Bumetanide protects diabetic hearts from ischemic injury

R. Ramasamv, Saul Schaefer

Research output: Contribution to journalArticlepeer-review


Abnormalities in ion transport and pH regulation at the myocyte level may contribute to cardiovascular complications in diabetes, potentially due to impaired Na+-K+-ATPase activity and increased levels of intracellular sodium [Na]i via the Na+-K+-2Cr cotransporter. This hypothesis was tested by inhibiting the Na+-K+-2CI cotransporter with bumetanide in diabetic hearts prior to global ischemia. Changes in pH, ATP, phosphocreatine (PCr) were measured using 31P NMR spectroscopy; creatine kinase (CK) release was measured enzymatically as a marker of myocardial injury. Diabetic Bio-Bred (BB/W) rats (n=12) were removed from insulin therapy 24 hours before isolated heart experiments. Diabetic (DC) hearts and non-diabetic control (C) rats (n=6) were subjected to 20 min of control perfusion, 20 min of global ischemia and 60 min of reperfusion. Six BB/W hearts received bumetanide (DB) 10 min before ischemia. DB hearts had reduced CK release (126+27 vs 432±27 IU/gdw, p < 0.05), higher ATP levels during ischemia, and higher pH at the end of ischemia (DB: 6.42±0.03, DC: 6.03±0.02, C: 5.98±0.03, p <0.05) The rate of pH recovery on reperfusion in untreated diabetics was slower than either bumetanide/diabetics or controls. These findings are consistent with bumetanide reducing the inward flux of sodium, with resultant lowering of ATP requirements of the sodium pump, preservation of ATP and reduced acidosis.

Original languageEnglish (US)
JournalFASEB Journal
Issue number3
StatePublished - 1996

ASJC Scopus subject areas

  • Agricultural and Biological Sciences (miscellaneous)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Biochemistry
  • Cell Biology


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