Inhibition by alcohols, halothane and chloroform of the Ca current in single frog ventricular cells

Biphasic changes in cardiac excitation-contraction coupling early in chronic alcohol exposure

“…In any event, our results still concur with the proposed mechanism of EtOH acting at lower concentrations to interfere with myofilament cross-bridge formation and thus decreasing myofilament sensitivity to Ca 2ϩ released from the SR, which is then exaggerated by reduced global SR Ca 2ϩ release that occurs at higher EtOH concentrations (7,14,15,20). Further contributing to these negative inotropic effects is attenuation in cardiac L-type Ca 2ϩ channel current (I Ca-L ) reported by our group (3) and others (18,35), which constitutes an EtOH-induced reduction in EC coupling trigger Ca 2ϩ .…”

Effect of ethanol on action potential and ionic membrane currents in rat ventricular myocytes

“…One more important remark should be mentioned here. Mongo & Vassort (1990), who first documented the inhibitory effect of ethanol on I Ca , described also an opposite stimulatory response to a low concentration of ethanol (10 m m ) and biphasic response to higher concentrations. Their experiments were performed on isolated frog ventricular myocytes.…”

Alteration of the L‐type calcium current in guinea‐pig single ventricular myocytes by heptaminol hydrochloride

“…The effects of hydrocarbons including n-alkanols and amines are widely studied in excitable cells but there is no common view on the mechanisms of action of these molecules. Changes in ionic channels activity (Haydon & Urban, 1983a,b;Mongo & Vassort, 1990), in ionic cotransport (Michaelis & Michaelis, 1983;Philipson, 1984;Haworth et al, 1989), in enzymatic activities (Ohnishi et al, 1984;Chatelain et al, 1986;Swann, 1990), in [Ca2 ], (Vassort et al, 1986;Daniell & Harris, 1988;Davidson et al, 1990) and in [H+]i (Vassort et al, 1986) have been shown to occur in various tissues as a consequence of the interaction of these hydrocarbons with biological membranes. In cardiac muscle, general and local anaesthetics (amines, straight chain alcohols and inhalation compounds) are known to alter most of ionic currents including Ca current (ICa) which is decreased (Ikemoto et al, 1985;Hiroto et al, 1988;Terrar & Victory, 1988;Mongo & Vassort, 1990).…”

“…At more negative values of HP the rapid recovery of ICa is usually associated with the well known phenomenon of 'overshoot or 'Ca facilitation' (see Argibay et al, 1988;Tseng, 1988;Mongo & Vassort, 1990). This is illustrated in Figure 4b, Figure 4c is an expanded graph of the first 500 ms of Figure 4b normalized to maximum value and it shows that, despite the marked Meszaros & Pappano, 1990 and ethanol by Mongo & Vassort, 1990). Although, the molecular basis of the action of membrane active substances is not well understood, it is generally admitted that two pathways, one hydrophobic the other hydrophilic, are used by these compounds to reach their site of action and this depends on the fact that molecules are or not amphiphile.…”

“…This increase in [Ca2+]i may result from: (1) a release of membrane bound Ca2" (Vassort et al, 1986); (2) an inhibition of Na'-Ca2" exchange mechanism (Michaelis & Michaelis, 1983;Philipson, 1984;Haworth et al, 1989) and of sarcolemmal and intracellular membrane Ca-ATPases (Salama & Scarpa, 1983;Ohnishi et al, 1984). In order to explain their effects on ICa characteristics, Mongo & Vassort (1990) have proposed the participation of an increase in [Ca2+]i as a mechanism of action of n-alkanols and halogenated compounds in addition to those previously described (see Introduction and also Meszaros & Pappano, 1990 (Mentrard et al, 1984;Argibay et al, 1988;Tseng, 1988) (Mentrard et al, 1984). This reduction, although significant (P <0.02, n = 8), appeared to be not very pronounced; this may be due to the use of EGTA (10 mM) in the patch pipette to buffer intracellular Ca2+ to avoid cell contraction.…”