AJP - Heart Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Am J Physiol Heart Circ Physiol 256: H247-H255, 1989;
0363-6135/89 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
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 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 Swain, D. P.
Right arrow Articles by Pittman, R. N.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Swain, D. P.
Right arrow Articles by Pittman, R. N.

AJP - Heart and Circulatory Physiology, Vol 256, Issue 1 247-H255, Copyright © 1989 by American Physiological Society


ARTICLES

Oxygen exchange in the microcirculation of hamster retractor muscle

D. P. Swain and R. N. Pittman
Department of Physiology, Medical College of Virginia, Virginia Commonwealth University, Richmond 23298-0551.

We determined percent hemoglobin oxygen saturation (SO2) in arterioles and venules of the hamster retractor muscle at rest. We found that SO2 decreased from 69.9 +/- 1.4% (SE) in large input arterioles (first order, 1A, ID = 60 +/- 3 micron) to flow-weighted values of 56.7% in small arterioles (4A, ID = 20 +/- 1 micron), 51.3% in small venules (4V, ID = 28 +/- 1 micron), and to 50.6 +/- 1.0% in large venules (1V, ID = 147 +/- 13 micron). Thus approximately two-thirds of the net decline in SO2 for this tissue occurred by diffusion of oxygen from arterioles, whereas only about one-third occurred by diffusion from capillaries. Furthermore, no net shunting of oxygen from the arterioles to the venules was detected as evidenced by the absence of any significant change in venular SO2. By determining the SO2 at upstream and downstream ends of arterioles in four consecutive branching orders (1A-4A), we found that the decrease in SO2 per unit length (delta SO2/L) increased approximately 20-fold from 1A to 4A. This increase in delta SO2/L was directly proportional to estimated luminal minus tissue oxygen tension and inversely proportional to red blood cell flow.





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