Isoprenaline was infused into in utero fetal lambs to examine the effect of this beta-adrenoceptor agonist on left ventricular stroke volume and left ventricular output and test the generally held assumption that the fetal ventricle is markedly limited in its ability to increase ventricular output. 2. Seven in utero lambs (121-133 days of gestation) were instrumented with left ventricular dimension transducers, an ascending aortic electromagnetic flow transducer, a brachiocephalic arterial catheter and electrocardiographic and atrial pacing electrodes. 3. On the day of study, 5-8 days following surgery and 129-137 days of gestation, each lamb received infusions of isoprenaline, via the superior vena cava or left atrium, at rates which ranged from 0.005-0.5 microgram kg-1 min-1. 4. Heart rate and left ventricular stroke volume, output and end-diastolic and end-systolic dimensions were measured under control conditions and during various levels of isoprenaline infusion, with and without controlling heart rate. 5. Analysis of variance was done using the mean cell model. Least-square means and standard errors of the least-square means are reported. F ratios were calculated from type III sums-of-squares; P less than 0.05 was considered significant. 6. The mean heart rate increased with isoprenaline (P less than 0.0001) from a mean control level of 169 +/- 8 to 281 +/- 9 beats min-1 (+/- S.E.M.). 7. Mean left ventricular end-diastolic and end-systolic minor axis dimensions decreased significantly with isoprenaline from 16.7 +/- 0.1 mm (control) to 15.7 +/- 0.2 mm (P less than 0.0004) and from 11.7 +/- 0.1 mm (control) to 10.4 +/- 0.2 mm (P less than 0.0001) respectively. When heart rate was controlled with atrial pacing, mean end-diastolic dimension increased significantly at the higher isoprenaline doses from 14.6 +/- 0.1 mm (control) to 15.3 +/- 0.2 mm (control) (P = 0.0002), while mean end-systolic dimension fell significantly from 10.9 +/- 0.1 to 10.5 +/- 0.1 mm (P less than 0.003). Inasmuch as stroke volume increased, the increase in end-diastolic dimension and the fall in end-systolic dimension indicate an increase in venous return to the left ventricle. 8. During spontaneous rhythm, isoprenaline increased stroke volume from 2.45 +/- 0.06 ml (control) to 2.63 +/- 0.09 ml, not statistically significant. When heart rate was controlled, stroke volume increased with isoprenaline dose from 1.68 +/- 0.06 ml (control) to 2.40 +/- 0.08 ml (P less than 0.0001).(ABSTRACT TRUNCATED AT 400 WORDS)
