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AJP - Regulatory, Integrative and Comparative Physiology, Vol 266, Issue 2 321-R327, Copyright © 1994 by American Physiological Society
ARTICLES |
J. A. Carrithers, F. Liu, H. W. Shirer and J. A. Orr
Department of Physiology and Cell Biology, University of Kansas, Lawrence 66045.
These experiments were designed to determine if intravenous infusion of the thromboxane A2 mimetic, U-46,619, would elicit tachypnea in the rabbit, and if so whether the afferent signal was generated by receptors innervated by myelinated or unmyelinated vagal nerve fibers. Intravenous infusion of U-46,619 (0.5 microgram/kg delivered over 10 s) increased breathing frequency (26%) and right ventricular blood pressure (59%) in the anesthetized rabbit (n = 10). Systemic arterial blood pressure, heart rate, and tidal volume were unaffected by the infusion of U-46,619. When myelinated fiber conduction in the vagus nerve was eliminated by bilaterally cooling the nerve to 6 degrees C, the increase in breathing frequency was only 5% above baseline levels. The tachypneic response to U-46,619 was totally eliminated when both myelinated and unmyelinated fiber conduction was abolished by cooling the vagi to 0 degree C. The increase in right ventricular blood pressure after U-46,619 infusion was unaffected by vagal cooling. Because most (> 80%) of the tachypneic response to U-46,619 was eliminated by blockade of myelinated vagal fiber conduction, we conclude that the tachypneic response to U-46,619 is mediated mostly by receptors innervated by myelinated vagal afferent fibers in the anesthetized rabbit.
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