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This Article Full Text Full Text (PDF) All Versions of this Article: 288/6/R1783    most recent 00524.2004v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (3) Citing Articles via Google Scholar Google Scholar Articles by Whyte, D. G. Articles by Johnson, A. K. Search for Related Content PubMed PubMed Citation Articles by Whyte, D. G. Articles by Johnson, A. K.

NEUROHUMORAL CONTROL OF CARDIOVASCULAR FUNCTION

Lesions of the anteroventral third ventricle region (AV3V) disrupt cardiovascular responses to an elevation in core temperature

Departments of ¹Physiology and Biophysics, Psychology, Pharmacology, Exercise Science, and ²the Cardiovascular Center, University of Iowa, Iowa City

Submitted 2 August 2004 ; accepted in final form 7 January 2005

Blood flow is redistributed from the viscera to the periphery during periods of heat stress to maximize heat loss. The heat-induced redistribution of blood flow is strongly influenced by nonthermal inputs such as hydration status. At present, little is known about where thermal and nonthermal information is integrated to generate an appropriate effector response. Recently, the periventricular tissue that surrounds the anteroventral third ventricle (AV3V) has been implicated in the integration of thermal and osmotic information. The purpose of the present study was to determine the effects of electrolytic lesions of the AV3V on the cardiovascular response to a passive heat stress in unanesthetized, free-moving male Sprague-Dawley rats. Core temperature was elevated at a constant rate of 0.03°C/min in sham- and AV3V-lesion rats using an infrared heat lamp. Changes in mesenteric and hindquarter vascular resistance were determined using Doppler flow probes, and heat-induced salivation was estimated using the spit-print technique. The rise in mean arterial pressure (MAP), heart rate (HR), and mesenteric resistance in response to elevations in core temperature were all attenuated in AV3V-lesion rats; however, hindquarter resistance was unaffected. Heat-induced salivation was also diminished. In addition, AV3V-lesion rats were more affected by the novelty of the experimental environment, resulting in a higher basal core temperature, HR, and MAP. These results indicate that AV3V lesions disrupt the cardiovascular and salivatory response to a passive heat stress in rats and produce an exaggerated stress-induced fever triggered by a novel environment.

thermoregulation; mesenteric resistance; Doppler flowmetry; salivation; novel environment

This article has been cited by other articles:

				D. G. Whyte and A. K. Johnson Lesions of the anteroventral third ventricle region exaggerate neuroendocrine and thermogenic but not behavioral responses to a novel environment Am J Physiol Regulatory Integrative Comp Physiol, January 1, 2007; 292(1): R137 - R142. [Abstract] [Full Text] [PDF]