Reperfusion-induced arrhythmias and lethality are reduced by a 2KDa heparin fragment |
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| Institution: | 1. Department of Cell and Molecular Pharmacology and Experimental Therapeutics, Medical University of South Carolina, 70 President Street, DDB410, Charleston, SC 29425, United States;2. Department of Pharmaceutical and Biomedical Sciences, Medical University of South Carolina, 274 Calhoun Street, MSC141, Charleston, SC 29425, United States;1. Department of Molecular and Cellular Physiology, Stanford University School of Medicine, Stanford, CA 94305, USA;2. Graduate School of Pharmaceutical Sciences, Tohoku University, 6-3, Aoba, Aramaki, Aoba-ku, Sendai, Miyagi 980-8578, Japan;3. Department of Cellular and Molecular Pharmacology, University of California, San Francisco, School of Medicine, San Francisco, CA 94158, USA;4. Department of Psychiatry, University of California, San Francisco, School of Medicine, San Francisco, CA 94158, USA;5. Department of Structural Biology, Stanford University School of Medicine, Stanford, CA 94305, USA;6. Howard Hughes Medical Institute, Stanford University School of Medicine, Stanford, CA 94305, USA;1. Klinik für Innere Medizin III, Universitätsklinikum des Saarlandes, 66421 Homburg, Germany;2. Department of Biophysics, CIPMM, School of Medicine, Saarland University, 66421 Homburg, Germany;3. Johns Hopkins University, Baltimore, MD 21218, USA;4. Department of Structural Biology, Saarland University, 66421 Homburg, Germany;5. Department of Cell and Developmental Biology, University College London, London WC1E 6BT, UK;6. Department of Physics and Astronomy, University College London, London WC1E 6BT, UK;7. The Hatter Cardiovascular Institute, University College London, London WC1E 6BT, UK;8. Institut für Zellbiologie, Universität des Saarlandes, 66421 Homburg, Germany;9. Klinik für Allgemeine und Interventionelle Kardiologie, Universitäres Herzzentrum Hamburg, 20246 Hamburg, Germany;10. Deutsches Zentrum für Herzkreislaufforschung (DZHK e.V.), Partner Site Hamburg/Lübeck/Kiel, Germany;1. Section of Cardiology, Department of Medicine, Huddinge, Karolinska Institutet, and Department of Cardiology, Karolinska University Hospital, Stockholm, Sweden;2. Department of Clinical Sciences, Danderyd University Hospital, Karolinska Institutet, Stockholm, Sweden;3. Uppsala Clinical Research Center and Department of Medical Sciences, Uppsala University, Uppsala, Sweden;1. Guang’an Men Hospital, China Academy of Chinese Medicine, Beijing 100053, China;2. LongHua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200032, China |
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| Abstract: | The influence of a low molecular weight heparin (Oligo-H, m.w. 2KDa) on ventricular arrhythmias and lethality induced by heart reperfusion following a 5 min coronary occlusion was studied in anesthetized rats. Both intravenous (i.v.) and subcutaneous (s.c.) injection of the compound doseand time-dependently prevented the reperfusion syndrome: in all salinepretreated animals post-ischemic reperfusion induced ventricular tachycardia (VT), which degenerated into ventricular fibrillation (VF) in 25 out of 30 rats, with a mortality rate of 73%; on the other hand, in rats I.V. Or s.c. pretreated with Oligo-H (20 mg/kg, 30 and 90 min, respectively, before coronary occlusion), VT occurred in 4 out of 10–11 animals and degenerated into VF in 2–3 out of 10–11 animals, with a mortality rate of 18–20%. Even more effective was a low molecular weight dermatan sulfate (Oligo-Ds, M.w. 2.1KDa). In rats treated with lidocaine, used as reference compound, at the dose of 5 mg/kg i.v. 10 min before coronary occlusion, VT occurred in 2 out of 10 animals and degenerated into VF in 1 out of 10 animals, with a mortality rate of 10%. It is concluded that low molecular weight glycosaminoglycans significantly reduce the consequences of heart reperfusion. |
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