Cardiac output in xenopus laevis tadpoles during development and in response to an adenosine agonist. Tang, Yen-Yee, and Carl M. Rovainen. Department of Cell Biology and Physiology, Washington University School of Medicine, St. Louis, MO 63110
APStracts 2:0269R, 1995.
We test the hypothesis that the heart and arteries enlarge with increased cardiac output during development and volume overload. Transparent albino tadpole of Xenopus laevis at stages 43-50 were anesthetized in 0.3-0.5 mM benzocaine. Areas and radii (Rmax, Rmin) of the ventricle were measured in digitized video frames during the cardiac cycle. Stroke volume (SV) and cardiac output (CO) were calculated from Rmax and Rmin. Maximal velocities of 3.4 [mu]m 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 [mu]l/gm) and CO (70 [mu]l/gm/min) with wet weights. Volume overload was induced by a vasodilatory adenosine agonist 5'-N-ethylcarboxamido-adenosine (NECA) in the aquarium water. Acute (0.5-4 hr) NECA significantly increased Rmax and heart rate. Chronic (&GT1 week) NECA significantly increased both Rmax and Rmin. SV and CO increased &GT2X, blood pressures decreased, and specific vascular conductances increased &GT5X. It is concluded that NECA increases cardiac output in Xenopus tadpoles through a combination of increased filling and accelerated growth.

Received 21 November 1994; accepted in final form 22 September
1995.
APS Manuscript Number R671-4.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 14 November 95