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 258: H1865-H1871, 1990;
0363-6135/90 $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 Engels, W.
Right arrow Articles by Van der Vusse, G. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Engels, W.
Right arrow Articles by Van der Vusse, G. J.

AJP - Heart and Circulatory Physiology, Vol 258, Issue 6 1865-H1871, Copyright © 1990 by American Physiological Society

ARTICLES

Ischemia and reperfusion induced formation of eicosanoids in isolated rat hearts

W. Engels, M. Van Bilsen, M. J. De Groot, P. J. Lemmens, P. H. Willemsen, R. S. Reneman and G. J. Van der Vusse
Department of Physiology, University of Limburg, Maastricht, The Netherlands.

Isolated, ejecting rat hearts, perfused with Krebs-Henseleit buffer, were exposed to various periods of global ischemia. Arachidonic acid (AA) accumulated significantly in the ischemic heart when the duration of ischemia exceeded 45 min. During 30 min of reperfusion, tissue levels of AA raised steadily to values of 10.5, 17.7, and 63.1 nmol/g, after 30, 45, and 60 min of ischemia, respectively. During reperfusion, significant amounts of AA metabolite prostacyclin (determined as stable metabolite 6-ketoprostaglandin F1 alpha, by radioimmunoassay and high-performance liquid chromatography) were released after 30, 45, and 60 min of ischemia. Beside prostacyclin, only small amounts of thromboxane B2 could be found during reperfusion. In contrast to increasing amounts of AA in reperfused tissue, prostacyclin release was maximal during the first 5 min of reperfusion and declined rapidly thereafter. Relatively small proportions of the accumulated AA are converted into prostacyclin, i.e., less than 1%. When hearts were treated with mepacrine, AA accumulation was almost completely abolished during 60 min of ischemia. The cumulative release of prostacyclin was found to be reduced to 134 pmol/g during 30 min of subsequent reperfusion. A close, rectilinear correlation could be established between AA accumulation and cumulative prostacyclin release during reperfusion. It is likely, however, that the site of bulk AA accumulation and that of conversion of AA into eicosanoids does not coincide in the ischemic and reperfused heart because of the low conversion rates of AA into prostacyclin and the different time courses of AA accumulation and prostacyclin production after reinstallation of flow.


This article has been cited by other articles:


Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
K. Shinmura, M. Nagai, K. Tamaki, M. Tani, and R. Bolli
COX-2-derived prostacyclin mediates opioid-induced late phase of preconditioning in isolated rat hearts
Am J Physiol Heart Circ Physiol, December 1, 2002; 283(6): H2534 - H2543.
[Abstract] [Full Text] [PDF]

Home page
 CirculationHome page
C.-Y. Xiao, A. Hara, K.-i. Yuhki, T. Fujino, H. Ma, Y. Okada, O. Takahata, T. Yamada, T. Murata, S. Narumiya, et al.
Roles of Prostaglandin I2 and Thromboxane A2 in Cardiac Ischemia-Reperfusion Injury: A Study Using Mice Lacking Their Respective Receptors
Circulation, October 30, 2001; 104(18): 2210 - 2215.
[Abstract] [Full Text] [PDF]


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