创伤性二尖瓣关闭不全心肌间质血管改建及相关细胞因子调节研究

Study on the interstitial revascularization and related cytokine regulation in myocardium of traumatic mitral regurgitation

目的 探讨创伤性二尖瓣关闭不全心肌间质血管改建及相关细胞因子调节。方法 首先在超声引导下经心导管介入法造成二尖瓣关闭不全动物实验模型 ,在不同时间点宰杀切取心肌标本 ,然后用苏木素 伊红 (HE)染色检测模型犬心肌内小动脉内外径比值 ,用免疫组织化学方法检测心肌中α 平滑肌肌动蛋白 (α SMA)、碱性成纤维细胞生长因子 (bFGF)、血管内皮生长因子(VEGF)的表达量 ,并将其与心肌内小动脉内外径比值对比分析。结果 创伤性二尖瓣关闭不全模型犬心肌组织中α SMA、bFGF、VEGF的表达量较正常对照明显升高 ,术后 5个月升高最为明显 ,后期呈下降趋势 (P1m比 3m <0 .0 5 ,P1m比 5m <0 .0 1,P1m比 7m >0 .0 5 ) ,且都与血管密度呈正相关 (r血管比α SMA =0 .5 0 9,P <0 .0 5 ;r血管比bFGF =0 .5 0 1,P <0 .0 5 ;r血管比VEGF =0 .5 37,P <0 .0 5 )。病变早期间质血管增多 ,管壁无明显增厚 ,间质纤维有减少趋势。病变后期可见间质血管相对较为减少 ,管壁稍增厚 ,心肌间质纤维明显增多。结论 bFGF、VEGF等细胞因子及血管内皮细胞、血管周细胞都参与了早期心肌内小血管的改建。

Objective To investigate the interstiti al revascularization and related cytokine regulation in myocardium of the traumati c mitral regurgitation.Methods Percutaneous transluminal catheteriztion under the guiding of B-dimensional echocardiography was performe d to establish the animal model of traumatic mitral regurgitation.The specimens were obtained from canine model of traumatic mitral regurgitation and stained by HE in order to examine the ratio of arteriolar inner to outer diameter and by i mmunohischemical staining and in situ hybridization to measure the expression of the protein of bFGF,VEGF and α-SMA and mRNA of bFGF.Relationship between th e vascular density and the expression of bFGF,VEGF and α-SMA was analyzed. WT 5'HZ Results The imaging analysis indicated that vascular density was significantly increased,but the arteriolar wall did not change in the early phase of disease.The vascular density and the expression of bFGF,VEGF and α -SMA reached the peak at 5th mouth after operation,then gradually decreased at the late phase of disease (P1m vs 3m <0.05,P1m vs 5m<0.01,P1m vs 7m>0.05).The e xpression of bFGF,VEGF andα-SMA in the myocardium of traumatic mitral regurgit ation was significantly higher than in the normal canine control group.There wer e a positive relationship between vascular density and expression of bFGF,VEGF a nd α-SMA (r vessel vs a-SMA=0.509,P<0.05;r vessel vs b-FGF=0.501,P <0.05;r vessel vs VEGF=0.537,P<0.05).Conclusion Cy tokines of bFGF,VEGF and vascular endothelia,pericytes might take par t in the interstitial revascularization at the early stage of traumatic mitral r egurgitation.