充血性心力衰竭时神经体液因素变化与证候衍变的实验研究

An Experimental Study of the Changes of Neurohumoral Factors and Syndromes in Rats with Congestive Heart Failure

本研究测定大鼠充血性心力衰竭(CHF)模型,心气虚(心功能代偿)至心阳虚(心功能失代偿)证衍变时神经体液因素变化:CHF 大鼠交感神经系统(SNS)、肾素-血管紧张素-醛固酮系统(RAAS)、内皮素(ET)、血浆心钠素(ANP)激活。大鼠心气虚随 ANP 增高、环磷酸鸟苷(cGMP)、排钠及尿量增加,去甲肾上腺素(NE)排泄、血管紧张素Ⅱ(AngⅡ)、醛固酮(Aldo)水平下降,血浆肾素活性(PRA)、ET 未继续增高,CHF 表现缓解,而心阳虚大鼠 ANP 较前者继续增高,cGMP、尿量及排钠减少,尿 NE、血浆 PRA、AngⅡ、Aldo及 ET 持续增高,CHF 表现加重。这表明在前者 ANP 抑制 SNS、RAAS 及 ET,发挥代偿作用,后者衍变为心阳虚,SNS、RAAS、ET 过度激活,ANP 作用钝化,为 CHF 加重心气虚的实质。

In the present study,the authors measured the neurohumoral factors in rats model with congestive beart failure (CHF) and with syndromes changing from insufficiency of Heart-Qi to insufficiency of Heart-Yang.The results showed that in rats with CHF,sympathetic nervous system(SNS),renin-angiotensin-aldo-sterone-sodium(RAAS),endothelial (ET) and atrial natriuretic peptide(ANP) were activated in either of the two syndromes.In the rats with insufficiency of Heart-Qi,plasma ANP elevated,cGMP,urine Na excreation(UNa) and the urinary volume increased;urine nor- pinephrine(NE),Ang ,Aldo,PRA and ET were all decreasing continuously,and the rats' CHF symptoms relieved. On the contrary,in rats with insufficiency of Heart-Yang,although ANP were much higher than that in the previous con- dition(P<0.05),cGMP,UV,and UNa tended to decrease,RAJAS,ET and urine NE elevated persistantly,and CHF aggravated.The results suggested that in rats with insufficiency of Heart-Qi,ANP secretion increases and inhibits SNS, RAAS,ET and has a compensatory effect,but in rats with severe CHF,the syndrome insufficiency of Heart-Qi trans- formed into insufficiency of Heart-Yang.SNS,RAAS,ET are overactivated and the ANP effect is blunted,which re- flects the essence of the Syndromic change of rats with CHF.