• 1 January 1982
    • journal article
    • research article
    • Vol. 61  (5) , 403-409
Abstract
The effect of halothane on the availability of different sources of activator Ca for myocardial contraction was evaluated in relationship to the negative inotropic effect of the anesthetic. This was studied in rabbit papillary muscle under various simulation conditions that vary the importance of one or another of 2 sources of Ca2+ for production of contraction. The rested-state contraction depends primarily on the transsarcolemmal influx of Ca2+ for its activation; the potentiated-state contraction is dependent largely on Ca2+ released from intracellular stores. In the presence of 0.6% halothane (gas phase) the rested-state and potentiated-state contractions were depressed (mean .+-. SEM [standard error of the mean]) 38% .+-. 5% (n = 15) and 32% .+-. 3% (n = 7), respectively (no statistically significant difference). Halothane accelerated the decay of the potentiated state, indicating that it stimulated the loss of Ca2+ from internal stores. Halothane showed the time course of force increase following restimulation of rested muscles, indicating that it inhibits the filling of internal stores. The negative inotropic effect of halothane is apparently caused by a combination of quantitatively similar effects of the anesthetic on the transsarcolemmal and intracellular sources of activator Ca2+.