botulism/potassium

Clostridium botulinum and type-B C botulinum toxin were isolated from a necrotic wound that developed subsequent to castration in a 2-year-old Thoroughbred gelding. The horse had clinical signs of botulism and was successfully treated with wound debridement, C botulinum type-B antitoxin, potassium

Guanidine and its alkyl analogs stimulate the neuromuscular junction presynaptically by inhibiting voltage-gated potassium (Kv) channels, leading to enhanced release of acetylcholine in the synaptic cleft. This stimulatory effect of guanidine underlies its use in the therapy for the neuromuscular

Toosendanin, a triterpenoid from Melia toosendan Sieb et Zucc, has been found before to be an effective anti-botulism agent, with a bi-phasic effect at both motor nerve endings and central synapse: an initial facilitation followed by prolonged depression. Initial facilitation may be due to

Botulinum neurotoxins (BoNTs) are potent neuroparalytic toxins that cause mortality through respiratory paralysis. The approved medical countermeasure for BoNT poisoning is infusion of antitoxin immunoglobulins. However, antitoxins have poor therapeutic efficacy in symptomatic patients; thus, there

Content of lactic and pyruvic acids, glycogen, sodium and potassium ions are well as the total LDH activity and its isoenzyme spectrum were not distinctly altered, when secretion of salivary glands was inhibited by administration of botulinic toxin into rats (within 48 hrs after the toxin

Several tick species have been demonstrated, described, or suspected to cause paralysis in their host during the repletion process, presumably by impairing neurotransmission. The resulting polyneuropathy gradually spreads to the upper limbs causing incoordination and ends in respiratory failure.

Botulinum neurotoxins (BoNTs) are exceedingly potent neurological poisons that prevent neurotransmitter release from peripheral nerve terminals by cleaving presynaptic proteins required for synaptic vesicle fusion. The ensuing neuromuscular paralysis causes death by asphyxiation. Although no

Levels of sodium and potassium ions in muscle tissue, blood plasma and red cells were measured, and the index characterizing the capacity of tissue to accumulate cations from the environment and the discrimination coefficient were calculated in experiments on white rats subjected to experimental

Botulism is a disease characterized by neuromuscular paralysis and is produced from botulinum neurotoxins (BoNTs) found within the Gram positive bacterium Clostridium botulinum. This bacteria produces the most deadliest toxin known, with lethal doses as low as 1 ng/kg. Due to the relative ease of

4-aminopyridine is the first of the aminopyridines to be used in clinical practice. It blocks potassium channels and thereby increases acetylcholine, and possibly noradrenaline, release at nerve terminals. In man the drug has a significant action at the neuromuscular junction, but has little effect

This review summarizes those neurological diseases which are accompanied by a drooping of the upper lid, due to weakness of the m. levator palpebrae or m. tarsalis respectively. After connatal ptosis with or without involvement of other bulbar muscles the different types of muscular dystrophies are

Botulinum neurotoxins (BoNT) are the etiological agents responsible for botulism, a disease characterized by peripheral neuromuscular blockade and a characteristic flaccid paralysis of humans. BoNT/A is the most toxic protein known to man and has been classified by the Centers of Disease Control

A large number of intellectually engaging and potentially serious neuromuscular diseases have been presented. The emergency medicine physician must be able to recognize those entities that have the potential to clinically deterioration. The evaluation of weakness requires a comprehensive,

Human exposure to botulinum toxin typically occurs in two settings: 1) as an etiologic agent in the disease botulism and 2) as a therapeutic agent for the treatment of dystonia. Epidemiologic studies on botulism suggest that the human nervous system is susceptible to five toxin serotypes (A, B, E, F