Key result
Incubation with 0.5 mmol/L ryanodine caused a 52.2% increase in peak 45Ca2+ accumulation in nonfailing myocardium microsomes and a 24.3% increase in failing myocardium microsomes.
Why the study?
Does ryanodine affect sarcoplasmic reticulum Ca2+ accumulation differently in microsomes from failing versus nonfailing human myocardium?
Population
Microsomes prepared from nonfailing (n=8) and failing (n=10) human left ventricular myocardium
Comparison
0.5 mmol/L ryanodine vs Absence of ryanodine
Design
Preclinical
Authors
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May implicate SR Ca2+ efflux in HF; hypothesis-generating, should not yet change practice.
Does ryanodine affect sarcoplasmic reticulum Ca2+ accumulation differently in microsomes from failing versus nonfailing human myocardium?
Ryanodine causes a diminished stimulation of Ca2+ accumulation in sarcoplasmic reticulum-derived microsomes from failing human myocardium compared to nonfailing myocardium, suggesting increased Ca2+ efflux may contribute to abnormal Ca2+ homeostasis in heart failure.
Nimer et al. (1995) studied Heart failure (n=18). Ryanodine vs. Absence of ryanodine was evaluated on Peak 45Ca2+ accumulation. Incubation with 0.5 mmol/L ryanodine caused a 52.2% increase in peak 45Ca2+ accumulation in nonfailing myocardium microsomes and a 24.3% increase in failing myocardium microsomes.
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