AJP - Heart Calcium Transients and Cell-Sarcomere
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Heart Circ Physiol 269: H734-H742, 1995;
0363-6135/95 $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 HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Decking, U. K.
Right arrow Articles by Kammermeier, H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Decking, U. K.
Right arrow Articles by Kammermeier, H.

AJP - Heart and Circulatory Physiology, Vol 269, Issue 2 734-H742, Copyright © 1995 by American Physiological Society

ARTICLES

Hypoxia-induced activation of KATP channels limits energy depletion in the guinea pig heart

U. K. Decking, T. Reffelmann, J. Schrader and H. Kammermeier
Institut fur Herz und Kreislaufphysiologie, Heinrich-Heine-Universitat Dusseldorf, Germany.

The functional role of ATP-dependent potassium (KATP) in hypoxic cardiac failure was investigated in isolated guinea pig hearts with glibenclamide and rimalkalim as inhibitor and activator, respectively. Monophasic action potential duration at 90% of repolarization (MAP50), left ventricular function, and cardiac energy status (31P nuclear magnetic resonance spectroscopy) were measured during normotoxic (95% O2) and hypoxic (20% O2) perfusion. In normoxic hearts, 1 microM glibenclamide did not affect MAP50, left ventricular function, and coronary flow (n = 4). In contrast, rimalkalim rapidly shortened MAP50 and left ventricular pressure (LVP) in a dose-dependent fashion (e.g., by 60.2 +/- 3.5 and 80.8 +/- 8.2%, respectively, with 0.6 microM rimalkalim). This latter effect was reversed by 1 microM (glibenclamide (n = 4). With hypoxic perfusion, a reduction in LVP was observed, along with a shortening of the action potential (MAP90; 202 +/- 13 vs. 164 +/- 9 ms) and an increase in coronary flow. Glibenclamide (1 microM) reversed the MAP90 shortening and the increase in coronary flow. In addition, glibenclamide increased LVP transiently (n = 4). When coronary flow of hypoxic hearts was kept constant, however, glibenclamide elicited a sustained positive inotropic effect (n = 7). After glibenclamide, an increase in LVP from 54 +/- 4 to 64 +/- 3 mmHg was observed, along with a reduction in the free energy change of ATP hydrolysis from -54.5 +/- 1.9 to -52.9 +/- 0.2 nJ/mol and a further increase in the coronary venous adenosine from 269 +/- 48 to 1,680 +/- 670 nmol/l.(ABSTRACT TRUNCATED AT 250 WORDS)


This article has been cited by other articles:


Home page
 J. Appl. Physiol.Home page
K. Schulze, C. Duschek, R. D. Lasley, and R. Bunger
Adenosine enhances cytosolic phosphorylation potential and ventricular contractility in stunned guinea pig heart: receptor-mediated and metabolic protection
J Appl Physiol, March 1, 2007; 102(3): 1202 - 1213.
[Abstract] [Full Text] [PDF]

Home page
 HeartHome page
T Reffelmann, H G Klues, P Hanrath, and E R Schwarz
Post-stenotic coronary blood flow at rest is not altered by therapeutic doses of the oral antidiabetic drug glibenclamide in patients with coronary artery disease
Heart, January 1, 2002; 87(1): 54 - 60.
[Abstract] [Full Text] [PDF]

Home page
 J. Thorac. Cardiovasc. Surg.Home page
F. Monti, K. Iwashiro, S. Picard, A. Criniti, S. La Francesca, G. Ruvolo, U. Papalia, P. P. Campa, B. Marino, and P. E. Puddu
ADENOSINE TRIPHOSPHATE-DEPENDENT POTASSIUM CHANNEL MODULATION AND CARDIOPLEGIA-INDUCED PROTECTION OF HUMAN ATRIAL MUSCLE IN AN IN VITRO MODEL OF MYOCARDIAL STUNNING
J. Thorac. Cardiovasc. Surg., April 1, 2000; 119(4): 842 - 848.
[Abstract] [Full Text] [PDF]

Home page
 Physiol. Rev.Home page
G. HEUSCH
Hibernating Myocardium
Physiol Rev, October 1, 1998; 78(4): 1055 - 1085.
[Abstract] [Full Text] [PDF]

Home page
 FASEB J.Home page
P. P. Dzeja and A. Terzic
Phosphotransfer reactions in the regulation of ATP-sensitive K+ channels
FASEB J, May 1, 1998; 12(7): 523 - 529.
[Abstract] [Full Text]

Home page
 Cardiovasc ResHome page
M. Kelm, S. Schafer, R. Dahmann, B. Dolu, S. Perings, U. K.M Decking, J. Schrader, and B. E Strauer
Nitric oxide induced contractile dysfunction is related to a reduction in myocardial energy generation
Cardiovasc Res, November 1, 1997; 36(2): 184 - 194.
[Abstract] [Full Text] [PDF]

Home page
 Circ. Res.Home page
U. K. M. Decking, G. Schlieper, K. Kroll, and J. Schrader
Hypoxia-Induced Inhibition of Adenosine Kinase Potentiates Cardiac Adenosine Release
Circ. Res., August 19, 1997; 81(2): 154 - 164.
[Abstract] [Full Text]

Home page
 J. Biol. Chem.Home page
J. R. Elvir-Mairena, A. Jovanovic, L. A. Gomez, A. E. Alekseev, and A. Terzic
Reversal of the ATP-liganded State of ATP-sensitive K+ Channels by Adenylate Kinase Activity
J. Biol. Chem., December 13, 1996; 271(50): 31903 - 31908.
[Abstract] [Full Text] [PDF]

Home page
 J. Thorac. Cardiovasc. Surg.Home page
M. Yamashita, R. A. Schmid, S. Fujino, J. D. Cooper, and G. A. Patterson
NICORANDIL, A POTENT ADENOSINE TRIPHOSPHATE-SENSITIVE POTASSIUM-CHANNEL OPENER, AMELIORATES LUNG ALLOGRAFT REPERFUSION INJURY
J. Thorac. Cardiovasc. Surg., November 1, 1996; 112(5): 1307 - 1314.
[Abstract] [Full Text]


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