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


     


J Appl Physiol 99: 1272-1277, 2005; doi:10.1152/japplphysiol.00428.2005
8750-7587/05 $8.00
This Article
Right arrow Full Text Free
Right arrow Full Text (PDF) Free
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
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
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 ISI Web of Science (1)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Rogers, J.
Right arrow Articles by Sheriff, D. D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Rogers, J.
Right arrow Articles by Sheriff, D. D.

Is there a threshold duration of vascular occlusion for hindlimb reactive hyperemia?

Jennifer Rogers and Don D. Sheriff

Department of Exercise Science, The University of Iowa, Iowa City, Iowa

Submitted 15 April 2005 ; accepted in final form 21 May 2005

Relatively brief changes in perfusion pressure and flow through arterioles occur in a number of conditions, such as in the flying environment and during such common everyday activities such as bending forward at the waist. Also, brief periods of negative vertical acceleration (Gz) stress, which reduces perfusion in the lower body, has been shown to impair the regulation of arterial pressure during subsequent positive Gz stress. To examine the contribution that reactive hyperemia makes in these settings, studies on the hindlimb circulation of anesthetized rats (n = 8) were carried out by imposing graded duration vascular occlusion (1, 2, 4, 10, and 30 s) to test the hypothesis that there is a threshold duration of reduction in perfusion that must be exceeded for reactive hyperemia to be triggered. Vascular conductance responses to 1 s of terminal aortic occlusion were no different before and after myogenic responses were blocked with nifedipine, indicating that 1 s of occlusion failed to elicit reactive hyperemia. Two seconds of occlusion elicited a small but significant elevation in hindlimb vascular conductance. The magnitude of the reactive hyperemia was graded in direct relation to the duration of occlusion for the 2-, 4-, and 10-s periods of occlusion and appeared to be approaching a plateau for the 30-s occlusion. Thus there is a threshold duration of terminal aortic occlusion (~2 s) required to elicit reactive hyperemia in the hindlimbs of anesthetized rats, and the reactive hyperemia that results possesses a threat to the regulation of arterial pressure.

rat; blood flow; blood pressure regulation



Address for reprint requests and other correspondence: D. D. Sheriff, Dept. of Exercise Science, Univ. of Iowa, 424 Field House, Iowa City, IA 52242.don-sheriff{at}uiowa.edu




This article has been cited by other articles:


Home page
J. Appl. Physiol.Home page
D. D. Sheriff, I.-H. Nadland, and K. Toska
Hemodynamic consequences of rapid changes in posture in humans
J Appl Physiol, August 1, 2007; 103(2): 452 - 458.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 2005 by the American Physiological Society.