国际麻醉学与复苏杂志
國際痳醉學與複囌雜誌
국제마취학여복소잡지
INTERNATIONAL JOURNAL OF ANESTHESIOLOGY AND RESUSCITATION
2012年
12期
807-810,844
,共5页
宋秀梅%王慎会%商丽梅%王月兰
宋秀梅%王慎會%商麗梅%王月蘭
송수매%왕신회%상려매%왕월란
机械通气诱发肺损伤%肺表面活性物质%基因表达%丝裂原活化蛋白激酶
機械通氣誘髮肺損傷%肺錶麵活性物質%基因錶達%絲裂原活化蛋白激酶
궤계통기유발폐손상%폐표면활성물질%기인표체%사렬원활화단백격매
Ventilation induced lung injury%Pulmonary surfactant%Genes expression%Mitogen-activated protein kinases
目的 丝裂原活化蛋白激酶(mitogen-activated protein kinases,MAPK)在机械通气过程中对肺表面活性物质及特异蛋白基因表达的影响和可能机制. 方法 采用健康成年雄性Sprague-Dawley大鼠48只,体重250 g～320 g.采用3％戊巴比妥35 mg/kg～40 mg/kg腹腔注射麻醉后行气管切开置管术,完全随机分组方法分为6组(每组8只):①C组(对照组,麻醉后仅做气管切开不做机械通气)；②LV组[正常通气组,潮气量(Vt):6ml/kg,余同过度通气组]；③HV组[过度通气组,Vt:40 ml/kg,呼吸频率(RR)40次/min,吸呼比(I∶E)1∶2～1∶3,呼气末正压通气(PEEP) =0,吸入氧浓度(FiO2)21％,通气4 h]；④SP600125组(SP600125+ HV组,高潮气量通气前30 min给予MAPK拮抗剂SP600125)；⑤PD98059组(PD98059+ HV组,高潮气量通气前30 min给予MAPK拮抗剂PD98059)；⑥SB203580组(SB203580+ HV组,高潮气量通气前30 min给予MAPK拮抗剂SB203580).机械通气4h后(对照组气管切开后4h),采用RT-PCR方法测定肺表面活性蛋白(SP)-A、B、C和RTI40 mRNA表达量. 结果 ①与C组比较,LV组、HV组大鼠肺组织中RTI40表达均增加(P＜0.05),而HV组、SP600125 +HV组及SB203580+HV组肺组织中SP-A、SP-C表达均减少(P＜0.05),LV组中和PD98059+HV组中的SP-A、C变化均无统计学意义(P＞0.05)；②与HV组比较,SP600125+HV组、PD98059+HV组、SB203580+HV组肺组织中SP-A、C基因表达增加(P＜0.05),RTI40基因表达降低(P＜0.05)；③SP-A、C基因表达量在PD98059+HV组较SP600125+HV组、SB203580+HV组升高(P＜0.05)；④SP-B在各组中变化无统计学意义(P＞0.05). 结论 高潮气量机械通气致肺上皮细胞特异蛋白SP-A、C基因表达下降和RTI40基因表达上调,而MAPK拮抗剂可以防止该现象发生,提示MAPK影响呼吸机相关性肺损伤(ventilator-induced lung injury,VILI)过程中对肺上皮细胞的分泌功能.
目的 絲裂原活化蛋白激酶(mitogen-activated protein kinases,MAPK)在機械通氣過程中對肺錶麵活性物質及特異蛋白基因錶達的影響和可能機製. 方法 採用健康成年雄性Sprague-Dawley大鼠48隻,體重250 g～320 g.採用3％戊巴比妥35 mg/kg～40 mg/kg腹腔註射痳醉後行氣管切開置管術,完全隨機分組方法分為6組(每組8隻):①C組(對照組,痳醉後僅做氣管切開不做機械通氣)；②LV組[正常通氣組,潮氣量(Vt):6ml/kg,餘同過度通氣組]；③HV組[過度通氣組,Vt:40 ml/kg,呼吸頻率(RR)40次/min,吸呼比(I∶E)1∶2～1∶3,呼氣末正壓通氣(PEEP) =0,吸入氧濃度(FiO2)21％,通氣4 h]；④SP600125組(SP600125+ HV組,高潮氣量通氣前30 min給予MAPK拮抗劑SP600125)；⑤PD98059組(PD98059+ HV組,高潮氣量通氣前30 min給予MAPK拮抗劑PD98059)；⑥SB203580組(SB203580+ HV組,高潮氣量通氣前30 min給予MAPK拮抗劑SB203580).機械通氣4h後(對照組氣管切開後4h),採用RT-PCR方法測定肺錶麵活性蛋白(SP)-A、B、C和RTI40 mRNA錶達量. 結果 ①與C組比較,LV組、HV組大鼠肺組織中RTI40錶達均增加(P＜0.05),而HV組、SP600125 +HV組及SB203580+HV組肺組織中SP-A、SP-C錶達均減少(P＜0.05),LV組中和PD98059+HV組中的SP-A、C變化均無統計學意義(P＞0.05)；②與HV組比較,SP600125+HV組、PD98059+HV組、SB203580+HV組肺組織中SP-A、C基因錶達增加(P＜0.05),RTI40基因錶達降低(P＜0.05)；③SP-A、C基因錶達量在PD98059+HV組較SP600125+HV組、SB203580+HV組升高(P＜0.05)；④SP-B在各組中變化無統計學意義(P＞0.05). 結論 高潮氣量機械通氣緻肺上皮細胞特異蛋白SP-A、C基因錶達下降和RTI40基因錶達上調,而MAPK拮抗劑可以防止該現象髮生,提示MAPK影響呼吸機相關性肺損傷(ventilator-induced lung injury,VILI)過程中對肺上皮細胞的分泌功能.
목적 사렬원활화단백격매(mitogen-activated protein kinases,MAPK)재궤계통기과정중대폐표면활성물질급특이단백기인표체적영향화가능궤제. 방법 채용건강성년웅성Sprague-Dawley대서48지,체중250 g～320 g.채용3％무파비타35 mg/kg～40 mg/kg복강주사마취후행기관절개치관술,완전수궤분조방법분위6조(매조8지):①C조(대조조,마취후부주기관절개불주궤계통기)；②LV조[정상통기조,조기량(Vt):6ml/kg,여동과도통기조]；③HV조[과도통기조,Vt:40 ml/kg,호흡빈솔(RR)40차/min,흡호비(I∶E)1∶2～1∶3,호기말정압통기(PEEP) =0,흡입양농도(FiO2)21％,통기4 h]；④SP600125조(SP600125+ HV조,고조기량통기전30 min급여MAPK길항제SP600125)；⑤PD98059조(PD98059+ HV조,고조기량통기전30 min급여MAPK길항제PD98059)；⑥SB203580조(SB203580+ HV조,고조기량통기전30 min급여MAPK길항제SB203580).궤계통기4h후(대조조기관절개후4h),채용RT-PCR방법측정폐표면활성단백(SP)-A、B、C화RTI40 mRNA표체량. 결과 ①여C조비교,LV조、HV조대서폐조직중RTI40표체균증가(P＜0.05),이HV조、SP600125 +HV조급SB203580+HV조폐조직중SP-A、SP-C표체균감소(P＜0.05),LV조중화PD98059+HV조중적SP-A、C변화균무통계학의의(P＞0.05)；②여HV조비교,SP600125+HV조、PD98059+HV조、SB203580+HV조폐조직중SP-A、C기인표체증가(P＜0.05),RTI40기인표체강저(P＜0.05)；③SP-A、C기인표체량재PD98059+HV조교SP600125+HV조、SB203580+HV조승고(P＜0.05)；④SP-B재각조중변화무통계학의의(P＞0.05). 결론 고조기량궤계통기치폐상피세포특이단백SP-A、C기인표체하강화RTI40기인표체상조,이MAPK길항제가이방지해현상발생,제시MAPK영향호흡궤상관성폐손상(ventilator-induced lung injury,VILI)과정중대폐상피세포적분비공능.
Objective To investigate the effects of mitogen-activated protein kinases (MAPK) on the genes expression of the pulmonary surfactants from alveolar epithelial cells during ventilation induced lung injury in rats.Methods Anesthetized male SD rats were randomized into six groups:① Control group(C) received no mechanical ventilation.② Low-volume ventilation(LV) group received mechanical ventilation with Vt=6 ml/kg,RR=40 bmp,I∶E=1∶2,FiO2=21％,positive end-expiratory pressure =0.③ Hyperventilation(HV) group received mechanical ventilation with the same respiratory parameters as the LV group and the Vt was 40 ml/kg.The inhibitors of MAPK including the JNK's:SP600125,the ERK's:PD98059 and the p38's:SB203580 were pretreated 30 min before ventilation just like in the HV group.④ SP600125 group (SP600125 + HV group).⑤ PD98059 group (PD98059 + HV group).⑥ SB203580 group (SB203580 + HV group).After 4 h ventilation,the animals in each group were killed and the lungs were removed for detecting the expression of SP-A,B,C and RTI40 mRNA by RT-PCR.Results ① Compared with group C,the expression of RTI40 mRNA of lung tissue increased significantly in the LV group and the HV group (P＜0.05),but the expression of SP-A,SP-C mRNA decreased in the HV group,SP600125 group and SB203580 group (P＜0.05),while there was no significant difference in the expression of SP-A、C mRNA in LV groups and PD98059 group (P＜0.05).② Compared with the HV group,the SP-A,C gene expressions of lung tissue in SP600125 group,PD98059 group and SB203580 group increased significantly (P＜0.05),but RTI40 gene expressions decreased(P＜0.05).③ The SP-A,C gene expressions of lung tissue in PD98059 group increased significantly than those of SP600125 group and SB203580 group.④ The SP-B gene expression had no difference in all groups.Conclusions The results of our study show that mechanical ventilation inhibited the expressions of the SP-A and SP-C,but upregulated RTI40 gene expressions.The inhibitors of MAPK attenuated the changes of SP-A,C and RTI40 mRNA during the process of high volume ventilation,which indicates that MAPK,at least in part,may play a role in the functions of Ⅰ and Ⅱ alveolar epithelial cells in the lung injury induced by mechanical ventilation.
