AJP - Heart pressure measurements
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Am J Physiol Heart Circ Physiol 262: H84-H90, 1992;
0363-6135/92 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Buy
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 HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Yokota, J.
Right arrow Articles by Shires, G. T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Yokota, J.
Right arrow Articles by Shires, G. T.

AJP - Heart and Circulatory Physiology, Vol 262, Issue 1 84-H90, Copyright © 1992 by American Physiological Society


ARTICLES

Oxygen free radicals affect cardiac and skeletal cell membrane potential during hemorrhagic shock in rats

J. Yokota, J. J. Chiao and G. T. Shires
Department of Surgery, New York Hospital-Cornell Medical Center, New York 10021.

Oxygen free radical (OFR) damage of excitable cell membranes (heart and skeletal muscle) during hemorrhagic shock and after resuscitation was studied in control rats and in rats pretreated with superoxide dismutase (SOD) and catalase (CAT; 6,000 U each) before hemorrhage. Their mean arterial pressure (MAP) was lowered to and maintained at 45 mmHg until 30% of the shed blood was spontaneously reinfused. The remaining blood and twice that volume of lactated Ringer solution were then infused. Cardiac output and organ blood flow were measured by the microsphere technique. The resting membrane potential (Em) and tissue ATP content in the heart and skeletal muscle were determined. There was no significant difference between the control and SOD + CAT groups in shock duration, maximal shed blood, hemodynamics, regional blood flow, or in ATP content in both heart and skeletal muscle, both during shock and after resuscitation. Radical scavenger treatment did not prevent muscle depolarization during shock. After resuscitation, however, significant repolarization in hearts and skeletal muscle of the SOD + CAT group (heart, -70.0 +/- 1.1; muscle, -87.0 +/- 0.6 mV) was noted when compared with the controls (heart, -62.5 +/- 1.2; muscle, -82.7 +/- 1.1 mV; P less than 0.05). This implicates OFRs as mediators of excitable cell membrane injury following resuscitation.


This article has been cited by other articles:


Home page
Am. J. Respir. Crit. Care Med.Home page
M.-C. LIN, S. EBIHARA, Q. E. DWAIRI, S. N. A. HUSSAIN, L. YANG, S. B. GOTTFRIED, A. COMTOIS, and B. J. PETROF
Diaphragm Sarcolemmal Injury Is Induced by Sepsis and Alleviated by Nitric Oxide Synthase Inhibition
Am. J. Respir. Crit. Care Med., November 1, 1998; 158(5): 1656 - 1663.
[Abstract] [Full Text] [PDF]


Home page
Circ. Res.Home page
A. Bhatnagar
Electrophysiological Effects of 4-Hydroxynonenal, an Aldehydic Product of Lipid Peroxidation, on Isolated Rat Ventricular Myocytes
Circ. Res., February 1, 1995; 76(2): 293 - 304.
[Abstract] [Full Text]




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