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Nicholas S. Assali Perinatal Research Laboratory, Department of Obstetrics and Gynecology, and Brain Research Institute, University of California Los Angeles School of Medicine, Los Angeles, California 90095-1740
CGS-21680 (CGS), a highly selective
adenosine A2a receptor agonist,
may excite the fetal carotid bodies. This study was
designed to determine 1) whether CGS
stimulates fetal breathing and 2) whether sinoaortic denervation abolishes CGS-induced
tachycardia. In eight intact fetuses (>0.8 term),
intra-arterial CGS infusion (6 µg · min
1 · kg
estimated fetal
wt1)
increased mean arterial PCO2 by
3-7 Torr, reduced fetal arterial
PO2 by 2-5 Torr, and produced a
mild metabolic acidemia. Heart rate increased from 154 ± 7 (control) to 249 ± 12 beats/min, but mean arterial pressure was not
significantly affected. CGS initially increased the
frequency, amplitude, and incidence of fetal breathing, but this
hyperpnea was followed by prolonged respiratory depression that was not
reversed with blockade of adenosine
A1 receptors. Denervation of both
carotid bodies together with interruption of the vagi abolished the
hyperpnea without altering the respiratory depression or the maximum
rise in heart rate. We conclude that CGS induces
1) tachycardia by a mechanism
independent of the peripheral arterial chemoreceptors, 2) hyperpnea by stimulating
peripheral adenosine A2a
receptors, and 3) respiratory
depression by activating central
A2a receptors.
CGS-21680; chemoreceptors; heart rate; metabolism; respiration
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