Аннотация
The reduced power of the failing heart can be ascribed to a combination
of reduced force and slower contraction. We hypothesized that these
two properties are due to different cellular mechanisms. We measured
contraction parameters both in vivo and in isolated left ventricular
(LV) cardiomyocytes from a rat model of post infarction congestive
heart failure (CHF). ECG was measured simultaneously with echocardiography
and LV pressure, respectively. Shortening and shortening velocity
(SV) in isolated cardiomyocytes were measured during different stimulation
protocols. LV end diastolic pressure (LVEDP) was 24.6 +/- 0.7 mmHg
in CHF. LV systolic pressure was decreased by 20\%, maximum rate
of pressure development in the LV (+dP/dtmax) by 36\% and time in
systole increased by 20\% in CHF compared to sham. Electrical remodelling
occurred in CHF cells, which were depolarized and had prolonged action
potentials (AP) compared to sham cells. Fractional shortening (FS)
was increased in CHF compared to sham independent of stimulation
protocol. Larger FS was accompanied by increased sarcoplasmic reticulum
(SR) Ca2+ load and depended on the electrical remodelling. Time to
peak contraction (TTP) was increased in CHF compared to sham cells,
but in contrast to FS, TTP was only slightly affected when the cells
were stimulated with sham APs and sham diastolic membrane potential
(DMP). Contraction duration (corresponding to systolic duration)
was 25\% longer in CHF than in sham independent on stimulation protocol.
We conclude that electrical remodelling affecting DMP and AP duration
(APD) significantly affects the size of contraction, whereas the
mechanism for slowing of contraction in CHF is different.
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