Experiment 1a - Intravenous (IV) Injection Decamethonium
After establishing a control response 0.02 mg/kg of DECAMETHONIUM is injected intravenously.
Describe the change in twitch tension immediately following injection but before appearance of the block.
|Tubocurarine causes a reversible decrease in twitch tension|
|Decamethonium produces an initial increase in twitch tension followed by a reversible decrease|
|Tubocurarine produces a peak fall in twitch tension of about 75%|
|The pattern of the response to decamethonium is the same as that for tubocurarine|
Competitive (non-depolarizing) neuromuscular blocking agents such as tubocurarine bind to nicotinic ACh receptors on the muscle end plate and so reduce excitability. The ACh released by electrical stimulation of the nerve now has fewer available ACh receptors and the twitch tension is decreased.
Depolarizing agents such as decamethonium are long-acting agonists of the ACh receptors and so produce a maintained depolarization of the end plate. This inactivates the Na+ channels and there is a loss of transmission. The increase in twitch tension seen immediately after injection is due to the depolarizing action of decamethonium at the end plate.