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


     


Am J Physiol Regul Integr Comp Physiol 258: R684-R689, 1990;
0363-6119/90 $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
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 Chiao, J. J.
Right arrow Articles by Shires, G. T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Chiao, J. J.
Right arrow Articles by Shires, G. T.

AJP - Regulatory, Integrative and Comparative Physiology, Vol 258, Issue 3 684-R689, Copyright © 1990 by American Physiological Society


ARTICLES

In vivo myocyte sodium activity and concentration during hemorrhagic shock

J. J. Chiao, J. P. Minei, G. T. Shires 3rd and G. T. Shires
Department of Surgery, New York Hospital-Cornell Medical Center, New York 10021.

The increase in intracellular Na+ concentration ([ Na+]i) and H2O content and decrease in K+ concentration during hemorrhagic shock have been observed. However, the state of the increased [Na+]i has never been defined. In this investigation double-barreled Na(+)-selective microelectrodes were used to directly measure in vivo intracellular Na+ activity (alpha Na) in skeletal muscle cells during prolonged hemorrhagic shock. Resting membrane potential, [Na+]i, and H2O content were also studied concomitantly. Sustained hemorrhagic shock with metabolic acidosis was produced in 12 rabbits after removal of approximately 40% of estimated blood volume under light anesthesia. During prolonged shock, resting membrane potentials of skeletal muscle cells depolarized to -74.7 +/- 1.7 mV from a base-line value of -92.6 +/- 0.4 mV. [Na+]i increased to 14.22 +/- 0.45 mmol/l from a base-line value of 11.50 +/- 0.32 mmol/l. Intracellular H2O content also had a 2.2% increase, whereas levels of [K+]i and extracellular H2O content decreased significantly. However, alpha i(Na) remained unchanged (4.07 +/- 0.19 mmol/l in base line and 4.04 +/- 0.20 mmol/l during shock). This makes the intracellular apparent activity coefficient for Na+ fall significantly from 0.356 in base line to 0.286 during shock. This result indicates that the extra Na+ that diffused into cell because of membrane dysfunction was bound to the fixed charges and/or compartmentalized into subcellular organelles. The unchanged alpha i(Na) also indicates that the depolarization of resting membrane potentials during sustained severe hypovolemia was not caused by the increased [Na+]i. The increase in extracellular [K+] during shock could account for the fall of the resting membrane potentials.(ABSTRACT TRUNCATED AT 250 WORDS)





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