| pubmed-article:2812894 | pubmed:abstractText | In the stage 24 chick embryo, a paced increase in heart rate reduces stroke volume, presumably by rate-dependent decrease in passive filling. We hypothesized that rate-dependent stroke volume reduction could be abolished by volume loading. Dorsal aortic blood velocity was measured with a 20 mHz pulsed-Doppler meter from a 0.75-mm piezoelectric crystal (eight embryos), and atri-oventricular velocity was simultaneously measured from the ventricular apex (six embryos). Sinus venosus pacing (stimuli of 1 ms duration and less than 4 mA) was performed at intrinsic rate (P:I) and at 150% of intrinsic rate (P:150%I). Volume loading was performed during P:150%I by intravenous injection of 7.5 microL of chick Ringer's solution. Using atrioventricular velocity profile, stroke volume was divided into the proportion due to passive (E-phase) and active (A-phase) filling. Stroke volume was compared during P:I, P:150%I, immediately (P:150%I') and 30 s after (P:150%I") volume loading. Data (mean +/- SEM) were compared by ANOVA. During pacing, stroke volume (mm2/cycle) decreased but increased after volume loading (I, 0.43 +/- 0.03; P:I, 0.37 +/- 0.03; P:150%I, 0.19 +/- 0.03; P:150%I', 0.24 +/- 0.05; P:150%I", 0.28 +/- 0.04 (p less than 0.005). During P:150%I, E-phase filing disappeared and was not restored by volume loading, whereas, A-phase filling diminished but was restored by volume loading. In stage 24 chick embryos, rate-dependent stroke volume decrease is reversed by volume loading that restores stroke volume due to an increase in active filling but not passive filling. Thus, even at rapid heart rate, the embryonic ventricle responds to volume loading, indicating that the Frank-Starling relationship functions during tachycardia in the embryonic heart. | lld:pubmed |
