中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2013年
2期
208-210
,共3页
蛋白激酶C%呼吸,人工%呼吸窘迫综合征,成人
蛋白激酶C%呼吸,人工%呼吸窘迫綜閤徵,成人
단백격매C%호흡,인공%호흡군박종합정,성인
Protein kinase C%Respiration,artificial%Respiratory distress syndrome,adult
目的 探讨蛋白激酶C(PKC)在大鼠机械通气相关性肺损伤中的作用.方法 健康雄性Wistar大鼠30只,体重250 ～ 300 g,采用随机数字表法,将大鼠分为5组(n=6):对照组(C组)、小潮气量组(S组)、小潮气量+ PKC抑制剂组(S+P组)、大潮气量组(L组)、大潮气量+PKC抑制剂组(L+P组).大潮气量组VT42 ml/kg,小潮气量组VT7 ml/kg,呼吸频率40次/min,I∶E 1∶2,呼吸末正压为0,FiO221％,机械通气4h.S+P组、L+P组于麻醉前1h肌肉注射PKC抑制剂bisindolvlmaleimide Ⅰ 0.12 mg/kg.C组于气管切开后即刻,其它4组机械通气4 h时处死大鼠,取肺组织,计算湿/干重比(W/D比),观察病理学结果；采用Western blot法测定肺组织occludin蛋白表达.结果 与C组比较,其余4组肺组织W/D比升高,occludin蛋白表达下调(P＜0.05)；与 S组比较,L组肺组织W/D比升高,occludin蛋白表达下调,S+P组肺组织W/D比降低,occludin蛋白表达上凋(P＜0.01)；与L组比较,L+P组肺组织W/D比降低,occludin蛋白表达上调(P＜0.01).S+P组和L+P组肺组织病理学损伤较S组和L组减轻.结论PKC参与了大鼠机械通气相关性肺损伤.
目的 探討蛋白激酶C(PKC)在大鼠機械通氣相關性肺損傷中的作用.方法 健康雄性Wistar大鼠30隻,體重250 ～ 300 g,採用隨機數字錶法,將大鼠分為5組(n=6):對照組(C組)、小潮氣量組(S組)、小潮氣量+ PKC抑製劑組(S+P組)、大潮氣量組(L組)、大潮氣量+PKC抑製劑組(L+P組).大潮氣量組VT42 ml/kg,小潮氣量組VT7 ml/kg,呼吸頻率40次/min,I∶E 1∶2,呼吸末正壓為0,FiO221％,機械通氣4h.S+P組、L+P組于痳醉前1h肌肉註射PKC抑製劑bisindolvlmaleimide Ⅰ 0.12 mg/kg.C組于氣管切開後即刻,其它4組機械通氣4 h時處死大鼠,取肺組織,計算濕/榦重比(W/D比),觀察病理學結果；採用Western blot法測定肺組織occludin蛋白錶達.結果 與C組比較,其餘4組肺組織W/D比升高,occludin蛋白錶達下調(P＜0.05)；與 S組比較,L組肺組織W/D比升高,occludin蛋白錶達下調,S+P組肺組織W/D比降低,occludin蛋白錶達上凋(P＜0.01)；與L組比較,L+P組肺組織W/D比降低,occludin蛋白錶達上調(P＜0.01).S+P組和L+P組肺組織病理學損傷較S組和L組減輕.結論PKC參與瞭大鼠機械通氣相關性肺損傷.
목적 탐토단백격매C(PKC)재대서궤계통기상관성폐손상중적작용.방법 건강웅성Wistar대서30지,체중250 ～ 300 g,채용수궤수자표법,장대서분위5조(n=6):대조조(C조)、소조기량조(S조)、소조기량+ PKC억제제조(S+P조)、대조기량조(L조)、대조기량+PKC억제제조(L+P조).대조기량조VT42 ml/kg,소조기량조VT7 ml/kg,호흡빈솔40차/min,I∶E 1∶2,호흡말정압위0,FiO221％,궤계통기4h.S+P조、L+P조우마취전1h기육주사PKC억제제bisindolvlmaleimide Ⅰ 0.12 mg/kg.C조우기관절개후즉각,기타4조궤계통기4 h시처사대서,취폐조직,계산습/간중비(W/D비),관찰병이학결과；채용Western blot법측정폐조직occludin단백표체.결과 여C조비교,기여4조폐조직W/D비승고,occludin단백표체하조(P＜0.05)；여 S조비교,L조폐조직W/D비승고,occludin단백표체하조,S+P조폐조직W/D비강저,occludin단백표체상조(P＜0.01)；여L조비교,L+P조폐조직W/D비강저,occludin단백표체상조(P＜0.01).S+P조화L+P조폐조직병이학손상교S조화L조감경.결론PKC삼여료대서궤계통기상관성폐손상.
Objective To investigate the role of protein kinase C (PKC) in mechanical ventilation-induced lung injury in rats.Methods Thirty healthy male Wistar rats,weighing 250-300 g,were randomly divided into 5 groups (n =6 each):control group (group C),small tidal volume group (group S),small tidal volume and PKC inhibitor group (group S + P),large tidal volume group (group L),and large tidal volume and PKC inhibitor group (group L + P).VT =42 ml/kg,RR =40 bpm,I∶E =1∶ 2,PEEP =0,FiO2 =21％ in groups L and L + P,while VT=7 ml/kg,RR=40 bpm,I∶E=1∶2,PEEP=0,FiO2 =21％ in groups S and S+P.The rats were only tracheostonized in group C,while the rats were mechanically ventilated for 4 h in the other four groups.PKC inhibitor bisindolylmaleinide Ⅰ 0.12 mg/kg was injected intramuscularly 1 h before anesthesia in groups S + P and L + P.The animals were sacrificed immediacy after tracheotomy in group C,and at 4 h of ventilation in the other four groups and lungs were removed for calculation of wet/dry lung weight ratio (W/D ratio) and for microscopic examination.The expression of occludin was determined in the lung tissues by Western blot.Results Compared with group C,W/D ratio was significantly increased and the expression of occludin was down-regulated in the other four groups (P ＜ 0.05).Compared with group S,W/D ratio was significantly increased and the expression of occludin was down-regulated in group L,and W/D ratio was decreased and the expression of occludin was up-regulated in group S + P (P ＜ 0.01).W/D ratio was significantly lower and the expression of occludin was higher in group L + P than in group L (P ＜ 0.01).The pathological changes were attenuated in groups S + P and L + P as compared with groups S and L.Conclusion PKC is involved in mechanical ventilation-induced lung injury in rats.
