Indeed, decrease in blood pressure produced by d-Tc have been shown to be less when the muscle relaxant was preceded by and antihistamine. The amount of histamine release substance depends on plasma levels of the drug achieved and thus on the rapidity of intravenous administration of that drug. If d-Tc produces histamine release, then slow intravenous injection would be associated with minimal histamine release and a resulting attenuation of the typical blood pressure reduction that follows' this drugs injection.
Therefore, we measured changes in mean arterial pressure MAP and heart rate in patients anesthetized with nitrous oxide-halothane during and after the intravenous injection of d-Tc at varying rates of administration. In the case of carbamylcholine, low doses inhibited histamine release, but higher doses allowed histamine to be liberated from mast cells. From these findings, it is concluded that some drugs like theophylline or isoproterenol may diminish the side effects of d-tubocurarine and perhaps some other muscle relaxants.
Also, as theophylline and isoproterenol are concerned, increase of cyclic AMP may play a role in the inhibition of histamine release. Both block of Na channels and block of pre-synaptic nicotinic autoreceptors have been implicated.
The presynaptic nicotinic receptors have a different subunit composition compared to the muscle-type nicotinic receptors. At high concentrations they can also produce a more intense motor blockade by blocking the pore of the nicotinic receptor-channel complex. Clients in whom release of histamine is hazardous.
Use with caution during pregnancy and lactation and in children. Of the nondepolarizing neuromuscular blockers, d-tubocurarine causes the most histamine release by a direct effect on mast cells.
Histamine release can cause bronchospasm, hypotension, salivary secretions. Its muscle relaxant properties are qualitatively similar to the other newer non-depolarizing relaxants such as pancuronium, vecronium, rocuronium to name just a few.
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