Why the study?
Does phosphocreatine depletion by beta-guanidinopropionate impair mechanical function and ATP homeostasis in rats after myocardial infarction?
Population
Rats subjected to sham operation or left coronary artery ligation (MI) to induce a heart failure model
Comparison
Feeding with 1% beta-guanidinopropionate for 8… vs 0% GP feeding (Sham or MI)
Design
Preclinical
Follow-up
8 weeks
Authors
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Severe PCr depletion precludes post-MI survival in rats; leaves open whether CK modulation affects human outcomes.
Does phosphocreatine depletion by beta-guanidinopropionate impair mechanical function and ATP homeostasis in rats after myocardial infarction?
Severe depletion of myocardial phosphocreatine content prevents survival after acute MI and impairs ATP homeostasis in chronically infarcted hearts.
Horn et al. (2001) studied this question.
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