OA iv, arterial partial pressure of oxygen ( PaO2 ) was measured, and the oxygenation index ( PaO2 /FiO2 ) as well as wet /dry weight ratio( W/D) of lung tissue were calculated respectively. The pathological changes of lung tissue was observed through light microspcope. Interlukin-8 ( IL-8 ) , myeloperoxidase ( MPO) and NF-κB in lung tissue homogenate were measured by enzyme linked immunosorbent assay ( ELISA ) . Results Extensive pneumonedema, pneumorrhagia, focal atelectasis and amout of inflammatory cells infiltration in lung tissues were all revealed in ARDS rats. Lung injury score ( 8. 63 ±2. 20 vs. 1. 38 ±0. 92) , W/D ratio ( 8. 37 ±0. 99 vs. 4. 08 ±0. 65) were all higher in the ARDS rats than those in group C( all P lt;0. 01) . PaO2 /FiO2 was lower in group A1 than that in group C [ ( 206 ±32) mm Hg vs. ( 428 ±28) mm Hg, P lt; 0. 01] . The concentrations of MPO [ ( 33. 91 ±1. 43) ng/mL vs. ( 20. 92 ±1. 40) ng/mL) ] , IL-8 [ ( 809 ±39) ng/L vs. ( 583 ±91) ng/L] and NF-κB [ ( 1163 ±105) ng/L vs. ( 803 ±130) ng/L] in lung tissue homogenate were significantly increased in the ARDS rats than those in group C ( all P lt;0. 01) . Pathological changes of lung tissue ( including pneumonedema, pneumorrhagia, atelectasis and inflammatory cell infiltration, etc. )obviously improved when treated by PHCD or/and PHCD combined with MV ( all P lt;0. 05) . PaO2 /FiO2 in group A2 and A3 were both significantly increased when compared with group A1 ( both P lt; 0. 05) .Meanwhile,W/D ratio, lung injury score, and concentrations of MOP, IL-8 and NF-κB were sharply decreased in group A2 and A3 ( all P lt;0. 05) . The improvement in all above indices were more significant in group A3 than those in group A2, despite all those indices failed to meet the levels of normal rats ( all P lt; 0. 05) .Conclusion PHCD can inhibit the inflammatory response in ARDS rats induced by OA iv, through which it protect the lung tissue frominjury induced by OA. The protective role of PHCD plus MV is superior to that of PHCD only.
Objective To investigate the changes of interleukin-17 ( IL-17) and the effects of propofol in rats with acute lung injury ( ALI) . Methods ALI model was established by hydrochloric acid ( HCl) inhalation in a dose of 2 mL/kg. 35 adultmale SD rats were randomly divided into seven groups, ie.a control group, a HCl group, and five propofol groups ( T24b , T12b , T0 , T1a , T3a groups, respectively) . The T0 ,T24b and T12b groups were pretreated with intraperitoneal propofol injection 0, 24 and 12 hours respectively before HCl inhalation. The T1a and T3a groups were managed by intraperitoneal propofol injection 1 and 3 hours respectively after HCl inhalation. Immunohistochemistry was used to determine the expression of IL-17 in lung tissue. ELISA was adopted to detect the levels of IL-17 and IL-8 in lung tissue homogenate as well as in bronchoalveolar lavage fluid ( BALF) , meanwhile arterial partial pressure of oxygen ( PaO2 ) and myeloperoxidase ( MPO) were measured. Results Those rats in the HCl group appeared respiratory distress, cyanosis, pulmonary edema, and inflammatory cells infiltration in lung tissues after HCl inhalation.The IL-17 levels in lung tissue homogenate as well as in BALF were higher in the HCl group than those in the control group( all P lt; 0. 01) . IL-17 was mainly expressed in alveolar epithelial cells and mononuclear cells in the ALI rats and its expression level was higher than that in the control group. IL-17 concentration in lung tissue homogenate was both correlated with IL-8 concentration in lung tissue homogenate ( r=0. 98, P =0.003) and with the activity of MPO in lung tissue( r=0. 981, P =0. 003) in the HCl group. Mainwhile, a same significant correlation was found between IL-8 level in lung tissue homogenate and the MPO activity in the HCl group( r =0. 961, P =0. 009) . Propofol attenuated lung injury induced by HCl inhalation, especially in T24b group. The concentrations of IL-17 in lung tissue homogenate and in BALF were lower in T24b group when compared with the HCl group( P = 0. 011, P =0. 003, respectively) . Conclusions The expression of IL-17 increases in ALI rats. Pretreatment with propofol by 24 hours has obvious inhibiting effects on inflammatory reaction. Inhibiting IL-17 expression may be one of the mechanisms through which propofol inhibits the inflammatory reaction of ALI.