Key result
Chronic unloading of the normal heart caused a time-dependent depression of myocyte contractile function, with prolonged relengthening and calcium decline at 5 weeks.
Population
Isogenic rats undergoing heterotopic heart transplantation to the abdominal aorta to induce cardiac unloading
Comparison
Chronic cardiac unloading for 2 and 5 weeks vs Native in situ hearts from recipient animals
Design
Preclinical
Follow-up
5 weeks
Authors
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May caution against prolonged unloading in mechanical support; leaves open effects in diseased human hearts.
Chronic unloading of the normal heart causes a time-dependent depression of myocyte contractile function and calcium regulation, suggesting potential impairment during prolonged cardiac atrophy.
Ito et al. (2003) studied Chronic cardiac unloading. Chronic cardiac unloading via heterotopic heart transplantation vs. Native in situ hearts from recipient animals was evaluated on Contractile function indices and [Ca(2+)](i) regulation in LV myocytes. Chronic unloading of the normal heart caused a time-dependent depression of myocyte contractile function, with prolonged relengthening and calcium decline at 5 weeks.
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