Attenuated L-type Ca$^2+$ current (I(Ca,L)), or current-contraction
gain have been proposed to explain impaired cardiac contractility
in congestive heart failure (CHF). Six weeks after coronary artery
ligation, which induced CHF, left ventricular myocytes from isoflurane-anesthetized
rats were current or voltage clamped from -70 mV. In both cases,
contraction and contractility were attenuated in CHF cells compared
with cells from sham-operated rats when cells were only minimally
dialyzed using high-resistance microelectrodes. With patch pipettes,
cell dialysis caused attenuation of contractions in sham cells, but
not CHF cells. Stepping from -50 mV, the following variables were
not different between sham and CHF, respectively: peak I(Ca,L) (4.5
+/- 0.3 vs. 3.8 +/- 0.3 pApF(-1) at 23 degrees C and 9.4 +/- 0.5
vs. 8.4 +/- 0.5 pApF(-1) at 37 degrees C), the bell-shaped voltage-contraction
relationship in Cs$^+$ solutions (fractional shortening, 15.2 +/-
1.0\% vs. 14.3 +/- 0.7\%, respectively, at 23 degrees C and 7.5 +/-
0.4\% vs. 6.7 +/- 0.5\% at 37 degrees C) and the sigmoidal voltage-contraction
relationship in K$^+$ solutions. Caffeine-induced Ca$^2+$
release and sarcoplasmic reticulum Ca$^2+$-ATPase-to-phospholamban
ratio were not different. Thus CHF contractions triggered by I(Ca,L)
were normal, and the contractile deficit was only seen in undialyzed
cardiomyocytes stimulated from -70 mV.