Troglitazone Attenuates High-Glucose–Induced Abnormalities in Relaxation and Intracellular Calcium in Rat Ventricular Myocytes
Key result
Troglitazone attenuated or prevented high-glucose-induced prolongation of relaxation and abnormally slow rates of Ca2+ transient decay in cultured rat ventricular myocytes.
Why the study?
Does troglitazone prevent high-glucose-induced relaxation defects and abnormal Ca2+ transient decay in isolated rat ventricular myocytes?
Population
Normal adult rat ventricular myocytes maintained in culture
Comparison
Troglitazone added to high-glucose medium for… vs High-glucose medium without troglitazone, and…
Design
Preclinical
Follow-up
1-2 days
Authors
Discussion
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Member takes
Implication
May support direct myocardial protection by troglitazone in hyperglycemia; leaves open translation to in vivo or human diabetes.
Structured PICO
Does troglitazone prevent high-glucose-induced relaxation defects and abnormal Ca2+ transient decay in isolated rat ventricular myocytes?
P
Population
Normal adult rat ventricular myocytes cultured in normal or high-glucose media for 1-2 days.
I
Intervention
Troglitazone (5 micromol/l) added to high-glucose medium (25 mmol/l glucose) for 1-2 days
C
Comparator
High-glucose medium (25 mmol/l glucose) without troglitazone, and normal medium (5 mmol/l glucose) with or without troglitazone
O
Outcome
Mechanical properties (relaxation from peak contraction) and intracellular Ca2+ transients (rate of decay)surrogate
Troglitazone protects against high-glucose-induced relaxation defects and abnormal calcium handling in isolated rat ventricular myocytes, suggesting potential direct beneficial cardiac properties in diabetes.
Cite This Study
Ren et al. (1996) studied High-glucose-induced cardiac dysfunction. Troglitazone vs. High-glucose medium without troglitazone was evaluated on Mechanical properties (relaxation from peak contraction) and Ca2+ transients. Troglitazone attenuated or prevented high-glucose-induced prolongation of relaxation and abnormally slow rates of Ca2+ transient decay in cultured rat ventricular myocytes.