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Effect of thiopental on Ca2+ release from sarcoplasmic reticulum in intact myocardium
Background:
While thiopental is known to inhibit the myocardial transsarcolemmal influx of Ca2+, the effect of thiopental on sarcoplasmic reticular Ca2+ release has not been characterized.
Methods:
Isolated papillary muscles of rabbits were used. We measured postrest contractions to assess the Ca2+ release by sarcoplasmic reticulum in response to electrical stimulation. Contractures induced by rapid cooling were used as an index of Ca2+ content of sarcoplasmic reticulum. The effect of thiopental on the availability of extracellularly derived Ca2+ was evaluated from measurements of contractions at 0.1 Hz in the presence of 1 microM ryanodine.
Results:
Thiopental sodium (10, 20, and 30 mg/l; 38, 76, and 113 microM) inhibited the postrest contraction but not the contracture induced by rapid cooling. In the presence ryanodine, thiopental inhibited the postrest contraction elicited after 10 s of rest after 2-Hz stimulation much less than the steady-state contraction at 0.1 Hz (beat interval 10 s). Thiopental inhibited the postrest contraction (no ryanodine present) more strongly than did Ni2+ (an inhibitor of the transsarcolemmal Ca2+ influx) when the contraction at 0.1 Hz in the presence of ryanodine was inhibited to the same extent.
Conclusions:
These results suggest that thiopental decreases sarcoplasmic reticulum Ca2+ release induced by electrical stimulation and inhibits the ryanodine-induced efflux of sarcoplasmic reticulum Ca2+.