NITROPRUSSIDE SELECTIVELY REDUCES VENTRICULAR PRELOAD IN THE STAGE-21CHICK-EMBRYO

Objective: Embryonic cardiovascular function is dynamically regulated at the tissue level. Nitric oxide (NO) regulates vascular tone and inf luences cardiovascular function in neonatal and mature circulations. H owever, the role of NO in regulating embryonic cardiovascular function is undefined. We hypothesized that NO released from nitroprusside alt ers embryonic vascular tone with secondary effects on ventricular func tion. Methods: We measured ventricular pressure and calculated ventric ular volume from area using ellipsoid geometry for 180 s after suffusi on of 0.0, 0.1, 1.0, or 2.5 mu g of nitroprusside in 10 mu l of KHB bu ffer, or after acute venous hemorrhage in stage 21 chick embryos (n gr eater than or equal to 8 per group). We plotted pressure-volume loops and analyzed standard parameters of cardiovascular function by ANOVA, regression analysis, and ANCOVA. Results: Following nitroprusside, hea rt rate was unchanged, end-diastolic volume (EDV), stroke volume (SV), and end-systolic pressure decreased (P < 0.05 at 180 s). For 1.0 mu g of nitroprusside, EDV decreased by 27 +/- 6%, SV decreased by 36 +/- 6%, and end-systolic pressure decreased by 28 +/- 3%. The EDV vs, SV r elationship was unchanged with the exception of the 2.5 mu g nitroprus side dose. Arterial elastance was unchanged with the exception of the 2.5 mu g nitroprusside dose. The EDV vs. SV relationship and arterial elastance during preload reduction suggest that ventricular afterload did not decrease following NO. Conclusions: In contrast to the mature circulation, NO reduced preload without decreasing ventricular afterlo ad. Thus, vasoactive agents may have unique roles in the regulation of cardiovascular structure and function during embryogenesis.