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


     


J Appl Physiol 79: 214-221, 1995;
8750-7587/95 $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 Shrier, I.
Right arrow Articles by Magder, S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Shrier, I.
Right arrow Articles by Magder, S.

Journal of Applied Physiology, Vol 79, Issue 1 214-221, Copyright © 1995 by American Physiological Society


ARTICLES

Pressure-flow relationships in in vitro model of compartment syndrome

I. Shrier and S. Magder
Herzl Family Practice Centre, Sir Mortimer B. Davis Jewish General Hospital, Montreal, Quebec, Canada.

Compartment syndrome is a condition in which an increase in intramuscular pressure decreases blood flow to skeletal muscle. According to the Starling resistor (i.e., vascular waterfall) model of blood flow, the decrease in flow could occur through an increase in arterial resistance (Rart) or an increase in the critical closing pressure (Pcrit). To determine which explains the decrease in flow, we pump perfused a canine gastrocnemius muscle placed within an airtight box, controlled box pressures (Pbox) so that flow ranged from 100 to 50%, and measured Pcrit, Rart, arterial compliance, small venular pressure (measured by the double-occlusion technique), and venous pressure. An increase in Pbox limited flow mainly through an increase in Pcrit (75-85%), with only small changes in Rart (15-25%) and no change in arterial compliance. Increases in Pbox also produced a vascular waterfall in the venous circulation, but small venular transmural pressure always remained less than control levels. We conclude that increases in Pbox mostly limit blood flow through increases in Pcrit and that Rart plays a minor role. Transmural pressure across the small venules decreases with increases in intramuscular pressure, which contradicts the currently held belief that compartment syndrome is due to a cycle of swelling-ischemia-swelling.


This article has been cited by other articles:


Home page
Am. J. Physiol. Heart Circ. Physiol.Home page
J.-J. Wang, N. G. Shrive, K. H. Parker, and J. V. Tyberg
Effects of vasoconstriction and vasodilatation on LV and segmental circulatory energetics
Am J Physiol Heart Circ Physiol, March 1, 2008; 294(3): H1216 - H1225.
[Abstract] [Full Text] [PDF]


Home page
J. Appl. Physiol.Home page
I. Shrier, A. Baratz, and S. Magder
Effects of adenosine on pressure-flow relationships in an in vitro model of compartment syndrome
J Appl Physiol, March 1, 1997; 82(3): 755 - 759.
[Abstract] [Full Text] [PDF]




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