AJP Legacy Track the topics, authors and articles important to you
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Am J Physiol 201: 791-794, 1961;
0002-9513/61 $5.00
This Article
Right arrow Full Text (PDF)
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 Google Scholar
Google Scholar
Right arrow Articles by Kanter, G. S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kanter, G. S.

Renal hemodynamics during hyperthermia caused by exposure to high environmental temperature

G. S. Kanter 1

1 Department of Physiology, Albany Medical College, Albany, New York

The GFR (glomerular filtration rate) and RPF (renal plasma flow), following an initial increase, fell significantly after 3–4 hr exposure of anesthetized dogs to an air temperature of 49 C. This alteration occurred with either dehydration or hydration present. Creatinine clearance was used as a measure of GFR and p-aminohippuric acid clearance at low plasma levels was used as a measure of RPF. Rectal temperature averaged 43 C at the conclusion of the experiment. The hematocrit increased 14%. The alteration in renal hemodynamics was shown to be due to a mild fall in mean systemic blood pressure, and a concomitant early decrease in intrarenal resistance followed a further decrease in blood pressure, combined with a progressively increasing intrarenal resistance. It can be concluded that while the fall in blood pressure, increasing intrarenal resistance during the latter part of the exposure, and decreased GFR and RPF are resultants of hyperthermia, the massive loss of plasma volume and increase in hematocrit previously reported in hyperthermia produced with heating pads (largely conductive heating) need not occur. Such major changes may be ascribed to tissue damage rather than to hyperthermia, per se.

Note:
With the Technical Assistance of R. H. Lubinski, I. M. Mielens, and J. Shorey

Submitted on November 2, 1960







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 1961 by the American Physiological Society.