心肌容量超负荷与脑钠肽分泌关系的研究

Relationship between myocardial capacity overload and brain natriuretic peptide secretion

目的探讨心肌容量超负荷是否是引起生物体内脑钠肽(BNP)分泌水平增高的直接原因。方法健康新西兰兔10只,随机分为对照组(n=5)和容量超负荷组(n=5)。建立心肌容量超负荷实验动物模型,对照组仅给输液,维持左房压于平均生理水平(6 mmHg)。运用电生理记录仪动态观察监测两组实验前、容量超负荷组于容量超负荷(对照组维持左房压于6 mmHg)后15 min、30 min左心收缩功能(LVSP)变化及其对应的心电图改变。采用酶联免疫吸附实验法(ELISA)测定两组实验前、容量超负荷组容量超负荷末和对照组维持左房压于6 mmHg后即刻、15 min、30 min动物血浆中BNP水平。结果容量超负荷组及对照组LVSP水平在该实验过程前后均未见明显变化,两组相比差异亦无统计学意义。容量超负荷组心肌经容量超负荷处理后测得即刻BNP水平较处理前明显增加,并且于容量超负荷处理末期升至最高点(269.17±17.78)pg/ml,于容量超负荷处理后30 min内恢复至处理前基线水平;对照组BNP水平则在整个实验前后无明显变化。容量超负荷组与对照组动物心电图监测在整个实验过程中均未见任何缺血和心律失常改变。结论心肌容量超负荷是引起生物体内脑钠肽分泌的一种最主要且直接的原因。

Objective To investigate whether myocardial volume overload is the direct cause of increased brain natriuretic peptide(BNP)secretion in vivo.Methods Ten healthy New Zealand rabbits were randomly divided into control group(n=5)and volume overload group(n=5).An experimental animal model of myocardial capacity overload was established.The control group only gave infusion and maintained the left atrial pressure at the average physiological level(6 mmHg).The electrocardiographic recorder was used to observe and monitor the changes of left ventricular systolic function(LVSP)and electrocardiogram at 15 minutes and 30 minutes after the two groups of pre-expansion and volume overload groups in the capacity overload(control group maintained left atrial pressure at 6 mmHg).Enzyme-linked immunosorbent assay(ELISA)was used to determine the BNP levels in the plasma of the two groups before the experiment,the capacity overload of the overload group and the control group to maintain the left atrial pressure at 6 mmHg immediately,15 minutes,30 minutes.Results There was no significant change in LVSP levels in the volume overload group and the control group before and after the experimental procedure.There was no significant difference between the two groups.Immediately after the capacity overload treatment,the myocardial volume of the overload group was significantly increased compared with that before treatment,and reached the highest point(269.17±17.78)pg/ml at the end of the capacity overload treatment,30 minutes after the capacity overload treatment.The internal recovery to the baseline level before treatment;the BNP level of the control group did not change significantly before and after the whole experiment.ECG monitoring of the volume overload group and the control group showed no changes in ischemia and arrhythmia throughout the experiment.Conclusion Myocardial volume overload is one of the most important and direct causes of brain natriuretic peptide secretion in vivo.