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Vol. 288, Issue 3, 1214-1222, March 1999
Cardiology Section, Wake Forest University School of Medicine,
Winston-Salem, North Carolina
Endothelin-1 (ET-1) is a positive inotrope in normal hearts; however,
the direct cardiac effects of endogenous ET-1 in congestive heart
failure (CHF) are unknown. We evaluated the cardiac responses to
endogenous ET-1 using an ETA and ETB receptor
blocker (L-754,142) in seven conscious dogs before and after
pacing-induced CHF. Before CHF, when the plasma ET-1 was 7.3 ± 1.7 fmol/ml, L-754,142 caused no significant alterations in heart rate,
left ventricular (LV) end-systolic pressure, total systemic resistance,
and the time constant of LV relaxation (
). LV contractile
performance, measured by the slopes of LV pressure (P)-volume (V)
relation (EES), dP/dtmax-end-diastolic V
relation (dE/dtmax), and stroke work-end-diastolic V
relation, was also unaffected. After CHF, when the plasma ET-1 was
significantly increased to 14.1 ± 3.0 fmol/ml
(p < .05), L-754,142 produced a significant
decreases in LV end-systolic pressure (101 ± 11 versus 93 ± 8 mm Hg) and total systemic resistance (0.084 ± 0.022 versus
0.065 ± 0.15 mm Hg/ml/min). The (42 ± 12 versus 38 ± 10 ms), mean left atrial P (22 ± 5 versus 18 ± 4 mm Hg)
(p < .05), and minimum LVP were also significantly
decreased. After CHF, the slopes of P-V relations, EES
(3.4 ± 0.4 versus 4.8 ± 0.8 mm Hg/ml), dE/dtmax
(42.4 ± 7.8 versus 50.0 ± 7.8 mm Hg/s/ml), and stroke
work-end-diastolic V relation (58.1 ± 3.3 versus 72.4 ± 5.2 mm Hg) (p < .05) all increased after L-754,142,
indicating enhanced contractility. Before CHF, low levels of endogenous
ET-1 have little cardiac effect. However, after CHF, elevated
endogenous ET-1 produces arterial vasoconstriction, slows LV
relaxation, and depresses LV contractile performance. Thus, elevated
endogenous ET-1 may contribute to the functional impairment in CHF in
this canine model.
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