Transient Elevation of Glucose Increases Arrhythmia Susceptibility in Non-Diabetic Rat Trabeculae With Non-Uniform Contraction

• Miura Masahito

  Department of Clinical Physiology, Health Science, Tohoku University Graduate School of Medicine

• Handoh Tetsuya

  Department of Clinical Physiology, Health Science, Tohoku University Graduate School of Medicine

• Taguchi Yuhto

  Department of Clinical Physiology, Health Science, Tohoku University Graduate School of Medicine

• Hasegawa Taiki

  Department of Clinical Physiology, Health Science, Tohoku University Graduate School of Medicine

• Takahashi Yui

  Department of Clinical Physiology, Health Science, Tohoku University Graduate School of Medicine

• Morita Natsuki

  Department of Clinical Physiology, Health Science, Tohoku University Graduate School of Medicine

• Matsumoto Ayana

  Department of Clinical Physiology, Health Science, Tohoku University Graduate School of Medicine

• Shindoh Chiyohiko

  Department of Clinical Physiology, Health Science, Tohoku University Graduate School of Medicine

• Sato Haruka

  Department of Clinical Physiology, Health Science, Tohoku University Graduate School of Medicine

Abstract

Background:In non-diabetic patients with acute coronary syndrome, stress hyperglycemia occasionally occurs and is related to their mortality. Whether transient elevation of glucose affects arrhythmia susceptibility in non-diabetic hearts with non-uniform contraction was examined. Methods and Results:Force, intracellular Ca²⁺([Ca²⁺]_i), and membrane potential were measured in trabeculae from rat hearts. Non-uniform contraction was produced by a jet of paralyzing solution. Ca²⁺waves and arrhythmias were induced by electrical stimulation (2.0 mmol/L [Ca²⁺]_o). The activity of Ca²⁺/calmodulin-dependent protein kinaseII (CaMKII) was measured. An elevation of glucose from 150 to 400 mg/dL increased the velocity of Ca²⁺waves and the number of spontaneous action potentials triggered by electrical stimulation. Besides, the elevation of glucose increased the CaMKII activity. In the presence of 1 μmol/L KN-93, the elevation of glucose did not increase the velocity of Ca²⁺waves and the number of triggered action potentials. In addition, in the presence of 1 μmol/L autocamtide-2 related inhibitory peptide or 50 μmol/L diazo-5-oxonorleucine, the elevation of glucose did not increase the number of triggered action potentials. Furthermore, the elevation of glucose by adding L-glucose did not increase their number. Conclusions:In non-diabetic hearts with non-uniform contraction, transient elevation of glucose increases the velocity of Ca²⁺waves by activating CaMKII,probably through glycosylation with O-linked β-N-acetylglucosamine, thereby increasing arrhythmia susceptibility.

Journal

• Circulation Journal

  Circulation Journal 84 (4), 551-558, 2020-03-25

  The Japanese Circulation Society

Keywords

• Arrhythmia
• Calcium wave
• Glucose

Details

• CRID: 1390283659863041280
• NII Article ID: 130007815608
• NII Book ID: AA11591968
• DOI: 10.1253/circj.cj-19-0715
• ISSN: 13474820
• ISSN: 13469843
• NDL BIB ID: 030332835
• PubMed: 32092718
• Web Site: https://ndlsearch.ndl.go.jp/books/R000000004-I030332835
• Web Site: https://www.jstage.jst.go.jp/article/circj/84/4/84_CJ-19-0715/_pdf
• Web Site: https://search.jamas.or.jp/link/ui/2020343389
• Text Lang: en
• Data Source:
  • JaLC
  • NDL
  • Crossref
  • PubMed
  • CiNii Articles
  • KAKEN
• Abstract License Flag: Disallowed