挤压伤大鼠早期心脏损伤的细胞机制

目的观察挤压伤大鼠血清对培养的新生大鼠心肌细胞的某些作用,拟阐明挤压伤早期心肌细胞损伤的细胞机制。方法培养1～3d龄SD大鼠心肌细胞,观察挤压伤大鼠血清对心肌细胞搏动频率、表面积、蛋白质含量、3H-亮氨酸掺入、胞内钙浓度和Fos蛋白表达的影响。结果与正常大鼠血清组比较,挤压伤大鼠血清培养的心肌细胞搏动频率(次/min)由88.3±20.6降为26.4±16.7,心肌细胞表面积、蛋白质含量、3H-Leu掺入、胞内游离钙浓度(nmol/L)和Fos蛋白表达阳性指数增加。结论挤压伤大鼠血清通过抑制细胞搏动,增加胞内钙浓度诱导Fos蛋白的表达,引起心肌细胞肥大,介导挤压伤早期的心脏损伤。

Cellular mechanism of heart injury in the early stage of crush injury in rats

Objective To study cellular mechanism of cardiomyocytes injury in the early stage of crush injury by observing some effects of crush injury rat sera on cultured neonatal rat cardiomyocytes. Methods One to three days old neonatal rat cardiomyocytes were cultured in vitro and some effects of crush injury rat sera on beating rate, cell surface area, total protein content, 3H-Leu incorporation, intracellular calcium concentration ([Ca2 ]i) and Fos protein expression were observed in cultured rat cardiomyocytes. Results Compared with normal rat serum group, crush injury rat sera decreased beating rate(beats/min) of cardiomyocytes from 88.3 to 26.4, cell surface area, total protein content, 3H-Leu incorporation, [Ca2 ]i(nmol/L) and PI of Fos protein expression were increased. Conclusion Crush injury rat sera suppress cell beating, increase intracellular calcium, induce Fos protein synthesis and cause cell hypertrophy, which may cause cardiac injury in the early stage of rush injury.