Denervation potentiated the cooling-induced
contractures and the
halothane-cooling
contractures of isolated extensor digitorum longus and soleus muscles of the mouse. These effects were more striking in extensor digitorum longus than in soleus muscles. Significant increases in the peak amplitudes of the
halothane-cooling
contractures of both muscles and of the cooling
contractures of soleus muscle were observed within 2 and 7 days of
denervation. The potentiation of the
contractures persisted for 90 days, the period of this study.
Denervation (greater than 2 days) endowed extensor digitorum longus with the ability to generate cooling
contractures in the absence of
halothane. The rate of tension development of cooling-induced
contractures in the absence or presence of
halothane was significantly greater in denervated (2-90 days) than in innervated muscles.
Denervation also reduced the effectiveness of
procaine in inhibiting the
halothane-cooling
contractures. It is proposed that the potentiation of cooling-induced
contractures in denervated muscles results primarily from an increase in the rate of efflux and in the quantity of Ca2+ released from the sarcoplasmic reticulum, upon cooling and (or) when challenged with
halothane.