压力负荷所致左室心肌肥大和原癌基因C-myc表达关系的研究

在腹主动脉狭窄所致心肌肥大模型上，分别于２ｈ、８ｈ、１２ｈ、４８ｈ、１ 周、２ 周用形态学计量法（Ｍｏｒｐｈｏｍ ｅｔｒｙ）检测单位体积心肌细胞核数［Ｎ（ｎ）ｖ］和每核平均细胞体积［Ｖ（ｍ ）ｎ］；用核酸原位杂交技术检测原癌基因Ｃ ｍ ｙｃ表达强度。结果显示：手术组与对照组相比，Ｎ（ｎ）ｖ 和Ｖ（ｍ ）ｎ ２ｈ、８ｈ、１２ｈ 时无显著差异（Ｐ＞ ０．０５），４８ｈ、１周、２ 周时，手术组明显大于对照组（Ｐ＜ ０．０５）；原癌基因Ｃ ｍ ｙｃ ２ｈ 开始在手术组左室心肌细胞中表达，８ｈ 达高峰，４８ｈ 消失。提示原癌基因Ｃ ｍ ｙｃ与压力负荷所致左室心肌肥大有密切关系

ASSOCIATIONS BETWEEN EXPRESSION OF PROTO-ONCOGENES C-myc AND LEFT VENTRICULAR HYPERTROPHY CAUSED BY OVERLOAD PRESSURE IN RATS

Left ventricular hypertrophy is a complex cellular response to a variety of pathologic states.Overload pressure is a major cause of cardiac hypertrophy, although the mechanisms by which mechanical load induces cardiac cellular hypertrophy have long been a subject of great interest for cardiologists.Our experiment were performed on hypertrophy model rats caused by abdominal aorta cramped.The N(n)v and V(m)n of left ventricular myocardial cell were assessed at 2h,8h,48h,1W,2W using Anversa Method.The levels of proto oncogene C myc mRNA in the left ventricle were measured at the same time using nonradioaction In Situ Hybridization techniques.We found that the morphogenetic change of left ventricular myocardial cellV(m)n,N(n)v]bagan at 48h.There was obvious difference between the SHAM and OP at 48h ,1W,2W(P<0.05).The expression of C myc was a transient process.It began at 2h,reached peak at 8h,disappeared at 48h,C myc expressions were increased significantly at 2h,8h,12h(P<0.01).We conclude that proto oncogene C myc may be a initiative factor of left ventricular hypertrophy which response to many kinds of factors and hormone caused by excessive pressure load.