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Volatile Anesthetics and Second Messengers in Cardiac Tissue

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Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 301))

Abstract

The depression of myocardial contractility induced by volatile anesthetics is well documented by in vivo and in vitro studies. These agents’ direct myocardial depressant effect has been attributed to a decreased availability of free intracellular calcium to the contractile proteins and to a decreased sensitivity of the contractile proteins to activation by calcium. The volatile anesthetics have been shown to depress slow inward calcium currents in the sarcolemma, as well as inhibit calcium uptake and release by the sarcoplasmic reticulum.1 All these processes are modulated by hormones, neurotransmitters and other endogenous factors which regulate calcium movements either directly or indirectly via a second messenger system. Therefore, the effect of volatile anesthetics on calcium homeostasis and myocardial contractility may be due either to a direct interaction of the anesthetic with proteins regulating calcium movements or may be secondary to an action of the anesthetic on metabolic pathways modulating myocardial contractility.

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© 1991 Plenum Press, New York

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Vulliemoz, Y. (1991). Volatile Anesthetics and Second Messengers in Cardiac Tissue. In: Blanck, T.J.J., Wheeler, D.M. (eds) Mechanisms of Anesthetic Action in Skeletal, Cardiac, and Smooth Muscle. Advances in Experimental Medicine and Biology, vol 301. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5979-1_15

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  • DOI: https://doi.org/10.1007/978-1-4684-5979-1_15

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4684-5981-4

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