Myocardial protection during ventricular fibrillation by reduction of proton-driven sarcolemmal sodium influx

Although the inhibition of proton-driven sarcolemmal sodium influx ameliorates ischemic injury in the quiescent myocardium, the effects when ventricular fibrillation is present are largely unknown. We used an isolated rat heart model to investigate whether inhibition of the sodium-hydrogen exchanger...

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Bibliographic Details
Published in:The Journal of laboratory and clinical medicine 2001-01, Vol.137 (1), p.43-55
Main Authors: Gazmuri, Raúl J., Hoffner, Elizabeth, Kalcheim, Jordan, Ho, Helen, Patel, Mukti, Ayoub, Iyad M., Epstein, Mike, Kingston, Skip, Han, Ye
Format: Article
Language:English
Subjects:
Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy
Animals
Biological and medical sciences
Buffers
Calcium - analysis
Carrier Proteins - antagonists & inhibitors
Carrier Proteins - metabolism
Emergency and intensive cardiocirculatory care. Cardiogenic shock. Coronary intensive care
Guanidines - pharmacology
Heart Rate - drug effects
HEPES - pharmacology
Intensive care medicine
Magnesium - analysis
Medical sciences
Membrane Proteins - antagonists & inhibitors
Membrane Proteins - metabolism
Myocardial Ischemia - drug therapy
Myocardial Ischemia - metabolism
Myocardium - chemistry
Myocardium - metabolism
Potassium - analysis
Protons
Rats
Rats, Sprague-Dawley
Sarcolemma - chemistry
Sarcolemma - metabolism
Sodium - analysis
Sodium - metabolism
Sodium-Bicarbonate Symporters
Sodium-Hydrogen Exchangers - antagonists & inhibitors
Sodium-Hydrogen Exchangers - metabolism
Sulfones - pharmacology
Ventricular Fibrillation - drug therapy
Ventricular Fibrillation - metabolism
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Summary:Although the inhibition of proton-driven sarcolemmal sodium influx ameliorates ischemic injury in the quiescent myocardium, the effects when ventricular fibrillation is present are largely unknown. We used an isolated rat heart model to investigate whether inhibition of the sodium-hydrogen exchanger isoform-1 (with the benzoylguanidine derivatives HOE-694 and cariporide) with or without concomitant inhibition of the sodium-bicarbonate co-transporter (with perfusate buffered with N-2-hydroxyethylpiperazine-N-2-ethanesulfonic acid [HEPES]) during ischemia and ventricular fibrillation could ameliorate functional myocardial abnormalities presumed to limit cardiac resuscitability. Ischemic contracture, which typically develops during ventricular fibrillation, was ameliorated by HOE-694 when either a bicarbonate-buffered (20 ± 7 mm Hg vs 15 ± 5 mm Hg, P
ISSN:0022-2143
1532-6543
DOI:10.1067/mlc.2001.111693