Motor responses of the urinary bladder and skeletal muscle inBotulinumintoxicated rats
Autor: | F. G. Carpenter |
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Rok vydání: | 1967 |
Předmět: |
Male
medicine.medical_specialty Sensory Receptor Cells Physiology Urinary Bladder Neural Conduction Neuromuscular Junction Neuromuscular transmission Stimulation In Vitro Techniques medicine.disease_cause complex mixtures Parasympathetic Nervous System Internal medicine Clostridium botulinum medicine Mydriasis Paralysis Animals Toxins Biological Motor Neurons Nerve Endings Urinary bladder Toxin business.industry Muscles Skeletal muscle Botulism Articles Botulinum toxin Acetylcholine Electric Stimulation Rats Endocrinology medicine.anatomical_structure Anesthesia Biological Assay Carbachol Female medicine.symptom business Muscle Contraction medicine.drug |
Zdroj: | The Journal of Physiology. 188:1-11 |
ISSN: | 0022-3751 |
DOI: | 10.1113/jphysiol.1967.sp008119 |
Popis: | 1. Type A or type D botulinum toxin administered to rats did not produce a generalized paralysis of skeletal muscles at the time of ventilatory arrest. However, if survival was extended by artificial ventilation complete blockade of neuromuscular transmission developed 6·5 hr after 100 MLD of type D and 5 hr after 1000 MLD of type A toxin. The onset of paralysis of a muscle was shortened by repetitive stimulation of the motor nerves. 2. There was no consistent blockade of parasympathetically innervated viscera in animals dying after type A toxin. Animals given type D toxin displayed mydriasis and urinary retention before death. 3. Motor responses to electrical stimulation, of bladder preparations in vitro were more vulnerable to type D than to type A toxin. When somatic paralysis was complete in animals treated with type A or type D toxin the excised bladders produced pressure elevations 45 and 25%, respectively, of control preparations. 4. During electrical stimulation of bladder preparations nearly paralysed by either toxin, the ACh release was significantly diminished from controls. In the rat bladder botulinum toxin specifically disrupted the liberation of mediator from post-ganglionic nerve endings. |
Databáze: | OpenAIRE |
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