Document Detail

Effect of ATP synthesis promoters on postischemic myocardial recovery.
MedLine Citation:
PMID:  2395365     Owner:  NLM     Status:  MEDLINE    
The use of cardioplegia during surgically induced ischemia greatly reduces myocardial metabolic requirements. However, adenosine triphosphate (ATP) depletion may occur, resulting in poor functional recovery after ischemia. This study investigated if augmentation of intracellular ATP could be achieved by delivering known ATP synthesis promoters (adenosine and/or phosphate) during cardioplegic arrest, and whether this could enhance myocardial functional and metabolic recovery following ischemia. Isolated, perfused rabbit hearts were subjected to 120 min of hypothermic (34 degrees C) cardioplegia-induced ischemia. Controls received St. Thomas cardioplegia (CTL); remaining hearts received cardioplegia containing 200 microM adenosine (ADO), or 25 microM phosphate (PO4), or both ADO and PO4. Following ischemia and reperfusion, recovery of developed pressure (%DP) and postischemic diastolic stiffness was significantly better in adenosine hearts when compared with control or PO4 hearts. To determine if ADO or PO4 minimized depletion of ATP during ischemia or accelerated synthesis of ATP in the postischemic period, nucleotide levels were obtained before, during, and after ischemia. During ischemia, ATP fell equally in all groups, indicating that ADO and PO4 did not alter ischemia-induced depletion of ATP. However, intracellular adenosine was augmented during ischemia in adenosine-treated hearts. Consequently, during reperfusion, ADO and ADO/PO4 hearts had significantly enhanced ATP levels, suggesting that augmenting myocardial adenosine accelerated synthesis of ATP postischemia. The addition of phosphate, a stimulus for ATP synthesis, did not augment postischemic ATP. In fact, the beneficial effect of adenosine may have been decreased when phosphate was added to adenosine. In conclusion, adenosine but not PO4 augments intracellular ATP by allowing better metabolic repletion following ischemia, thereby improving postischemic myocardial functional recovery.
S F Bolling; L E Bies; E L Bove
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The Journal of surgical research     Volume:  49     ISSN:  0022-4804     ISO Abbreviation:  J. Surg. Res.     Publication Date:  1990 Sep 
Date Detail:
Created Date:  1990-10-05     Completed Date:  1990-10-05     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  0376340     Medline TA:  J Surg Res     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  205-11     Citation Subset:  IM    
Section of Thoracic Surgery, University of Michigan Medical Center, Ann Arbor 48109.
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MeSH Terms
Adenosine / pharmacology*
Adenosine Triphosphate / biosynthesis*
Heart Arrest, Induced*
Myocardial Reperfusion
Myocardium / metabolism*
Phosphates / pharmacology*
Ventricular Function
Reg. No./Substance:
0/Phosphates; 56-65-5/Adenosine Triphosphate; 58-61-7/Adenosine

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