Аннотация
Altered cardiac workload has an important effect on myocyte structure
and function. Cardiac hypertrophy resulting from an increase in load
has been studied extensively in the past. However, the effects of
unloading and atrophy have recently become of more interest since
devices for mechanical left ventricular unloading have been introduced
into clinical practice for the treatment of patients with terminal
heart failure, and a resulting improved cardiac and myocyte contractility
have been reported. We used the heterotopic abdominal mouse heart
transplant model in order to study the effects of 5 days of unloading
on cell size (confocal microscopy), contractility (fractional shortening:
video motion), calcium homeostasis (Ca$^2+$(i)transients, SR
Ca$^2+$content); and L-type Ca$^2+$and sodium/calcium exchanger
currents (whole cell patch clamp technique). We found unloading caused
decreased cell volume consistent with atrophy. An increased fractional
shortening and Ca$^2+$(i)transient were observed in myocytes
from unloaded hearts as compared with controls. Transsarcolemmal
I(Ca,L)and I(Na/Ca)densities, and SR Ca$^2+$content were unaltered,
as was membrane capacitance. A reduction in cell volume with mainteinance
of internal and surface membrane areas, and/or a decrease in concentration
of cellular protein Ca$^2+$buffers, may contribute to the increase
in the Ca$^2+$(i)transient in this model.
- 10756115
- animal,
- animals,
- aortic
- atpase,
- balb
- c,
- calcium
- calcium,
- cardiac
- cardiomegaly,
- cells,
- channels,
- contraction,
- cultured,
- disease
- diseases,
- dysfunction,
- exchanger,
- female,
- gov't,
- heart
- heart,
- homeostasis,
- humans,
- inbred
- l-type,
- left,
- low,
- male,
- mice,
- models,
- muscle
- muscles,
- myocardial
- myocardium,
- non-p.h.s.,
- non-u.s.
- output,
- p.h.s.,
- research
- reticulum,
- sarcoplasmic
- sodium,
- sodium-calcium
- stenosis,
- support,
- u.s.
- valve
- ventricles,
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