THE EFFECTS OF COCAINE AND LIGNOCAINE ON THE RAT RIGHT VENTRICLE IN VITRO

Publisher Website
Google Scholar
Abstract
The effects of cocaine and lignocaine on the contractile responses to field stimulation and to exogenously applied agents, in the absence of other stimuli, were investigated in the rat right ventricle. The effects of 3H accumulation from (-)-[3H]-noradrenaline [norepinephrine, NE] and on the spontaneous and field stimulation-induced overflow of 3H, following preloading of the tissue with (-)-[3H]-NE, are reported. Cocaine, but not lignocaine, inhibited the accumulation of 3H from (-)-[3H]-NE. The spontaneous overflow of 3H, following preloading of the tissue with (-)-[3H]-NE was not altered by cocaine, 10 .mu.M or lignocaine 100 .mu.M. Lignocaine (10 .mu.M) had no effect on the overflow of 3H evoked by field stimulation at 5Hz. Lignocaine (100 .mu.M) increased and cocaine (1 and 10 .mu.M) reduced the decline in evoked release of 3H. This effect of lignocaine probably represented a decrease in nerve excitability and that of cocaine inhibition of neuronal uptake of NE. Cocaine 1 .mu.M reduced the rate of beat response to tyramine 1 .mu.M, alone, probably by inhibiting the neuronal uptake process. Cocaine (1 and 10 .mu.M) had no effect on the contractile responses to field stimulation (at 2 and/or 5 Hz). The rate of beat to (-)-NE or (-)-isoprenaline (1 .mu.M) alone was decreased by cocaine (10 .mu.M). Lignocaine (10 .mu.M) reduced the force of contractions to field stimulation at 5 Hz and the responses to (-)-NE or (-)-isoprenaline alone. The inhibitory effects of cocaine and lignocaine on responses to (-)-isoprenaline in the rat right ventricle were evidently due to a decreased post-junctional membrane excitability. The inability of 10 .mu.M cocaine to potentiate contractile responses to endogenous or exogenous (-)-NE as a consequence of the inhibition of neuronal uptake was probably due to decreased post-junctional excitability of the right ventricle.