Alcohol and Anesthetic Actions on Myocardial Contractility
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While volatile anesthetics typically depress cardiac contractility, the actions of the presently used volatile anesthetics (halothane, enflurane, isoflurane) upon the pattern and magnitude of myocardial tension development differ significantly, suggesting different sites of action.1–3 Previous physiological and biochemical studies have suggested multiple mechanisms of action for the volatile agents, primarily implicating altered control of Ca delivery to myofibrils (depression of Ca entry and depression of sarcoplasmic reticulum uptake and release of Ca).4 To better understand the alterations in myocardial tension development, which may in part be related to the lipid solubility of the anesthetic agents, the aliphatic alcohols were employed as model anesthetic compounds with known physical characteristics which vary in a systematic fashion. With increasing chain length, the aliphatic alcohols possess increasing general anesthetic potency as well as increasing ability to inhibit nerve conduction.5 The actions of alcohols can thus be compared not only with the volatile anesthetics, but also with effects of the local anesthetics (LAs), also known to selectively alter myocardial contractility.3,6 Effects of these various anesthetic compounds were also contrasted with the effects of ryanodine, a plant alkaloid which binds with very high affinity to the Ca release channel of the sarcoplasmic reticulum (SR) and reduces the release of Ca2+ from the SR.7–10
KeywordsSarcoplasmic Reticulum Benzyl Alcohol Aliphatic Alcohol Volatile Anesthetic Tension Development
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