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以培养乳鼠心肌细胞做为模型,排除了血液动力学的影响,可供对血管紧张素Ⅱ致心肌肥厚的直接作用进行评价。结果表明,血管紧张素Ⅱ1、10、100mmol/L作用细胞72小时,心肌细胞的总蛋白增加15％、19％、30％,但细胞数目未见明显变化。用[~3H)亮氨酸结合的方法,测得血管紧张素Ⅱ1、10,100mmol/L在48小时内,增加蛋白合成29％、53％、70％。但用[~3H)胸甙结合方法,测得DNA的合成未见明显增加,血管紧张素Ⅱ100mmol/L作用心肌细胞7天后,引起细胞体积增加9％。这说明血管紧张素Ⅱ可以引起心肌细胞的肥大,并提示培养心肌细胞这一模型可以用来探索非血液动力学因素所致心肌肥厚的调节。
Using cultured neonatal rat cardiomyocytes as a model, hemodynamic effects were excluded and a direct assessment of myocardial hypertrophy by angiotensin II was evaluated. The results showed that the total protein of cardiomyocytes increased by 15%, 19% and 30% in angiotensinⅡ1,10,100 mmol / L-treated cells for 72 hours, but there was no significant change in the number of cells. Angiotensin Ⅱ 1, 10 and 100 mmol / L were measured to increase the protein synthesis by 29%, 53% and 70% within 48 hours by binding to [~ 3H] leucine. However, with ~ 3H thymidine incorporation, DNA synthesis did not increase significantly. Angiotensin II induced a 9% increase of cell volume after treated with 100 mmol / L cardiomyocytes for 7 days. This shows that angiotensin II can cause hypertrophy of cardiomyocytes and suggests that this model of cardiomyocyte culture can be used to explore the regulation of cardiac hypertrophy induced by non-hemodynamic factors.