Nitroprusside selectively reduces ventricular preload in the stage 21 chick embryo

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.