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作 者:何昆仑[1] 盖鲁粤[1] 黄大显[1] 高焱章[1] 王所亭[1]
出 处:《解放军医学杂志》2000年第3期162-164,共3页Medical Journal of Chinese People's Liberation Army
基 金:国家自然科学基金资助项目!(编号39900059)
摘 要:为探讨冠状动脉内放射抑制再狭窄的机制,对23头小型猪冠状动脉行球囊过度扩张术,其中12头在术后即刻通过^(192)Ir血管内放射治疗系统局部给予20Gy的放射剂量,其余11头作为对照组。用反转录-聚合酶链反应(RT-PCR)方法定量检测血管组织血小板源生长因子(PDGF-B)和诱导型一氧化氮合成酶(iNOS)基因表达,并测定血管组织一氧化氮(NO)的含量。结果:冠状动脉内放射明显抑制了术后3天和术后30天 PDGF-BmRNA表达(38.3%,P<0.01;39.4%,P<0.05);明显增加了球囊扩张术后3天及术后30天血管组织iNOSmRNA的表达(32.5%,P<0.01;34.2%,P<0.05)和NO的含量(102.0%,P<0.01;90.8%,P<0.01)。To investigate the mechanisms of intracoronary radiation in inhibiting restenosis after coronary artery balloon injury in swine. Twenty-three Chinese swines underwent coronary balloon over-stretch. The catheter- based radiation system was used to deliver 20Gy to the dilated segments in 12 swines, and 11 swines were used as control group. The animals were sacrificed three and thirty days following the initial procedure. The injured segments were dissected and processed to examine the gene expression of iNOS and PDGF-B by reverse transcription- polymerase chain reaction (RT-PCR) and to measure the production of NO by biochemistry. RESULTS:Intracor- onary radiation significantly reduced PDGF-B mRNA (38. 3 %, P<0. 01; 39. 4%, P<0. 05 ) and increased iNOS mRNA(32. 5 %, P<0. 01 ; 34. 2%,P<0. 05) three days and thirty days after the initial injury. Furthermore,in- tracoronary radiation also increased the production of NO three and thirty days after the injury (102. 0%, P<0. 01; 90. 8%,P<0. 01). CONCLUSIONS: PDGF-B and NO system may be involved in the mechanisms by which intracoronary radiation inhibits restenosis after balloon injury.
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