Neuromuscular block (1956), pt 1 of 2

Description:

An unconventional and delightful presentation by means of animated diagrams, actual experiments and stop-frame animated cartoon characters of the theory and clinical practice of muscle relaxants, with particular reference to tubocurarine, succinylcholine and decamethonium. Also discusses the electrical aspects of neuromuscular transmission. 2 segments. Made by Wellcome Foundation. Find out more: http://catalogue.wellcomelibrary.org/record=b1675532~S3

Complete Record: An unconventional and delightful presentation by means of animated diagrams, actual experiments and stop-frame animated cartoon characters of the theory and clinical practice of muscle relaxants, with particular reference to tubocurarine, succinylcholine and decamethonium. Also discusses the electrical aspects of neuromuscular transmission. 2 segments. Made by Wellcome Foundation. Find out more: http://catalogue.wellcomelibrary.org/record=b1675532~S3

Transcription

I think you'd better use a relaxant why all this Panic friend it's not so difficult to comprehend but since you find it such a tussle come let's have a diagram here's a muscle and over here a nerve down which an Impulse travels and observe a chemical is formed atile Coline whose action is to produce a muscular contraction this role played it rapidly destroyed by an enzyme Colin esteras and as you see the cycle just completed with each succeeding impulse is repeated now for a relaxant there are as you see a host but a tubocurarine is better known than most this blocks the atile choline's tracts and the muscle stays relaxed a small dose of neostigmine note is quite an effective antidote it combines with cholin esteras and some of the atile choline stays accumulates overcomes the barrier and the muscle can contract again but be careful there's a danger here give too much neostigmine and all the Colin esteras may disappear the atile choline will thus remain and you see the muscles paralyzed again let us now proceed to another relaxant suxy choline akin to atile choline in action it even produces an initial contraction but the effect of Colin esteras on this is slow and the Anis lasts a few minutes or so and now decamethonium similar to the last one and in fact it too can cause a muscle to contract but unaffected by Colin Rays it will stay until the bloodstream carries it away its effect is protracted therefore the paralysis May last half an hour or more well and now that we've seen the simple abstract scheme let's see how well all this makes sense when tested on the laboratory bench at some stage in your education you must have seen this preparation a rat diaphragm in ringer solution stimulated into regular contraction to B curine is added and here we Trace its action and in a short time we're not surprised to see the muscle fully paralyzed the bath is emptied the tubocurarine removed and upon refilling muscular conditions might improve after a second wash to make all sweet muscular recovery is complete another dose of tubocurarine is given the tracing follows its expected path then Neo stigmes added to the bath as we anticipate from what has gone before the muscle is recovering once more but if a second larger dose of antidote we add conditions quickly go from good to bad quite soon the muscles paralyzed again and note carefully excess atile choline is to blame now suxin choline first a paralysis then the bath washed twice suxy choline added once more and the muscles paralyzed give a small dose of neosine again but this time as you see there is no change and if we give a larger dose still the contractions quickly reduce to nil from this of course you will deduce that neostigmine is no use for suy choline overdose nor indeed as this Trace shows for too much decamethonium I'm sure youve not found it hard to follow all the facts so far but as you must already know there's an electrical side to this story so just have a look at this micro slide which when it's greatly magnified shows the nerve endings on a


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