烧伤,电%肝素,低分子量%肿瘤坏死因子α%内皮素1
燒傷,電%肝素,低分子量%腫瘤壞死因子α%內皮素1
소상,전%간소,저분자량%종류배사인자α%내피소1
Burns,electric%Heparin,low-molecular-weight%Tumor necrosis factor-alpha%Endothelin-1
目的 观察低分子量肝素(LMWH)对电烧伤大鼠血管损伤以及炎症反应的影响.方法 取60只Wistar大鼠,用自制调压器和变压器制成右后肢内侧中段(电流出口)约0.5 cm×0.5 cm大小Ⅲ～Ⅳ度电烧伤模型,伤后即刻以20 g/L磺胺嘧啶银糊剂外涂创面后暴露,每日观察创面情况.按随机数字表法将致伤后大鼠分为LMWH组与对照组,每组30只.LMWH组从致伤日起每日腹壁皮下注射LMWH 1 U/g,每天2次;对照组不行其他处理.伤后3、5、10 d,2组分别处死10只大鼠,在创面及创周损伤组织取样约1.0 cm ×0.5 cm并同时心脏采血,分别行HE、Masson、醛品红染色,观察病理变化及血栓形成情况,计算血栓形成率;ELISA法检测血清中TNF-α及内皮素1含量;RT-PCR法检测损伤组织中TNF-α mRNA表达.对数据行Levene齐性检验、析因设计方差分析、LSD-t检验、SNK-q检验、Friedman M非参数检验. 结果 (1)电烧伤后大鼠伤肢红肿明显,深达肌肉及骨质.与对照组比较,LMWH组大鼠各时相点红肿消退稍快,炎症反应较轻.(2)组织学观察见损伤组织坏死,大量炎性细胞浸润;组织内血管扩张,淤血及血栓形成,血管内皮细胞肿胀、坏死及脱落.2组大鼠损伤组织中均可见血管壁结构破坏、弹力纤维断裂、内弹力膜僵直等病变.以上病变随时间推移逐渐好转,LMWH组伤后5、10d情况好于对照组.(3)LMWH组大鼠血栓形成率总体明显低于对照组(处理因素主效应F=4.921,P＜0.05).LMWH组大鼠伤后3、10d血栓形成率分别为(0.07±0.11)％、(0.03±0.05)％,明显低于对照组的(0.16±0.15)％、(0.1 3±0.18)％(t值分别为2.17、2.07,P值均小于0.05).LMWH组大鼠伤后10d血栓形成率低于本组伤后3 d(t=3.61,P ＜0.05).(4)LMWH组大鼠血清TNF-α、内皮素1含量总体明显低于对照组(处理因素主效应F=47.161,x2 =81.46,P值均小于0.01).LMWH组大鼠伤后3、5、10 d TNF-α含量分别为(71±24)、(74±14)、(72 ±20) pg/mL,内皮素1含量分别为(20.9±3.2)、(19.8±5.2)、(18.6±1.1) ng/mL,分别明显低于对照组的(195±148)、(96 ±20)、(159±46) pg/mL与(38.8±15.4)、(27.9±3.6)、(25.6±7.6) ng/mL(t值为3.81 ～8.05,q值为4.41 ～7.85,P＜0.05或P＜0.01).(5)LMWH组大鼠损伤组织中TNF-α mRNA的表达量总体明显低于对照组(处理因素主效应F=199.113,P＜0.01).LMWH组大鼠伤后3、5、10 d TNF-α mRNA表达量分别为0.93 ±0.10、1.15±0.12、1.21±0.11,分别明显低于对照组的1.68±0.15、1.43±0.12、1.50±0.13(t值为3.75 ～6.12,P＜0.05或P＜0.01).LMWH组大鼠伤后10 d TNF-α mRNA表达量明显高于本组伤后3 d(t=3.61,P＜0.05).结论 LMWH干预可减轻电烧伤大鼠血管损伤和炎症反应,降低伤肢血管的血栓形成率.
目的 觀察低分子量肝素(LMWH)對電燒傷大鼠血管損傷以及炎癥反應的影響.方法 取60隻Wistar大鼠,用自製調壓器和變壓器製成右後肢內側中段(電流齣口)約0.5 cm×0.5 cm大小Ⅲ～Ⅳ度電燒傷模型,傷後即刻以20 g/L磺胺嘧啶銀糊劑外塗創麵後暴露,每日觀察創麵情況.按隨機數字錶法將緻傷後大鼠分為LMWH組與對照組,每組30隻.LMWH組從緻傷日起每日腹壁皮下註射LMWH 1 U/g,每天2次;對照組不行其他處理.傷後3、5、10 d,2組分彆處死10隻大鼠,在創麵及創週損傷組織取樣約1.0 cm ×0.5 cm併同時心髒採血,分彆行HE、Masson、醛品紅染色,觀察病理變化及血栓形成情況,計算血栓形成率;ELISA法檢測血清中TNF-α及內皮素1含量;RT-PCR法檢測損傷組織中TNF-α mRNA錶達.對數據行Levene齊性檢驗、析因設計方差分析、LSD-t檢驗、SNK-q檢驗、Friedman M非參數檢驗. 結果 (1)電燒傷後大鼠傷肢紅腫明顯,深達肌肉及骨質.與對照組比較,LMWH組大鼠各時相點紅腫消退稍快,炎癥反應較輕.(2)組織學觀察見損傷組織壞死,大量炎性細胞浸潤;組織內血管擴張,淤血及血栓形成,血管內皮細胞腫脹、壞死及脫落.2組大鼠損傷組織中均可見血管壁結構破壞、彈力纖維斷裂、內彈力膜僵直等病變.以上病變隨時間推移逐漸好轉,LMWH組傷後5、10d情況好于對照組.(3)LMWH組大鼠血栓形成率總體明顯低于對照組(處理因素主效應F=4.921,P＜0.05).LMWH組大鼠傷後3、10d血栓形成率分彆為(0.07±0.11)％、(0.03±0.05)％,明顯低于對照組的(0.16±0.15)％、(0.1 3±0.18)％(t值分彆為2.17、2.07,P值均小于0.05).LMWH組大鼠傷後10d血栓形成率低于本組傷後3 d(t=3.61,P ＜0.05).(4)LMWH組大鼠血清TNF-α、內皮素1含量總體明顯低于對照組(處理因素主效應F=47.161,x2 =81.46,P值均小于0.01).LMWH組大鼠傷後3、5、10 d TNF-α含量分彆為(71±24)、(74±14)、(72 ±20) pg/mL,內皮素1含量分彆為(20.9±3.2)、(19.8±5.2)、(18.6±1.1) ng/mL,分彆明顯低于對照組的(195±148)、(96 ±20)、(159±46) pg/mL與(38.8±15.4)、(27.9±3.6)、(25.6±7.6) ng/mL(t值為3.81 ～8.05,q值為4.41 ～7.85,P＜0.05或P＜0.01).(5)LMWH組大鼠損傷組織中TNF-α mRNA的錶達量總體明顯低于對照組(處理因素主效應F=199.113,P＜0.01).LMWH組大鼠傷後3、5、10 d TNF-α mRNA錶達量分彆為0.93 ±0.10、1.15±0.12、1.21±0.11,分彆明顯低于對照組的1.68±0.15、1.43±0.12、1.50±0.13(t值為3.75 ～6.12,P＜0.05或P＜0.01).LMWH組大鼠傷後10 d TNF-α mRNA錶達量明顯高于本組傷後3 d(t=3.61,P＜0.05).結論 LMWH榦預可減輕電燒傷大鼠血管損傷和炎癥反應,降低傷肢血管的血栓形成率.
목적 관찰저분자량간소(LMWH)대전소상대서혈관손상이급염증반응적영향.방법 취60지Wistar대서,용자제조압기화변압기제성우후지내측중단(전류출구)약0.5 cm×0.5 cm대소Ⅲ～Ⅳ도전소상모형,상후즉각이20 g/L광알밀정은호제외도창면후폭로,매일관찰창면정황.안수궤수자표법장치상후대서분위LMWH조여대조조,매조30지.LMWH조종치상일기매일복벽피하주사LMWH 1 U/g,매천2차;대조조불행기타처리.상후3、5、10 d,2조분별처사10지대서,재창면급창주손상조직취양약1.0 cm ×0.5 cm병동시심장채혈,분별행HE、Masson、철품홍염색,관찰병리변화급혈전형성정황,계산혈전형성솔;ELISA법검측혈청중TNF-α급내피소1함량;RT-PCR법검측손상조직중TNF-α mRNA표체.대수거행Levene제성검험、석인설계방차분석、LSD-t검험、SNK-q검험、Friedman M비삼수검험. 결과 (1)전소상후대서상지홍종명현,심체기육급골질.여대조조비교,LMWH조대서각시상점홍종소퇴초쾌,염증반응교경.(2)조직학관찰견손상조직배사,대량염성세포침윤;조직내혈관확장,어혈급혈전형성,혈관내피세포종창、배사급탈락.2조대서손상조직중균가견혈관벽결구파배、탄력섬유단렬、내탄력막강직등병변.이상병변수시간추이축점호전,LMWH조상후5、10d정황호우대조조.(3)LMWH조대서혈전형성솔총체명현저우대조조(처리인소주효응F=4.921,P＜0.05).LMWH조대서상후3、10d혈전형성솔분별위(0.07±0.11)％、(0.03±0.05)％,명현저우대조조적(0.16±0.15)％、(0.1 3±0.18)％(t치분별위2.17、2.07,P치균소우0.05).LMWH조대서상후10d혈전형성솔저우본조상후3 d(t=3.61,P ＜0.05).(4)LMWH조대서혈청TNF-α、내피소1함량총체명현저우대조조(처리인소주효응F=47.161,x2 =81.46,P치균소우0.01).LMWH조대서상후3、5、10 d TNF-α함량분별위(71±24)、(74±14)、(72 ±20) pg/mL,내피소1함량분별위(20.9±3.2)、(19.8±5.2)、(18.6±1.1) ng/mL,분별명현저우대조조적(195±148)、(96 ±20)、(159±46) pg/mL여(38.8±15.4)、(27.9±3.6)、(25.6±7.6) ng/mL(t치위3.81 ～8.05,q치위4.41 ～7.85,P＜0.05혹P＜0.01).(5)LMWH조대서손상조직중TNF-α mRNA적표체량총체명현저우대조조(처리인소주효응F=199.113,P＜0.01).LMWH조대서상후3、5、10 d TNF-α mRNA표체량분별위0.93 ±0.10、1.15±0.12、1.21±0.11,분별명현저우대조조적1.68±0.15、1.43±0.12、1.50±0.13(t치위3.75 ～6.12,P＜0.05혹P＜0.01).LMWH조대서상후10 d TNF-α mRNA표체량명현고우본조상후3 d(t=3.61,P＜0.05).결론 LMWH간예가감경전소상대서혈관손상화염증반응,강저상지혈관적혈전형성솔.
Objective To observe the effects of low molecular weight heparin (LMWH) on the inflammatory response and vascular injury in rat after electric burn.Methods A homemade regulator and transformer apparatus was used to reproduce the model of electric burn (0.5 cm × 0.5 cm in size) with depth from full-thickness to full-thickness skin plus muscle and bone on the middle of the inside of right hind limb in 60 Wistar rats.The open wounds were covered with 20 g/L sulfadiazine silver paste immediately after injury.The wound condition was observed every day.The injured rats were divided into group LMWH and control group (C) according to the random number table,with 30 rats in each group.Rats in group LMWH were given subcutaneous injection of LMWH (1 U/g) in abdominal wall,2 times a day.No other treatment was given in rats in group C.On post burn day (PBD) 3,5,and 10,10 rats respectively of two groups were sacrificed.The damaged tissue of wound and that around the wound (1.0 cm × 0.5 cm in size) were excised,and heart blood was obtained.The pathological changes and thrombosis in damaged tissue were observed with HE,Masson,and aldehyde fuchsin staining,and the thrombosis rate was calculated.Serum contents of TNF-α and endothelin-1 were determined with ELISA.The mRNA expression of TNF-α in damaged tissue was detected with RT-PCR.Data were processed with Levene homogeneity test,analysis of variance of factorial design,LSD-t test,SNK-q test,and Friedman M nonparametric test.Results (1) The injured limb of rats was obviously swollen after electric burn,which reached deeply to the muscle and bone.Compared with those of group C,the swelling of rats subsided slightly faster and the inflammatory response was lighter in group LMWH at each time point.(2) The necrosis of damaged tissue and profuse infiltration of inflammatory cells were observed.Dilatation of blood vessels,congestion and thrombosis,and swelling,necrosis,and desquamation of vascular endothelial cells were observed in the damaged tissue.Damaged blood vessel wall,ruptured elastic fiber,loss of internal elastic membrane,and other pathological changes were observed in the damaged tissue of rats in the two groups.Above lesions were improved gradually along with the passage of time,and the improvement was more obvious in rats of group LMWH compared with that of group C on PBD 5 and 10.(3) The thrombosis rates of rats in group LMWH were obviously lower than those of rats in group C (F =4.921,P ＜0.05).The thrombosis rates of rats in group LMWH on PBD 3 and 10 were respectively (0.07 ± 0.11) ％ and (0.03 ± 0.05) ％,which were significantly lower than those of rats in groupC [(0.16±0.15)％ and (0.13 ±0.18)％,with t values respectively 2.17 and 2.07,P values below 0.05].In group LMWH,the thrombosis rate of rats on PBD 10 was obviously lower than that on PBD 3 (t =3.61,P ＜ 0.05).(4) The serum contents of TNF-o and endothelin-1 of rats in group LMWH were significantly lower than those of rats in group C (F =47.161,x 2 =81.46,P values below 0.01).In group LMWH,TNF-α contents were respectively (71 ±24),(74 ± 14),(72 ±20) pg/mL,and endothelin-1 contents were respectively (20.9 ± 3.2),(19.8 ±5.2),(18.6 ± 1.1) ng/mL on PBD 3,5,and 10,and they were significantly lower than those of rats in group C [(195 ± 148),(96 ±20),(159 ± 46) pg/mL and (38.8 ± 15.4),(27.9 ± 3.6),(25.6 ± 7.6) ng/mL,with t values from 3.81 to 8.05,q values from 4.41 to 7.85,P ＜0.05 or P ＜0.01].(5) The mRNA expression levels of TNF-α in damaged tissue of rats in group LMWH were significantly lower than those of rats in group C (F =199.113,P ＜ 0.01).The mRNA expression levels of TNF-α of rats in group LMWH were respectively 0.93 ± 0.10,1.15 ±0.12,1.21 ±0.11 on PBD 3,5,and 10,and they were significantly lower than those of group C (1.68±0.15,1.43±0.12,1.50±0.13,with t values from 3.75 to 6.12,P ＜0.05 orP ＜0.01).In group LMWH,the mRNA expression level of TNF-α of rats on PBD 10 was obviously higher than that on PBD 3 (t =3.61,P ＜ 0.05).Conclusions LMWH intervention can ameliorate vascular injury and inflammatory response of electrically burned wounds in rats,and it decreases thrombosis rate in the vessels of injured limb.
