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PubMed1986

Infant botulism.

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Botulism↗
PubMedDate not supplied

[Changes in Na, K-ATPase activity in subcellular fractions of the lumbar region of the spinal cord in botulism and the possibility of their pharmacological correction].

Inhibition of Na, K-ATPase in fractions of unpurified synaptosomes and of heavy microsomes from lumbar part of spinal cord was found in dynamics of botulinic intoxication of the C type in rats. Both competitive and noncompetitive types of inhibition of the enzymatic activity were found in kinetic studies. Inhibition of transport functions across biological membranes caused by botulinic toxin was shown to have a reversible character. The inhibition might be prevented within the early periods of botulinic intoxication by administration of serotonin and guanidine hydrochloride.

Adenosine Triphosphate↗
PubMed1985

[Possibilities of pharmacologic correction of Na, K-ATPase activity in the spinal cord in botulism].

The experiments on white rats have shown that gutimin is capable of reactivating Na, K-ATPase of the synaptosomes of the jugular spinal cord in type C botulinic intoxication. Serotonin prevented Na, K-ATPase activity inhibition only in preclinical period of intoxication. Parmidin injection did not prevent suppression of Na, K-ATPase activity either in preclinical period or in skeletal muscle paresis.

Animals↗
PubMed1985

[Effect of 4-aminopyridine on the development of experimental botulism].

The studies of survival and the life span of mice and the toxin in LD50 have shown that 4-aminopyridine (4-AP) at doses of 1, 2 and 5 mg/kg has a therapeutic effect on type C botulinic intoxication. Maximum protective effect is observed when 4-AP at a dose of 2 mg/kg is injected twice daily. Therefore, 4-AP, enhancing the transmitter release into cholinergic synapses, weakens the toxic effect of botulinic toxin.

4-Aminopyridine↗