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
2013年
12期
1067-1070,1086
,共5页
翟丽梅%燕宪亮%王厚清%赵宁军%梁高永%许铁
翟麗梅%燕憲亮%王厚清%趙寧軍%樑高永%許鐵
적려매%연헌량%왕후청%조저군%량고영%허철
盐酸戊乙奎醚%肺间质纤维化%百草枯%转化生长因子-β1
鹽痠戊乙奎醚%肺間質纖維化%百草枯%轉化生長因子-β1
염산무을규미%폐간질섬유화%백초고%전화생장인자-β1
Penehyclidine hydrochloride%Pulmonary interstitial fibrosis%Paraquat%Transforming growth factor-β1
目的 研究盐酸戊乙奎醚(penehyclidine hydrochloride,PHC)对急性百草枯(paraquat,PQ)中毒所致大鼠肺间质纤维化(pulmonary interstitial fibrosis,PIF)的影响. 方法 SD雄性大鼠48只,采用随机数字表法分为4组:对照组(Con 组)、模型组(Mod组)、PHC治疗组(PHC组)、地塞米松(dexamethasone,Dex)治疗组(Dex组);每组再分为第7天和第22天两个亚组,每组6只.腹腔注射质量分数20％ PQ溶液(18 mg/kg,生理盐水稀释至1 ml)的方法制备大鼠PQ中毒模型;Con组腹腔注射1 ml生理盐水.染毒后30 min,PHC组和Dex组大鼠分别向其腹腔注射PHC(0.1 mg/kg)和Dex(3 mg/kg),药物用生理盐水稀释至1 ml,每24 h重复1次;Con组和Mon组在对应时间点腹腔注射1 ml生理盐水.于染毒后第7天和第22天处死实验动物,检测动脉血氧分压(partial pressure of oxygen in artery,PaO2)和动脉血二氧化碳分压(partial pressure of carbon dioxide in artery,PaCO2),测定肺组织湿/干重比(wet/dry ratio,W/D),检测肺组织转化生长因子-β1(transforming growth factor-β1,TGF-β1)的表达,苏木精-伊红(hematoxylin-eosin,HE)、Masson染色观察肺组织病理形态学变化. 结果 与Con组比较,Mod组、PHC组和Dex组大鼠第7天/第22天PaO2显著降低[(79±6) mm Hg/(78±8) mm Hg vs (39±6) mm Hg/(44±5) mm Hg、(46±4) mm Hg/(52±5)mm Hg、(54±6) mm Hg/(60±-6)mm Hg(1 mm Hg=0.133 kPa)],PaCO2显著增加[(44±7) mm Hg/(45±7) mm Hg vs(92±5)mm Hg/(82±4) mm Hg、(84±8) mm Hg/(73±8) mm Hg、(75±7) mm Hg/(65±7) mm Hg],肺组织W/D显著升高[(2.60±0.25)/(2.58±0.22) vs(5.67±0.61)/(4.57±0.39)、(4.25±0.44)/(3.85±0.34)、(3.69±0.40)/(3.40±o.28)],TGF-β1表达显著增加[(136±7)/(140±7) vs (215±23)/(322±29)、(193±11)/(246±16)、(186±11)/(214±14)];与Mon组比较,PHC组和Dex组大鼠PaO2升高、PaCO2降低,肺W/D和TGF书-β1表达降低,差异均有统计学意义(P＜0.05或P＜0.01);PaO2、PaCO2和肺W/D在第7天变化更明显,TGF-β1表达增加在第22天更明显;第7天组织形态学以急性肺炎性改变为主、第22天以PIF为主,PHC组和Dex组大鼠肺组织炎性侵润和PIF程度较Mon组轻. 结论 PHC能抑制肺组织TGF-β1的表达,减轻急性PQ中毒大鼠肺组织的炎性侵润和PIF.
目的 研究鹽痠戊乙奎醚(penehyclidine hydrochloride,PHC)對急性百草枯(paraquat,PQ)中毒所緻大鼠肺間質纖維化(pulmonary interstitial fibrosis,PIF)的影響. 方法 SD雄性大鼠48隻,採用隨機數字錶法分為4組:對照組(Con 組)、模型組(Mod組)、PHC治療組(PHC組)、地塞米鬆(dexamethasone,Dex)治療組(Dex組);每組再分為第7天和第22天兩箇亞組,每組6隻.腹腔註射質量分數20％ PQ溶液(18 mg/kg,生理鹽水稀釋至1 ml)的方法製備大鼠PQ中毒模型;Con組腹腔註射1 ml生理鹽水.染毒後30 min,PHC組和Dex組大鼠分彆嚮其腹腔註射PHC(0.1 mg/kg)和Dex(3 mg/kg),藥物用生理鹽水稀釋至1 ml,每24 h重複1次;Con組和Mon組在對應時間點腹腔註射1 ml生理鹽水.于染毒後第7天和第22天處死實驗動物,檢測動脈血氧分壓(partial pressure of oxygen in artery,PaO2)和動脈血二氧化碳分壓(partial pressure of carbon dioxide in artery,PaCO2),測定肺組織濕/榦重比(wet/dry ratio,W/D),檢測肺組織轉化生長因子-β1(transforming growth factor-β1,TGF-β1)的錶達,囌木精-伊紅(hematoxylin-eosin,HE)、Masson染色觀察肺組織病理形態學變化. 結果 與Con組比較,Mod組、PHC組和Dex組大鼠第7天/第22天PaO2顯著降低[(79±6) mm Hg/(78±8) mm Hg vs (39±6) mm Hg/(44±5) mm Hg、(46±4) mm Hg/(52±5)mm Hg、(54±6) mm Hg/(60±-6)mm Hg(1 mm Hg=0.133 kPa)],PaCO2顯著增加[(44±7) mm Hg/(45±7) mm Hg vs(92±5)mm Hg/(82±4) mm Hg、(84±8) mm Hg/(73±8) mm Hg、(75±7) mm Hg/(65±7) mm Hg],肺組織W/D顯著升高[(2.60±0.25)/(2.58±0.22) vs(5.67±0.61)/(4.57±0.39)、(4.25±0.44)/(3.85±0.34)、(3.69±0.40)/(3.40±o.28)],TGF-β1錶達顯著增加[(136±7)/(140±7) vs (215±23)/(322±29)、(193±11)/(246±16)、(186±11)/(214±14)];與Mon組比較,PHC組和Dex組大鼠PaO2升高、PaCO2降低,肺W/D和TGF書-β1錶達降低,差異均有統計學意義(P＜0.05或P＜0.01);PaO2、PaCO2和肺W/D在第7天變化更明顯,TGF-β1錶達增加在第22天更明顯;第7天組織形態學以急性肺炎性改變為主、第22天以PIF為主,PHC組和Dex組大鼠肺組織炎性侵潤和PIF程度較Mon組輕. 結論 PHC能抑製肺組織TGF-β1的錶達,減輕急性PQ中毒大鼠肺組織的炎性侵潤和PIF.
목적 연구염산무을규미(penehyclidine hydrochloride,PHC)대급성백초고(paraquat,PQ)중독소치대서폐간질섬유화(pulmonary interstitial fibrosis,PIF)적영향. 방법 SD웅성대서48지,채용수궤수자표법분위4조:대조조(Con 조)、모형조(Mod조)、PHC치료조(PHC조)、지새미송(dexamethasone,Dex)치료조(Dex조);매조재분위제7천화제22천량개아조,매조6지.복강주사질량분수20％ PQ용액(18 mg/kg,생리염수희석지1 ml)적방법제비대서PQ중독모형;Con조복강주사1 ml생리염수.염독후30 min,PHC조화Dex조대서분별향기복강주사PHC(0.1 mg/kg)화Dex(3 mg/kg),약물용생리염수희석지1 ml,매24 h중복1차;Con조화Mon조재대응시간점복강주사1 ml생리염수.우염독후제7천화제22천처사실험동물,검측동맥혈양분압(partial pressure of oxygen in artery,PaO2)화동맥혈이양화탄분압(partial pressure of carbon dioxide in artery,PaCO2),측정폐조직습/간중비(wet/dry ratio,W/D),검측폐조직전화생장인자-β1(transforming growth factor-β1,TGF-β1)적표체,소목정-이홍(hematoxylin-eosin,HE)、Masson염색관찰폐조직병리형태학변화. 결과 여Con조비교,Mod조、PHC조화Dex조대서제7천/제22천PaO2현저강저[(79±6) mm Hg/(78±8) mm Hg vs (39±6) mm Hg/(44±5) mm Hg、(46±4) mm Hg/(52±5)mm Hg、(54±6) mm Hg/(60±-6)mm Hg(1 mm Hg=0.133 kPa)],PaCO2현저증가[(44±7) mm Hg/(45±7) mm Hg vs(92±5)mm Hg/(82±4) mm Hg、(84±8) mm Hg/(73±8) mm Hg、(75±7) mm Hg/(65±7) mm Hg],폐조직W/D현저승고[(2.60±0.25)/(2.58±0.22) vs(5.67±0.61)/(4.57±0.39)、(4.25±0.44)/(3.85±0.34)、(3.69±0.40)/(3.40±o.28)],TGF-β1표체현저증가[(136±7)/(140±7) vs (215±23)/(322±29)、(193±11)/(246±16)、(186±11)/(214±14)];여Mon조비교,PHC조화Dex조대서PaO2승고、PaCO2강저,폐W/D화TGF서-β1표체강저,차이균유통계학의의(P＜0.05혹P＜0.01);PaO2、PaCO2화폐W/D재제7천변화경명현,TGF-β1표체증가재제22천경명현;제7천조직형태학이급성폐염성개변위주、제22천이PIF위주,PHC조화Dex조대서폐조직염성침윤화PIF정도교Mon조경. 결론 PHC능억제폐조직TGF-β1적표체,감경급성PQ중독대서폐조직적염성침윤화PIF.
Objective To investigate the effect of penehyclidine hydrochloride(PHC) on pulmonary interstitial fibrosis(PIF) induced by paraquat (PQ) in rats.Methods Forty-eight male SD rats were randomly divided into four groups,control group(Con group),model group(Mod group),PHC group and dexamethasone(Dex) group.Then every group was randomly divided into 7th day and 22th day subgroup,there were 6 rats in every group.20％ PQ (18 mg/kg,diluted to 1 ml) was injected peritoneally to make poisoning model,while in the Con group 1 ml normal saline was used.30 min after exposed to PQ,rats in PHC group and Dex group were respectively intraperitoneally injected with PHC (0.1 mg/kg) and Dex (3 mg/kg),and then repeated injection once per 24 h,all intervention drug were diluted to 1 ml with normal saline.Rats in Con group and Mod group at corresponding time points were given with equal volume of normal saline.On the 7th day and 22th day respectively,experimental animals were killed to detect the partial pressure of oxygen in artery (PaO2) and partial pressure of carbon dioxide in artery (PaCO2),the lung wet/dry ratio (W/D),the pathological changes of lung tissue by hematoxylin-eosin (HE) staining and Masson staining,and the transforming growth factor-β1 (TGF-β1) expression in lung tissue with immunohistochemistry.Results Comparing with Con group,the PaO2 was significantly lower[(79±6) mm Hg/(78±8) mm Hg vs(39±6) mm Hg/(44±5) mm Hg,(46±4) mm Hg/(52±5) mm Hg,(54±6) mm Hg/(60±6) mm Hg(1 mm Hg=0.133 kPa)],the PaCO2[(44±7) mm Hg/(45±7) mm Hg vs(92±5) mm Hg/(82±4) mm Hg,(84±8) mm Hg/(73±8) mm Hg,(75±7) mm Hg/(65±7) mm Hg],pulmonary W/D[(2.60±0.25)/(2.58±0.22) vs(5.67±0.61)/(4.57±0.39),(4.25±0.44)/(3.85±0.34),(3.69±0.40)/(3.40±0.28)] and TGF-β1[(136±7)/(140±7) vs(215±23)/(322±29),(193±11)/(246±16),(186±11)/(214±14)] expression was significantly increased in rats exposed to PQ.The morphological changes presented acute pulmonary inflammatiuon on the 7th day,while on the 22th day,PIF appeared.Penehyclidine hydrochloride and Dex,could significantly increase PaO2,decrease PaCO2.Inhibit lung inflammation infiltration,reduce PIF,significantly reduce lung W/D and TGF-β1 expression in the lung tissue,and there were no obvious difference in PHC group and Dex group.Conclusions PHC can inhibitting the expression of TGF-31,then reduce lung inflammation infiltration and suppress the occurrence of PIF of PQ poisoning in rats.
