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