Effects of isoflurane and halothane on rapid cooling contractures in myocardial tissue

Abstract

The effects of isoflurane and halothane on the availability of Ca2+ stored in and released from the sarcoplasmic reticulum (SR) were studied in isolated rabbit papillary muscles by measuring the effects of the anesthetics on rapid cooling contractures, which are known to be activated by Ca2+ released from the SR. Isoflurane (0.3%) reduced the force of the rapid cooling contracture to 57% of control with a marked slowing of the average rate of contracture development and increased the force of the first contraction after rewarming to 133% of control. In contrast, 1.7% halothane, which reduced the rapid cooling contracture to 51% of control (comparable to the value in the presence of 0.3% isoflurane), had little effect on the rate of contracture development and strongly inhibited the first contraction after rewarming to 5% of control. Halothane, but not isoflurane, strongly inhibited postrest potentiated-state contractions, which are also known to be activated by Ca2+ released from the SR. These results suggest that 1) isoflurane inhibits rapid cooling-induced Ca2+ release from the SR without inhibiting Ca2+ release triggered by rapid depolarization as occurs in the potentiated-state contraction, and 2) halothane inhibits contractile activity dependent on Ca2+ released from the SR regardless of mechanism involved.