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 259: R849-R856, 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 HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by White, F. C.
Right arrow Articles by Merhoff, E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by White, F. C.
Right arrow Articles by Merhoff, E.

AJP - Regulatory, Integrative and Comparative Physiology, Vol 259, Issue 4 849-R856, Copyright © 1990 by American Physiological Society

ARTICLES

Responses of harbor seal and pig heart to progressive and acute hypoxia

F. C. White, R. Elsner, D. Willford, E. Hill and E. Merhoff
Department of Pathology, School of Medicine, University of California, San Diego, La Jolla 92093.

Myocardial oxidative and glycolytic reserves were evaluated in four harbor seals, Phoca vitulina richardsi, and six domestic pigs, Sus scrofa (hematocrits: 58 +/- 5 and 34 +/- 1%., respectively). Progressive hypoxia was induced by lowering arterial hemoglobin-oxygen saturation in 10% decrements, each maintained for 10-min periods, until the onset of heart failure. Myocardial oxygen consumption rate (VO2), lactate release/uptake rate (L), and triple product, an index of myocardial energetic demand, were determined at each saturation level. Onset of L began in pigs at Sao2 = 57 +/- 5% and in seals at Sao2 = 35 +/- 4%. Cumulative oxygen consumption (VO2) during hypoxia, determined from the onset of cardiac lactate release, was 435 ml O2/100 g in seals and 172 ml O2/100 g in pigs. Cumulative lactate release during the same period was 14 mM/100 g in seals and 4.6 mM/100 g in pigs. The pigs' left ventricular contractile response (dP/dtmax) was greater than that of seals throughout the time of lactate release. Total myocardial energetic sources were higher in seals than in pigs, and seals were better able to tolerate myocardial hypoxia than were pigs. In a separate experiment, two seals and six pigs were made acutely hypoxic until cessation of cardiac output (seals, 17.5 min; pigs, 7.4 min) and were then reoxygenated. Both seals recovered promptly to control levels of cardiac mechanical function, whereas none of the pigs recovered. Additionally, five pigs were beta-blocked with 0.10 mg/kg of propranolol and were subjected to acute hypoxia. Tolerance to cardiac hypoxia in beta-blocked pigs was significantly increased compared with that of control animals.(ABSTRACT TRUNCATED AT 250 WORDS)


This article has been cited by other articles:


Home page
 J. Appl. Physiol.Home page
S. B. Kanatous, R. Elsner, and O. Mathieu-Costello
Muscle capillary supply in harbor seals
J Appl Physiol, May 1, 2001; 90(5): 1919 - 1926.
[Abstract] [Full Text] [PDF]


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