Diethyl ether and nitrous oxide at clinical concentrations were shown to slightly but significantly decrease the maximal Ca2+-activated tension. Measured caffeine-induced tension transients of functionally skinned papillary muscle fibers indicate that diethyl ether inhibited the CA2+ release mechanism in the sarcoplasmic reticulum and increased the amount of Ca2+ sequestered into the sarcoplasmic reticulum. The overall effect of continuously exposing the fibers to 6% or higher concentrations of diethyl ether was to depress the amount of Ca2+ released from the sarcoplasmic reticulum. We therefore conclude that the mechanisms of myocardial depression by diethyl ether may be due in part to an inhibition of the Ca2+ release mechanism of the sarcoplasmic reticulum and in part to a decrease in the maximal Ca2+-activated tension. Nitrous oxide-induced myocardial depression could only partly be due to a decrease in the maximal Ca2+-activated tension.
ASJC Scopus subject areas
- Anesthesiology and Pain Medicine