[Mechanism of the disturbance in muscle energy allowance in botulin poisoning].

Development of botulinic pareses of cat sceletal muscles was followed by an inhibition of oxygen utilization simultaneously with a still sufficient compensation of external respiration impairment. The inhibitory effect of botulinic toxins on tissue respiration was apparently mediated via impairment of cetecholamine metabolism; utilization of O2 in the muscles was unaltered during the preclinical period of the toxin intensive sorption by tissues. Also a definite relationship was observed between the development of tissue hypoxia and an increase in content of tissue catecholamines. Stimulation of tissue hypoxia was accompanied by impairments in glycolytic process, deficiency of potassium, ascorbic acid and phosphocreatine in muscle tissue.