Bowers P N, Tinney J P, Keller B B
NIH SCOR in Pediatric Cardiovascular Diseases, Strong Children's Research Center, University of Rochester School of Medicine and Dentistry, NY 14642, USA.
Cardiovasc Res. 1996 Feb;31 Spec No:E132-8.
Embryonic cardiovascular function is dynamically regulated at the tissue level. Nitric oxide (NO) regulates vascular tone and influences cardiovascular function in neonatal and mature circulations. However, the role of NO in regulating embryonic cardiovascular function is undefined. We hypothesized that NO released from nitroprusside alters embryonic vascular tone with secondary effects on ventricular function.
We measured ventricular pressure and calculated ventricular volume from area using ellipsoid geometry for 180 s after suffusion of 0.0, 0.1, 1.0, or 2.5 micrograms of nitroprusside in 10 microliters of KHB buffer, or after acute venous hemorrhage in stage 21 chick embryos (n > or = 8 per group). We plotted pressure-volume loops and analyzed standard parameters of cardiovascular function by ANOVA, regression analysis, and ANCOVA.
Following nitroprusside, heart rate was unchanged, end-diastolic volume (EDV), stroke volume (SV), and end-systolic pressure decreased (P < 0.05 at 180 s). For 1.0 microgram of nitroprusside, EDV decreased by 27 +/- 6%, SV decreased by 36 +/- 6%, and end-systolic pressure decreased by 28 +/- 3%. The EDV vs. SV relationship was unchanged with the exception of the 2.5 micrograms nitroprusside dose. Arterial elastance was unchanged with the exception of the 2.5 micrograms nitroprusside dose. The EDV vs. SV relationship and arterial elastance during preload reduction suggest that ventricular afterload did not decrease following NO.
In contrast to the mature circulation, NO reduced preload without decreasing ventricular afterload. Thus, vasoactive agents may have unique roles in the regulation of cardiovascular structure and function during embryogenesis.
胚胎心血管功能在组织水平受到动态调节。一氧化氮（NO）调节血管张力，并影响新生儿和成熟循环中的心血管功能。然而，NO在调节胚胎心血管功能中的作用尚不清楚。我们假设硝普钠释放的NO会改变胚胎血管张力，并对心室功能产生继发影响。
在10微升KHB缓冲液中注入0.0、0.1、1.0或2.5微克硝普钠后，或在第21阶段鸡胚急性静脉出血后（每组n≥8），我们测量心室压力，并使用椭圆几何形状从面积计算心室容积，持续180秒。我们绘制压力-容积环，并通过方差分析、回归分析和协方差分析来分析心血管功能的标准参数。
注入硝普钠后，心率不变，舒张末期容积（EDV）、每搏输出量（SV）和收缩末期压力降低（180秒时P<0.05）。对于1.0微克硝普钠，EDV降低27±6%，SV降低36±6%，收缩末期压力降低28±3%。除2.5微克硝普钠剂量外，EDV与SV的关系未发生变化。除2.5微克硝普钠剂量外，动脉弹性未发生变化。预负荷降低期间的EDV与SV关系和动脉弹性表明，NO作用后心室后负荷并未降低。
与成熟循环不同，NO降低了前负荷，但未降低心室后负荷。因此，血管活性药物在胚胎发育过程中对心血管结构和功能的调节可能具有独特作用。
