Journal of Applied Physiology Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


J Appl Physiol 45: 521-527, 1978;
8750-7587/78 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Wright, G.
Right arrow Articles by Toraason, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Wright, G.
Right arrow Articles by Toraason, M.

Journal of Applied Physiology, Vol 45, Issue 4 521-527, Copyright © 1978 by American Physiological Society


ARTICLES

Cardiovascular effects of whole-body heating in spontaneously hypertensive rats

G. Wright, E. Knecht and M. Toraason

The cardiovascular response to severe whole-body heating was examined in anesthetized spontaneously hypertensive (SH) (mean BP = 140 Torr) and normotensive (N) rats (mean BP = 96 Torr). Elevation of colonic temperature to 44 degrees C resulted in an initial increase in arterial pressure (mean BP: SH = 199 Torr, N = 124 Torr) with a subsequent severe hypotension. There was little evidence to suggest that this collapse in systemic pressure was related to a direct heat impairment of cardiac function. It was more likely the result of a progressive venodilation which produced venous pooling and decreased venous return. The arterial blood pressure response to exogenous catecholamine challenge decreased at elevated temperatures. This suggests that there was a deterioration of the vasoconstrictor response and indicated a possible effect of heat at the receptor or effector level. There were significant differences between the responses of normotensive and hypertensive rats to whole-body heating suggesting an enhanced cardiovascular sensitivity in hypertensive rats that may partially explain earlier reports of inferior thermoregulation and heat intolerance in these animals.


This article has been cited by other articles:


Home page
Toxicol Ind HealthHome page
K.-S. You, M.-H. Lee, and K. H. Park
A rat model to evaluate the pesticide permeability and stress effects of protective clothing
Toxicology and Industrial Health, February 1, 2005; 21(1-2): 49 - 55.
[Abstract] [PDF]


Home page
J. Appl. Physiol.Home page
K. L. Ryan, M. R. Tehrany, and J. R. Jauchem
Nitric oxide does not contribute to the hypotension of heatstroke
J Appl Physiol, March 1, 2001; 90(3): 961 - 970.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online