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为探明压力超负荷性心脏肥厚转向心力衰竭过程中,心肌细胞形态与收缩功能的动态变化,本研究建立腹主动脉缩窄(transverse abdominal aortic constriction,TAC)高血压大鼠模型,观测在TAC后1、8、16与20周时,单个心肌细胞形态与无负荷缩短幅值的变化。结果显示:TAC手术后大鼠体重增长明显慢于同步对照假手术组,且用左心室质量与体重比不能准确衡量心肌肥厚程度,而用胶原酶分离心肌细胞后,直接测量单个心肌细胞长度与宽度的结果显示,TAC术后8、16和20周时,心肌细胞长度、宽度和表面面积均较同步对照组显著增加,较好地反映了心肌细胞的肥大程度。TAC心肌细胞面积的增长速率在早期至中期较快,后期明显下降。肥大心肌细胞的长度与宽度在TAC后8周开始明显增加,但肌节长度保持不变,而肌节数量呈显著性增加。与同步对照组相比,单个心肌细胞的无负荷缩短幅值在1周TAC组明显增加,8周组无统计学差别,16与20周组则显著降低。上述结果提示:肥大心肌细胞收缩功能降低与其细胞内分子功能改变有关。
To investigate the dynamic changes of myocardial cell morphology and systolic function during stress overload hypertrophic cardiomyopathy, we established a rat model of transverse abdominal aortic constriction (TAC) hypertension and observed the effects of TAC After 1, 8, 16 and 20 weeks, the change of single myocardial cell morphology and no-load shortening amplitude. The results showed that the weight gain of rats after TAC was significantly slower than that of the sham control group, and the left ventricular mass to body weight ratio could not accurately measure the degree of myocardial hypertrophy. However, after myocardial cells were separated by collagenase, the length of single cardiomyocytes The results of width show that at 8, 16 and 20 weeks after TAC, the length, width and surface area of cardiomyocytes were significantly increased compared with the control group, which better reflects the hypertrophy of cardiomyocytes. TAC cardiomyocyte area growth rate in the early to mid-fast, significantly decreased late. The length and width of hypertrophic cardiomyocytes began to increase at 8 weeks after TAC, but the length of sarcomere remained unchanged while the number of sarcomeres increased significantly. Compared with the synchronous control group, the unloaded shortening amplitude of single cardiomyocytes increased significantly in TAC group at 1 week, no significant difference at 8 weeks group, and significantly decreased at 16 and 20 weeks. The above results suggest that the reduction of contractile function of hypertrophic cardiomyocytes is related to the changes of intracellular molecular function.