Key result
Pressure overload-induced RVH in rats alters calcium transients, correlating with sarcoplasmic reticulum density.
In a rat model of pressure overload, changes in calcium transient amplitude correlate with sarcoplasmic reticulum number during the transition to heart failure, providing insights into calcium handling mechanisms.
No direct clinical implications from rat model; leaves open translation of calcium-SR correlations to human right heart failure.
We examined changes in intracellular calcium transients of separated single myocytes from the right ventricle (RV) of the rat heart during the change from adaptation to maladaptation in response to a pressure overload. 2. Right ventricular hypertrophy (RVH) secondary to pulmonary hypertension was induced by a subcutaneous injection of monocrotaline. Developed tensions of the RV-free wall were decreased as RVH progressed. Single myocytes were separated from the RV during different stages of RVH. Fura-2/AM-loaded cells were field stimulated, and changes in calcium transients were measured by Olympus OSP-3 system. We also examined membranous ultrastructures (sarcoplasmic reticulum, mitochondria, surface caveolae) involved in calcium metabolism in the hearts using scanning electron microscopy. 3. We observed characteristic changes in calcium transients during the change from adaptation to maladaptation, and also found that one parameter (amplitude) of calcium transients appeared to be correlated with the changes in the number of sarcoplasmic reticulum. 4. These results provided some insights into the mechanism of calcium handling of hypertrophied heart in response to a pressure overload from adaptation to maladaptation especially when stimulatory frequency was high, and suggested that heart rate control is a very important factor for the treatment of patients with congestive heart failure.
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Kuramochi et al. (1994) studied Right ventricular hypertrophy and heart failure. Pressure overload via monocrotaline injection was evaluated on Changes in intracellular calcium transients and membranous ultrastructures. Pressure overload-induced right ventricular hypertrophy in rats caused characteristic changes in calcium transients, with amplitude correlating with the number of sarcoplasmic reticulum.
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