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目的观察高血脂大鼠心肌微细结构的改变,评估其与冠心病形成发展的关系。方法 2014年9—11月选取6周龄健康雄性SD大鼠20只,随机分成对照组与实验组各10只,实验组制作高血脂病理模型。用排水称量法测定心脏的质量与体积,COD-PAP、CPO-PAP和CAT法检测血脂。心脏切片用HE和免疫组织化学(免疫组化)pv-9000二步法染色,光镜观察心肌微细结构及Fas-L与Actin表达,Mimics10.0行图像分析,计量资料采用t检验,P<0.05为差异有统计学意义。结果实验组大鼠心脏平均体积及质量明显大于对照组[(0.86±0.08)、(0.62±0.08)cm3、(1.63±0.03)、(1.43±0.05)g],差异均有统计学意义(均P<0.05)。实验组大鼠血清TCH与LDLC分别为(3.94±0.94)、(0.90±0.27)mmol/L,对照组为(1.27±0.15)、(0.11±0.02)mmol/L,实验组明显高于对照组,对比差异均有统计学意义(均P<0.05)。实验组血清TG与HDLC分别为(1.64±1.03)、(0.73±0.12)mmol/L,对照组为(0.75±0.09)、(0.61±0.08)mmol/L,实验组高于对照组,对比差异均有统计学意义(均P<0.05)。实验组心肌间质增宽,微静脉与毛细血管扩展、淤血分,小动脉与微动脉内皮增高、内膜增厚、局部隆起,管腔内可见微血栓,心肌内有小片状变质坏死区与散在变质坏死的肌纤维。对照组心肌呈Actin强阳性表达,平均灰度值为465.89±77.37,实验组呈阳性表达,平均灰度值为1 089.41±292.21;对照组心肌Fas-L呈阴性表达,平均灰度值为1 429.25±74.82,实验组呈强阳性表达,平均灰度值为976.42±219.51,两组大鼠心肌Actin与Fas-L表达的平均灰度值对比差异均有统计学意义(均P<0.05)。实验组Actin表达弱于对照组,而Fas-L表达明显强于对照组。结论各种致病因素引起的心肌及其微、小血管广泛性损伤,与冠心病的形成与发展有着极为密切的关系。
Objective To observe the changes of myocardial micro-structure in hyperlipidemic rats and evaluate its relationship with the development of coronary heart disease. Methods Twenty healthy 6-week-old male Sprague-Dawley rats were randomly divided into control group and experimental group (n = 10) each from September to November in 2014. The experimental group was given hyperlipidemia model. The quality and volume of the heart were measured by the drainage method, and the blood lipids were measured by COD-PAP, CPO-PAP and CAT methods. Cardiomyocytes were stained with HE and immunohistochemistry (IHC) pv-9000 two-step method. The myocardial microstructure and the expression of Fas-L and Actin were observed by light microscopy. The image analysis was performed on Mimics 10.0 with t test, P < 0.05 for the difference was statistically significant. Results The average volume and quality of heart in the experimental group were significantly higher than those in the control group [(0.86 ± 0.08), (0.62 ± 0.08) cm3, (1.63 ± 0.03), (1.43 ± 0.05) g] P <0.05). The serum levels of TCH and LDLC in the experimental group were (3.94 ± 0.94) and (0.90 ± 0.27) mmol / L respectively, while those in the control group were (1.27 ± 0.15) and (0.11 ± 0.02) mmol / L respectively , The differences were statistically significant (P <0.05). The levels of TG and HDLC in the experimental group were (1.64 ± 1.03) and (0.73 ± 0.12) mmol / L, respectively, and those in the control group were (0.75 ± 0.09) and (0.61 ± 0.08) mmol / L respectively All were statistically significant (P <0.05). Experimental group myocardial interstitial widened, venules and capillary expansion, congestion points, arterioles and arterioles increased endothelial, thickening of the intima, local uplift, visible micro-thrombosis within the lumen, there is a small piece of myocardial necrosis With the loose deterioration of muscle fibers. The control group myocardial positive Actin expression, the average gray value of 465.89 ± 77.37, the experimental group was positive expression, the average gray value of 1 089.41 ± 292.21; control group myocardial Fas-L was negative expression, the average gray value of 1 429.25 ± 74.82. The expression of Actin and Fas-L in the two groups were significantly different (P <0.05). The average gray value was 976.42 ± 219.51 in the experimental group. The expression of Actin in the experimental group was weaker than that in the control group, while the expression of Fas-L was stronger in the experimental group than in the control group. Conclusion Various pathogenic factors cause extensive damage of myocardium, microvessel and small blood vessel, which are closely related to the formation and development of coronary heart disease.