Cardiac output in Xenopus laevis tadpoles during development and in response to an adenosine agonist.

We test the hypothesis that the heart and arteries enlarge with increased cardiac output (CO) during development and volume overload. Transparent albino tadpoles of Xenopus laevis at stages 43-50 were anesthetized in 0.3-0.5 mM benzocaine. Areas and radii [maximum and minimum radius (Rmax and Rmin, respectively)] of the ventricle were measured in digitized video frames during the cardiac cycle. Stroke volume (SV) and CO were calculated from Rmax and Rmin. Maximal velocities of 3.4-microns fluorescent beads were measured in the aortic arches. Arterial pressure was estimated by the Landis method. During normal development, the radii of the ventricle and aortic arch diameters increased with lengths of tadpoles, and SV (0.7 microliters/g) and CO (70 microliters.g-1.min-1) with wet weights. Volume overload was induced by a vasodilatory adenosine agonist 5'-N-ethylcarboxamidoadenosine (NECA) in the aquarium water. Acute (0.5-4 h) NECA significantly increased Rmax and heart rate. Chronic (> 1 wk) NECA significantly increased both Rmax and Rmin. SV and CO increased more than two times, blood pressures decreased, and specific vascular conductances increased more than five times. It is concluded that NECA increases CO in Xenopus tadpoles through a combination of increased filling and accelerated growth.