NDLI: Mechanism of Cardioprotective Effect of Adenocine and Non-Glycoside Cardiotonic Drugs during Experimental Chronic Cardiac Insufficiency

Content Provider	Springer Nature Link
Author	Sukoyan, G. V. Gongadze, N. V.
Copyright Year	2011
Abstract	The therapeutic action of adenocine during cardiac insufficiency (heart failure) caused by ischemic (stenosis) or reperfusion (removal of ligature) injury to the myocardium prevents depletion of ATP, the major energy source for myocytes in the right and left ventricles, and a drop in NAD/NADH ratio. The development of energy shortage during heart failure cannot be eliminated by β-acetyldigoxin, levosimendan, or milrinone: the content of ATP in the right and left ventricular myocardium remained below the normal level by 28 and 29%, 37 and 33%, 32 and 28%, respectively; the NAD/NADH ratio of the energy supply system in cardiomyocytes did not return to normal. Adenocine increased the content of NAD to the normal level in both the right and left ventricles, while it remained below the normal level after administration of β-acetyldigoxin (by 24 and 19.5%, respectively), levosimendan (by 27 and 29%), and milrinone (by 26 and 24%). In contrast to β-acetyldigoxin, levosimendan, and milrinone, adenocine inhibited activity of poly(ADP-ribose) polymerase in both ventricles. It is concluded that adenocine directly inhibits the key enzyme triggering apoptosis; we also hypothesized that this drug activates the regulatory and signal mechanisms arresting apoptotic alterations in the myocardium during heart failure.
Starting Page	610
Ending Page	613
Page Count	4
File Format	PDF
ISSN	00074888
Journal	Bulletin of Experimental Biology and Medicine
Volume Number	150
Issue Number	5
e-ISSN	15738221
Language	English
Publisher	Springer US
Publisher Date	2011-03-25
Publisher Place	Boston
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	cardiac insufficiency adenocine apoptosis bioenergetic insufficiency Internal Medicine Biomedicine general Cell Biology Laboratory Medicine Pathology
Content Type	Text
Resource Type	Article
Subject	Medicine Biochemistry, Genetics and Molecular Biology

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