摘要
目的 了解慢性心脏后负荷增加导致慢性心力衰竭时肾脏细胞凋亡的情况 ,探讨慢性心脏后负荷增加及引起慢性心力衰竭时影响肾脏功能不全的机制 .方法 复制慢性后负荷增加引起心力衰竭大鼠 (n=2 4)模型 ,检测血液动力学(BP,L VSP)变化 ,应用末端转移酶介导的缺口末端标记法(TU NEL )检测肾脏细胞凋亡 .结果 对照组大鼠肾脏及慢性后负荷增加早期肾脏均未出现细胞凋亡 ,心力衰竭时肾脏出现细胞凋亡 ,细胞凋亡程度肾髓质 (36 - ND) >肾近曲小管(17- ND) >肾小球 (6 - ND) ,肾血管平滑肌细胞及致密斑亦出现细胞凋亡 .结论 慢性后负荷增加引起心力衰竭时肾脏出现细胞凋亡 ,它与慢性心力衰竭密切相关 ,是肾功能不全的重要原因 .
AIM To observe renal cells apoptosis in chronic heart failure which resulted from the chronic excessive heart post load. To study the molecular mechanism of renal failure in chronic heart failure resulting from the excessive post load. METHODS The models of chronic heart failure which resulted from chronic excessive post load were made in rats ( n =24). The change of blood dynamics was detected. The presence of apoptotic renal cells was demonstrated by the method of terminal deoxynucleotidyl transferase mediated dUTP nick end labeling (TUNEL). RESULTS The presence of apoptotic renal cells was not demonstrated in the control groups and the early stage of chronic excessive post load, and was demonstrated in chronic heart failure groups. The degree of renal medulla's apoptosis (36 ND) was highest. The degree of renal juxtaglomerular tubule's apoptosis (17 ND)was lower; the degree of glomerulu's (6 ND) was lowest. The apoptotic renal vascular smooth muscle cells and apoptotic macula densa were also present. CONCLUSION Renal apoptosis is demonstrated when excessive post load results in chronic heart failure, and is closely related with chronic heart failure, so is an important cause of renal failure.
出处
《第四军医大学学报》
北大核心
2002年第7期586-588,共3页
Journal of the Fourth Military Medical University
