不同剂量低分子肝素钠对急性DVT大鼠血管形态学影响的研究
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摘要
目的观察不同剂量低分子肝素钠对急性DVT大鼠在不同时期治疗后血管形态学的变化。方法将72只SD大鼠制备模型后,随机按血栓形成后1、3、7、14天分期,每期18只,分为Ⅰ期、Ⅱ期、Ⅲ期、Ⅳ期。然后每期再根据低分子肝素钠剂量分为:低分子肝素钠小剂量组(700U/kg、一次/24h,n=6)、低分子肝素钠大剂量组(700U/kg、一次/12h,n=6)、模型组(0 U/kg,n=6)。低分子肝素钠大、小剂量组均由大鼠腹壁皮下注射,连续7日。实验结束后获取病变段血管,观察内皮细胞数量变化,胶原阳性染色面积百分比变化,并与同期模型组进行比较。结果模型组在Ⅱ期、Ⅲ期分别死亡一只,低分子肝素钠治疗大剂量组Ⅰ期、Ⅲ期、Ⅳ期内死亡4只。在Ⅰ期低分子肝素钠大、小剂量组内皮细胞数量与模型组相比均有统计学差异(P<0.05),组间亦有差异.低分子肝素钠大、小剂量组胶原阳性染色面积百分比与模型组相比均有统计学差异(P<0.05),组间相比无差异;在Ⅱ期,低分子肝素钠大、小剂量组内皮细胞数量与模型组相比均有统计学差异(P<0.05),组间无差异;在Ⅲ期、Ⅳ期低分子肝素钠大、小剂量组内皮细胞数量与模型组相比无统计学差异(P>0.05);在Ⅱ期、Ⅲ期低分子肝素钠大、小剂量组胶原阳性染色面积百分比与模型组相比仍有统计学差异(P<0.05),组间亦有差异;在Ⅳ期低分子肝素钠大、小剂量组胶原阳性染色面积百分比与模型组相比无统计学差异(P>0.05)。结论血栓形成3天内,大、小剂量低分子肝素钠对内皮细胞均有保护作用,以大剂量效果较好。血栓形成7天内,大、小剂量低分子肝素钠对对胶原增生均有抑制作用,随着时间的延长,以大剂量低分子肝素钠抑制作用最强。
Objective To observe the effect of different dose,s Low molecular weight heparin( LMWH) on morphological changes of vein wall after differenct periods of deep vein thrombosis (DVT) in rats. Methods Firstly,72 sprague-dawley (SD) rats were randomly divided intoⅠ、Ⅱ、Ⅲ、Ⅳperiods on 1st,3rd,7th,14th day following thrombosis respectively, there were 18 SD rats in every period.Then the 18 SD rats in each period were separated to 4 group. Low dose’s Low molecular weight heparin( LMWH) group (700u/kg,1t/24h, n=6.)、high dose’s Low molecular weight heparin(LMWH) group(700u/kg, 1t/12h, n=6.)、thrombosis group(0,000u/kg, n=6). In each group, to observe the remain quantity of endothelial cells and the expression areas of collagen by dyeing. Results 2 SD rats in thrombosis group were died inⅡ、Ⅲperiod respectively. 4 SD rats in high dose’s Low molecular weight heparin( LMWH) group were died inⅠ、Ⅲ、Ⅳperiod in thrombolytic therapy. InⅠperiod, the quantity of endothelial cells in low、high dose’s LMWH group have significant difference with thrombosis group respectively (P<0.05). The difference exisited in interclass as well(P<0.05). InⅠperiod, the expression areas of collagen in low、high dose’s LMWH group have significant difference with thrombosis group respectively (P<0.05); InⅡperiod, the quantity of endothelial cells in low、high dose’s LMWH group have significant difference with thrombosis group respectively (P<0.05) ,The difference do not exisited in interclass (P>0.05);InⅢ、Ⅳperiods,the quantity of endothelial cells in low、high dose’s LMWH group haven,t significant difference with thrombosis group respectively(P>0.05). InⅡ、Ⅲperiod, the expression areas of collagen in low、high dose’s LMWH group have significant difference with thrombosis group respectively (P<0.05), The difference exisited in interclass as well(P<0.05)。InⅣperiod, The expression areas of collagen in low、high dose’s LMWH group haven,t significant difference with thrombosis group respectively (P<0.05). Conclusions Different dose,s LMWH have protective effect on the quantity of endothelial cells during 3 days after thrombosis, the effect of high dose’s LMWH is better; Different dose,s LMWH haven,t protective on the quantity of endothelial cells after 7 days following thrombosis,but they have inhibitary effect on the expression areas of collagen in every period, the effect of high dose’s LMWH is better.
Objective To observe the effect of different dose,s Low molecular weight heparin( LMWH) on morphological changes of vein wall after differenct periods of deep vein thrombosis (DVT) in rats. Methods Firstly,72 sprague-dawley (SD) rats were randomly divided intoⅠ、Ⅱ、Ⅲ、Ⅳperiods on 1st,3rd,7th,14th day following thrombosis respectively, there were 18 SD rats in every period.Then the 18 SD rats in each period were separated to 4 group. Low dose’s Low molecular weight heparin( LMWH) group (700u/kg,1t/24h, n=6.)、high dose’s Low molecular weight heparin(LMWH) group(700u/kg, 1t/12h, n=6.)、thrombosis group(0,000u/kg, n=6). In each group, to observe the remain quantity of endothelial cells and the expression areas of collagen by dyeing. Results 2 SD rats in thrombosis group were died inⅡ、Ⅲperiod respectively. 4 SD rats in high dose’s Low molecular weight heparin( LMWH) group were died inⅠ、Ⅲ、Ⅳperiod in thrombolytic therapy. InⅠperiod, the quantity of endothelial cells in low、high dose’s LMWH group have significant difference with thrombosis group respectively (P<0.05). The difference exisited in interclass as well(P<0.05). InⅠperiod, the expression areas of collagen in low、high dose’s LMWH group have significant difference with thrombosis group respectively (P<0.05); InⅡperiod, the quantity of endothelial cells in low、high dose’s LMWH group have significant difference with thrombosis group respectively (P<0.05) ,The difference do not exisited in interclass (P>0.05);InⅢ、Ⅳperiods,the quantity of endothelial cells in low、high dose’s LMWH group haven,t significant difference with thrombosis group respectively(P>0.05). InⅡ、Ⅲperiod, the expression areas of collagen in low、high dose’s LMWH group have significant difference with thrombosis group respectively (P<0.05), The difference exisited in interclass as well(P<0.05)。InⅣperiod, The expression areas of collagen in low、high dose’s LMWH group haven,t significant difference with thrombosis group respectively (P<0.05). Conclusions Different dose,s LMWH have protective effect on the quantity of endothelial cells during 3 days after thrombosis, the effect of high dose’s LMWH is better; Different dose,s LMWH haven,t protective on the quantity of endothelial cells after 7 days following thrombosis,but they have inhibitary effect on the expression areas of collagen in every period, the effect of high dose’s LMWH is better.
引文
[1]吴在德等.第5版.外科学[M].人民卫生出版社,2001:689-692
[2]中华医学会呼吸病分会,肺血栓栓塞症的诊断与治疗指南(草案)[J],中华结核和呼吸杂志, 2001,24(5):259-264
[3] NORDSTOM M, LINDBLAD B, BERGQVIST D, et al. A prospective study of the incidence of deep-vein thrombosis within a defined urban population[J].J Inter Med, 1992,232:155
[4] Meissner MH, Strandness DE. Pathophysiology and natural history of acute deep venous thrombsis. In:Rutherford HB: Vascular Surgery(5th ed)[M]. Philadelphia: Saunders Company,2000.1929-1930
[5] Danis KW, Menawatt S, von Thron J, et al. Efficacy of deep vein thrombosis promphylaxis in Trauma patients and dentification of high—risk groups[J]. Trauma, 1993,35(1):132
[6]董国祥,实用血管外科学及护理学[J].北京:中国医药科技出版社:1995,201
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[8]杨景文等.下肢深静脉血栓溶栓治疗机制研究[J],中华血液学杂志,1992,13:450
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[11] Sixma JJ, Vanzanten GH, Saelman EUM, et al. Platelet adhesion to collagen [J]. Thromb Haemost,1995,74:454-459
[12]魏立新.血小板胶原受体及其拮抗剂研究进展[J].国外医学临床生物化学与检验学分册, 2001,22:(5)271-272
[13]孙敏莉等.急性下肢静脉血栓形成治疗的选择及评价[J],北京,中国实用外科杂志, 2006,26,(10):756-757
[14]李晓强等.下肢深静脉血栓形成的外科治疗[J].中国普外基础与临床杂志. 2006, 13(6):638-639
[15] Gonzalez-Fajardo J, Arreba E, Castrodeza J, et al. Venographic comparison of subcutaneous low-molecular weight heparin with oral anticogulant therapy in the long-term tretment of deep venous thrombosis[J].J Vasc Surg,1999 30(2):283-292
[16] Douketis JD, Kearon c, Bates S, et al. risk of fatal pulmonary embolism in patients with venous thromboembolism9J).JAMA,1998,279(6):458-462
[17]谢树民,刘蓓.深静脉血栓形成的抗凝治疗[J],现代中西医结合杂志. 2007, 16(24): 3600-3602
[18]王振义,李家增,阮长耿.血栓与止血基础理论与临床[M]. 2版.上海:上海科学技术出版社,1996:401
[19]吴庆华.急性下肢深静脉血栓的溶栓、抗凝治疗[J].中国实用外科杂志, 2003, 234: 202–205
[20]曲乐丰,景在平.急性下肢深静脉血栓形成的抗凝治疗进展[J] .中华普通外科杂志, 2003,189:573–574
[21]方积乾主编.第5版.卫生统计学[M],人民卫生出版社,2003,132
[22]李晓云,蔡莹等,血栓性疾病发生的相关因素[J].中国微循环,2002,6(5):297
[23]张柏根.下肢深静脉血栓形成治疗和预后的几个问题[J].中华普通外科杂志, 2006, 21(2):81
[24]张纪蔚,张柏根,赵意平,等.兔静脉血栓形成后内皮细胞形态和功能演变的实验研究[J].中华外科杂志,1997,35(6):383- 384
[25]露慰萱,刘春萍.深静脉血栓形成和肺血栓栓塞症的自然病程[J].中华医学杂志, 2003,83(1):84-85
[26]武忠弼等.第4版.病理学[M].人民卫生出版社,1999,52-57
[27]杨军,奚九一.静脉血栓早期机化阶段动物模型的建立[J].中国中医基础医学杂志, 2005,11(3):105-107
[28] Brass LF, Vassallo RR. Structure and function of the human platelet thrombin receptor[J].J Biol Chem,1992,267:795-798
[29] Manabe I, Nagai R. Molecular mechanisms regulating phenotypic modulation of smooth musclecell[J].CircMed,1995,13(2):76-81
[30] Giachelli C, Bae N, Lombardi D, et al. Molecular cloning and Character ization of2b7,aratmRNA which distinguishes Smooth muscle cell phenotypes in vitro and isident icaltooseopontin[J]. Biochem Biophys Res Commun,1991,177(5):867-873
[31] Han TH, Prywes R. Regulation role of MEF2D in serumin-Duction of the c-jinpromoter [J].Mol Cell Biol,1995,15(10):2907-2915
[32] Michae lK, Klaus M. Endothelin and estnosis[J].Cardio vasc Res, 1998, 39(3): 550-555
[33] Tuan TL, Song A, Slavin J, et al. In vitrofibroplasias: Matrix contraction, cell growth, and collagen production of fibroblasts cultured in fibrin gels [J].Exp Cell Res, 1996, 223(1): 127-134
[1]王铁.肺血栓栓塞症和深静脉血栓形成的放射性核素诊断[J].中华医学杂志, 2003,83(4):348-349
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[2]中华医学会呼吸病分会,肺血栓栓塞症的诊断与治疗指南(草案)[J],中华结核和呼吸杂志, 2001,24(5):259-264
[3] NORDSTOM M, LINDBLAD B, BERGQVIST D, et al. A prospective study of the incidence of deep-vein thrombosis within a defined urban population[J].J Inter Med, 1992,232:155
[4] Meissner MH, Strandness DE. Pathophysiology and natural history of acute deep venous thrombsis. In:Rutherford HB: Vascular Surgery(5th ed)[M]. Philadelphia: Saunders Company,2000.1929-1930
[5] Danis KW, Menawatt S, von Thron J, et al. Efficacy of deep vein thrombosis promphylaxis in Trauma patients and dentification of high—risk groups[J]. Trauma, 1993,35(1):132
[6]董国祥,实用血管外科学及护理学[J].北京:中国医药科技出版社:1995,201
[7]姚德成,血管外科急诊,见兰锡纯,冯桌荣,心脏血管外科学[M],第2版,北京:人民卫生出版社2002,1057-1064.
[8]杨景文等.下肢深静脉血栓溶栓治疗机制研究[J],中华血液学杂志,1992,13:450
[9] Nachman RL,Silverstein R.Hypercoabulable states.Ann Inern Med,1993,119(8): 819
[10] Sun Y, Diaz-Arias M, Weber KT. Angiotensin-converting enzyme, bradykin in and Angiotens in II recepter hiding in rat skin, tendon and heart valves:An in vitro quantitative autoradiographic study[J]. J Lab Clin Med, 1994,123:372-377
[11] Sixma JJ, Vanzanten GH, Saelman EUM, et al. Platelet adhesion to collagen [J]. Thromb Haemost,1995,74:454-459
[12]魏立新.血小板胶原受体及其拮抗剂研究进展[J].国外医学临床生物化学与检验学分册, 2001,22:(5)271-272
[13]孙敏莉等.急性下肢静脉血栓形成治疗的选择及评价[J],北京,中国实用外科杂志, 2006,26,(10):756-757
[14]李晓强等.下肢深静脉血栓形成的外科治疗[J].中国普外基础与临床杂志. 2006, 13(6):638-639
[15] Gonzalez-Fajardo J, Arreba E, Castrodeza J, et al. Venographic comparison of subcutaneous low-molecular weight heparin with oral anticogulant therapy in the long-term tretment of deep venous thrombosis[J].J Vasc Surg,1999 30(2):283-292
[16] Douketis JD, Kearon c, Bates S, et al. risk of fatal pulmonary embolism in patients with venous thromboembolism9J).JAMA,1998,279(6):458-462
[17]谢树民,刘蓓.深静脉血栓形成的抗凝治疗[J],现代中西医结合杂志. 2007, 16(24): 3600-3602
[18]王振义,李家增,阮长耿.血栓与止血基础理论与临床[M]. 2版.上海:上海科学技术出版社,1996:401
[19]吴庆华.急性下肢深静脉血栓的溶栓、抗凝治疗[J].中国实用外科杂志, 2003, 234: 202–205
[20]曲乐丰,景在平.急性下肢深静脉血栓形成的抗凝治疗进展[J] .中华普通外科杂志, 2003,189:573–574
[21]方积乾主编.第5版.卫生统计学[M],人民卫生出版社,2003,132
[22]李晓云,蔡莹等,血栓性疾病发生的相关因素[J].中国微循环,2002,6(5):297
[23]张柏根.下肢深静脉血栓形成治疗和预后的几个问题[J].中华普通外科杂志, 2006, 21(2):81
[24]张纪蔚,张柏根,赵意平,等.兔静脉血栓形成后内皮细胞形态和功能演变的实验研究[J].中华外科杂志,1997,35(6):383- 384
[25]露慰萱,刘春萍.深静脉血栓形成和肺血栓栓塞症的自然病程[J].中华医学杂志, 2003,83(1):84-85
[26]武忠弼等.第4版.病理学[M].人民卫生出版社,1999,52-57
[27]杨军,奚九一.静脉血栓早期机化阶段动物模型的建立[J].中国中医基础医学杂志, 2005,11(3):105-107
[28] Brass LF, Vassallo RR. Structure and function of the human platelet thrombin receptor[J].J Biol Chem,1992,267:795-798
[29] Manabe I, Nagai R. Molecular mechanisms regulating phenotypic modulation of smooth musclecell[J].CircMed,1995,13(2):76-81
[30] Giachelli C, Bae N, Lombardi D, et al. Molecular cloning and Character ization of2b7,aratmRNA which distinguishes Smooth muscle cell phenotypes in vitro and isident icaltooseopontin[J]. Biochem Biophys Res Commun,1991,177(5):867-873
[31] Han TH, Prywes R. Regulation role of MEF2D in serumin-Duction of the c-jinpromoter [J].Mol Cell Biol,1995,15(10):2907-2915
[32] Michae lK, Klaus M. Endothelin and estnosis[J].Cardio vasc Res, 1998, 39(3): 550-555
[33] Tuan TL, Song A, Slavin J, et al. In vitrofibroplasias: Matrix contraction, cell growth, and collagen production of fibroblasts cultured in fibrin gels [J].Exp Cell Res, 1996, 223(1): 127-134
[1]王铁.肺血栓栓塞症和深静脉血栓形成的放射性核素诊断[J].中华医学杂志, 2003,83(4):348-349
[2] Tapson VF, Carroll BA, Davidson BL, et al. The diagnostis approach to acute venous thromboemlism[J].Am J Respir Cvit Car Med.1999,160:1043-1066
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