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目的探讨盐酸异丙肾上腺素(ISO)长期作用对大鼠左心室心肌细胞和间质Ⅰ/Ⅲ型胶原蛋白的影响。方法成年大鼠42只按4mg/(kg.d)剂量腹膜内注射ISO 1、4和8周,制备心肌缺血SD大鼠模型,用等体积生理盐水作对照组。利用电子/光学显微镜观察不同阶段左心室肌组织结构,免疫组织化学和Western blotting方法检测左心室肌组织Ⅰ/Ⅲ型胶原蛋白表达,并利用HAPIS-2000显微图像分析系统和SPSS10.0统计学软件对表达强度和面积百分比进行统计学处理。结果光镜下观察ISO诱导心内膜下出现心肌细胞缺血坏死区。缺血坏死区有Ⅰ/Ⅲ型胶原蛋白高表达,缺血坏死区所占面积百分比有减小趋势,组间比较1周与4周之间差异无统计学意义(P>0.05),4周与8周间差异具有统计学意义(P<0.05);表达强度组间比较差异无统计学意义(P>0.05)。非缺血坏死区心肌细胞早期表现为大量聚集糖原颗粒,后期以线粒体增多,肌原纤维松散为主要特征;免疫组织化学检测间质Ⅰ型胶原蛋白所占面积百分比无变化,组间比较差异均无统计学意义(P>0.05);表达强度实验组间比较差异无统计学意义(P>0.05),但与对照组相比,表达量减小,差异具有统计学意义(P<0.05)。免疫组织化学检测间质Ⅲ型胶原蛋白所占面积百分比呈增多趋势,组间比较,1周与4周间差异具有统计学意义(P<0.05);表达强度稳定,组间比较差异均无统计学意义(P>0.05)。Western blotting结果显示,实验组间Ⅰ/Ⅲ型胶原蛋白均呈现从增多到减少的趋势,组间比较差异均具有统计学意义(P<0.05)。结论 ISO长期诱导致心内膜下心肌细胞缺血坏死,且缺血坏死区面积总体趋势变小;缺血坏死区发生纤维化改变,与心壁僵硬度增大相关。非缺血坏死区心肌细胞肥大与能量代谢相关,间质Ⅰ/Ⅲ型胶原蛋白不参与心室壁僵硬度和顺应性变化。
Objective To investigate the effects of isoprenaline (ISO) on the left ventricular myocytes and interstitial collagen type Ⅰ / Ⅲ in rats. Methods Forty-two adult SD rats were injected intraperitoneally with 4 mg / (kg · d) for 1, 4 and 8 weeks respectively to establish a rat model of myocardial ischemia. Equal volumes of normal saline were used as the control group. The structures of left ventricular muscle at different stages were observed by electron / light microscopy. The expression of type Ⅰ / Ⅲ collagen in left ventricular muscle was detected by immunohistochemistry and Western blotting. The HAPIS-2000 microscopic image analysis system and SPSS 10.0 statistics The software performed a statistical treatment on the expression intensity and area percentage. Results Under light microscopy, ISO induced myocardial subepithelial cell necrosis area. There was a high expression of type Ⅰ / Ⅲ collagen in ischemic necrotic area, and the percentage of ischemic necrotic area had a decreasing trend. There was no significant difference between groups in 1 week and 4 weeks (P> 0.05), 4 weeks (P <0.05). There was no significant difference between the two groups (P> 0.05). Myocardial cells in the non-ischemic necrosis area showed a large number of aggregated glycogen granules in the early stage, mitochondria increased and myofibril loosened in the later stage. The percentage of area occupied by type Ⅰ collagen in immunohistochemistry was not changed, (P> 0.05). There was no significant difference in expression intensity between the experimental groups (P> 0.05), but the expression level was decreased compared with the control group (P <0.05) . Immunohistochemistry showed that the percentage of interstitial type Ⅲ collagen in the area increased with the increasing trend. The differences between the two groups were statistically significant (P <0.05), the expression intensity was stable and there was no statistical difference between the two groups Significance (P> 0.05). The results of Western blotting showed that the type Ⅰ / Ⅲ collagen between the experimental groups showed a trend of increasing from decreasing to decreasing. The difference between the two groups was statistically significant (P <0.05). Conclusion ISO induced cardiomyocyte cardiomyocyte necrosis in a long term, and the overall trend of ischemic necrosis area became smaller. Fibrosis changed in ischemic necrosis area, which was related to the increase of stiffness of cardiac wall. Myocardial hypertrophy in nonischemic necrosis area is related to energy metabolism, and interstitial type I / III collagen does not participate in changes of ventricular wall stiffness and compliance.