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Exhaustion of Frank-Starling mechanism in conscious dogs with heart failure
Ist Teil von
American journal of physiology. Heart and circulatory physiology, 1993-10, Vol.265 (4), p.H1119-H1131
Ort / Verlag
United States
Erscheinungsjahr
1993
Quelle
MEDLINE
Beschreibungen/Notizen
K. Komamura, R. P. Shannon, T. Ihara, Y. T. Shen, I. Mirsky, S. P. Bishop and S. F. Vatner
Department of Medicine, Harvard Medical School, Brigham & Women's Hospital, Boston, Massachusetts.
The goal of this study was to elucidate the ability of the left ventricle
to accommodate an increase in preload (Frank-Starling mechanism) in the
presence of congestive heart failure (CHF) but in the absence of the
complicating effects of hypertrophy and fibrosis. To accomplish this, the
effects of volume loading were examined in eight conscious dogs during the
control state and after 3 wk of right ventricular pacing (240 beats/min).
CHF increased heart rate (by 16 +/- 5 from 92 +/- 5 beats/min), left
ventricular (LV) end-diastolic pressure (by 17 +/- 2 from 10 +/- 1 mmHg),
and LV end-diastolic volume (EDV; by 23 +/- 4 from 57 +/- 3 ml). Despite
reduced LV ejection fraction (from 54 +/- 3 to 31 +/- 3%), there was no
significant change in cardiac output (2.5 +/- 0.3 l/min) compared with
control (2.7 +/- 0.2 l/min). Stroke volume was preserved (control 19 +/- 2
ml; CHF 18 +/- 2 ml) at a constant heart rate by a shift to the right in
the relationship between LV stroke volume and EDV, indicating the
importance of chronic ventricular dilatation in maintaining pump
performance. In the control state, acute volume load increased LV EDV (by
17 +/- 2 ml) and stroke volume (by 11 +/- 2 ml), whereas in CHF it did not
increase LV EDV or stroke volume. Scanning electron microscopy revealed
areas of reduced collagen weave pattern surrounding myofibers. Myocyte
cross-sectional area by transmission electron microscopy was significantly
reduced, and there were multiple electron-dense expansions of the Z lines
with disruption of the normal lateral sarcomere alignment. These
morphological findings suggest that chronic ventricular dilatation utilized
in CHF results from myocyte stretch and morphological intracellular
rearrangement. Furthermore, the failing heart cannot further augment stroke
volume by acutely increasing EDV in CHF, suggesting that the Frank-Starling
reserve is essentially exhausted.