Glucocorticoid enhancement of guanidine neuromuscular facilitation

The effects of an intensive short-term triamcinolone diacetate pretreatment regimen (8 mg/kg intramuscularly once daily for 7 days) on the facilitation of neuromuscular transmission produced by either intravenous or direct intraarterial administration of guanidine hydrochloride, were examined in the in vivo cat soleus nerve-muscle preparation. The ability of guanidine to activate a stimulus-bound repetitive after discharge (SBR) of soleus motor axons and to produce an obligatory enhancement of soleus muscle isometric contractile tension was measured in glucocorticoid-treated vs. untreated animals. Triamcinolone pretreatment significantly increased the guanidine-induced soleus contractile potentiation by 3 to 4 times with i.v. injection (P < 0.05) and by more than 30 times with i.a. administration (P < 0.01). The incidence of SBR in normal motor axons after i.v. guanidine was 58.5% in the treated animals and 25.0% in the untreated ones (P < 0.001). Also, the rate of development of the peak SBR incidence was almost doubled as a result of triamcinolone pretreatment (P < 0.05). This glucocorticoid enhancement of the facilitatory actions of guanidine may have relevance for the treatment of certain neuromuscular disorders.