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OtherCARDIOVASCULAR PHARMACOLOGY

Reduction of Myocardial Infarct Size In Vivo by Carbohydrate-Based Glycomimetics

Kenneth S. Kilgore, Elaine J. Tanhehco, James L. Park, Keith B. Naylor, Mark B. Anderson and Benedict R. Lucchesi
Journal of Pharmacology and Experimental Therapeutics January 1998, 284 (1) 427-435;
Kenneth S. Kilgore
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Elaine J. Tanhehco
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James L. Park
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Keith B. Naylor
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Mark B. Anderson
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Benedict R. Lucchesi
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Abstract

One of the foremost mechanisms involved in the pathogenesis of myocardial reperfusion injury is the adhesion of neutrophils within the myocardium. The initial neutrophil-endothelial cell interactions are mediated by the selectin family of adhesion molecules. Blockade of this group of adhesion molecules, through the use of synthetic carbohydrate analogs to the selectin ligand sialyl Lewisx and glycomimetics, has been beneficial in reducing neutrophil influx and infarct size. In the present study, glycyrrhizin (GM1292), a natural structural glycomimetic, was analyzed for the ability to decrease myocardial infarct size after regional myocardial ischemia/reperfusion. To determine the structural requirements for optimal cardioprotective activity, two additional compounds related to glycyrrhizin, GM3290 and GM1658 (glycyrrhetinic acid), were studied. The molecular structures of the latter two compounds differ in the number of glucuronic acid residues in their respective molecules. Open-chest, anesthetized rabbits were subjected to 30 min occlusion of the left coronary artery followed by 5 hr of reperfusion. Vehicle or glycomimetic (10 mg/kg/hr) was administered intravenously immediately before the onset of reperfusion and every hour during the reperfusion period. Myocardial infarct size in rabbits treated with GM1292 (two glucuronic acid residues) and GM3290 (one glucuronic acid residue) was reduced significantly when compared with vehicle-treated animals (P < .05). GM1658, which lacks glucuronic acid residues, did not provide a protective effect in vivo. The data suggest that GM1292 and GM3290, which contain carbohydrate moieties, are effective in reducing the degree of myocardial injury after an acute period of ischemia/reperfusion.

Footnotes

  • Send reprint requests to: Kenneth S. Kilgore, Ph.D., Department of Pharmacology, University of Michigan Medical School, 1301C Medical Science Research Building III, Ann Arbor, MI 48109-0632.

  • ↵1 This study was supported in part by a Grant #HL19782–16 from the National Institutes of Health, Heart, Lung and Blood Institute; and by a grant (36GB967) from the American Heart Association, Michigan Affiliate.

  • ↵2 Glycomed, Inc., Alameda, CA 94501.

  • Abbreviations:
    AAR
    area at risk
    HUVEC
    human umbilical vein endothelial cells
    ICAM-1
    intracellular adhesion molecule-1
    MPO
    myeloperoxidase
    Ni-LV
    non-infarcted tissue of left ventricle
    PBS
    phosphate buffered saline
    sLex
    sialyl Lewisx
    TTC
    triphenyltetrazolium chloride
    BCECF-AM
    2′,7′-bis-(2-carboxyethyl)-5(and 6)-carboxyfluorescein, acetoxymethyl
    • Received May 19, 1997.
    • Accepted September 8, 1997.
  • The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics
Vol. 284, Issue 1
1 Jan 1998
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OtherCARDIOVASCULAR PHARMACOLOGY

Reduction of Myocardial Infarct Size In Vivo by Carbohydrate-Based Glycomimetics

Kenneth S. Kilgore, Elaine J. Tanhehco, James L. Park, Keith B. Naylor, Mark B. Anderson and Benedict R. Lucchesi
Journal of Pharmacology and Experimental Therapeutics January 1, 1998, 284 (1) 427-435;

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OtherCARDIOVASCULAR PHARMACOLOGY

Reduction of Myocardial Infarct Size In Vivo by Carbohydrate-Based Glycomimetics

Kenneth S. Kilgore, Elaine J. Tanhehco, James L. Park, Keith B. Naylor, Mark B. Anderson and Benedict R. Lucchesi
Journal of Pharmacology and Experimental Therapeutics January 1, 1998, 284 (1) 427-435;
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