Adenovirus-mediated VEGF(121) gene transfer stimulates angiogenesis in normoperfused skeletal muscle and preserves tissue perfusion after induction of ischemia.
Adenovirus-mediated VEGF(121) gene transfer stimulates angiogenesis in normoperfused skeletal muscle and preserves tissue perfusion after induction of ischemia.
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腺病毒介导的 VEGF(121) 基因转移刺激正常灌注骨骼肌中的血管生成，并在诱导缺血后保留组织灌注。
DOI：
10.1161/01.cir.102.5.565
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发表时间：
2000
期刊：
影响因子：
37.8
通讯作者：
Capogrossi,MC
中科院分区：
文献类型：
--
作者：
Gowdak,LH;Poliakova,L;Wang,X;Kovesdi,I;Fishbein,KW;Zacheo,A;Palumbo,R;Straino,S;Emanueli,C;Marrocco-Trischitta,M;Lakatta,EG;Anversa,P;Spencer,RG;Talan,M;Capogrossi,MC
背景-血管生成因子的管理刺激缺血组织中的新血管形成。然而，没有证据表明，血管生成可以在正常灌注的骨骼肌中诱导。我们验证了腺病毒介导的121氨基酸形式的血管内皮生长因子肌肉内（IM）基因转移的假设，方法和结果-兔和大鼠接受AdCMV. VEGF 121、AdCMV. VEGF 121或盐水在大腿的IM注射，注射肢体股动脉切除前4周（兔）或2周（大鼠）。在未手术的大鼠中，在注射AdCMV.VEGF121的部位，我们发现小动脉和毛细血管的长度密度分别增加了96%和29%。早在术后第1天，通过放射性微球测量的缺血腓肠肌血流改善记录了AdCMV.VEGF 121组缺血肢体的组织灌注（TP）增加AdCMV.VEGF 121 = 5.69 ± 0.40，AdCMV. VEGF 121 = 2.97 ± 0.50，生理盐水= 2.78 ± 0.43 mL·min-1·100 g-1，P <0.001（血管评分）（AdCMV. VEGF 121 = 50.58 ± 1.48，AdCMV. VEGF 121 = 29.08 ± 4.22，saline = 11.83 ± 1.90，P <0.0001），并通过31P NMR光谱评估腓肠肌生物能量储备的改善。后续研究表明，上级TP缺血肢体的AdCMV.VEGF 121组持续，直到它是由自发的侧支血管发育untreated animals.Conclusions-IM管理的AdCMV.VEGF 121刺激血管生成normoperfused骨骼肌，和新形成的血管保存TP诱导缺血后。
Background—Administration of angiogenic factors stimulates neovascularization in ischemic tissues. However, there is no evidence that angiogenesis can be induced in normoperfused skeletal muscles. We tested the hypothesis that adenovirus-mediated intramuscular (IM) gene transfer of the 121-amino-acid form of vascular endothelial growth factor (AdCMV.VEGF121) could stimulate neovascularization in nonischemic skeletal muscle and consequently attenuate the hemodynamic deficit secondary to surgically induced ischemia.Methods and Results—Rabbits and rats received IM injections of AdCMV.VEGF121, AdCMV.Null, or saline in the thigh, 4 weeks (rabbits) or 2 weeks (rats) before femoral artery removal in the injected limb. In unoperated rats, at the site of injection of AdCMV.VEGF121, we found 96% and 29% increases in length density of arterioles and capillaries, respectively. Increased tissue perfusion (TP) to the ischemic limb in the AdCMV.VEGF121group was documented, as early as day 1 after surgery, by improved blood flow to the ischemic gastrocnemius muscle measured by radioactive microspheres (AdCMV.VEGF121=5.69±0.40, AdCMV.Null=2.97±0.50, and saline=2.78±0.43 mL · min−1· 100 g−1,P<0.001), more angiographically recognizable collateral vessels (angioscore) (AdCMV.VEGF121=50.58±1.48, AdCMV.Null=29.08±4.22, saline=11.83±1.90,P<0.0001), and improvement of the bioenergetic reserve of the gastrocnemius muscle as assessed by31P NMR spectroscopy. Follow-up studies showed that superior TP to the ischemic limb in the AdCMV.VEGF121group persisted until it was equalized by spontaneous collateral vessel development in untreated animals.Conclusions—IM administration of AdCMV.VEGF121stimulates angiogenesis in normoperfused skeletal muscles, and the newly formed vessels preserve TP after induction of ischemia.
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腺病毒介导的血管内皮生长因子基因转移至兔和大鼠骨骼肌对血管通透性的影响。
DOI：
10.1016/s0022-5223(99)70225-4
发表时间：
1999
期刊：
The Journal of thoracic and cardiovascular surgery
影响因子：
--
作者：
L. Poliakova;Imre Kovesdi;Xiatong Wang;M. Capogrossi;M. Talan
通讯作者：
M. Talan
影响因子：
37.8
作者：
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S. Takeshita;L. Q. Pu;L. Stein;A. Sniderman;S. Bunting;N. Ferrara;J. Isner;J. Symes;J. Symes
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影响因子：
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作者：
B. Authier;A. Rossi;J. Albrand;M. Décorps
通讯作者：
M. Décorps
影响因子：
37.8
作者：
Y. Tsurumi;S. Takeshita;Dongfen Chen;M. Kearney;S. Rossow;J. Passeri;J. Horowitz;J. Symes;J. Isner
通讯作者：
Y. Tsurumi;S. Takeshita;Dongfen Chen;M. Kearney;S. Rossow;J. Passeri;J. Horowitz;J. Symes;J. Isner
影响因子：
15.9
作者：
TAKESHITA, S;ZHENG, LP;ISNER, JM
通讯作者：
ISNER, JM