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Old 07-07-2013
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Drug Nitrous oxide + Malignant hyperthermia

Anybody knows why nitrous oxide is not associated with malignant hyperthermia? Thanks
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Old 07-07-2013
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Seems like you're comparing this to the Halothane anesthetics.

In susceptible patients (who have a 'structural' AD mutation of ryanodine receptors)...the Halothane's can act on these channel proteins, and cause the increase of Calcium release into the cell.

These ryanodine receptors are in fact, calcium channels on the Sarcoplasmic membrane of skeletal muscles. Certain drugs (including succinylcholine, halothanes, ???and others???)...can act on them, and cause this release of Calcium.

Now, these skeletal muscle cells have to 'use up' all their ATP, just to pump this 'leaked out' calcium, back into the SR...all this ATP consumption will increase the ETC, increase oxygen consumption which increaese metabolism, which caues acidosis. HEAT is generated (b/c inc ATP consumption)! SANS will kick in (to attempt to cool by sweating --> GOOD), but SANS will also cause an increase HR and inc risk of arrhytmias!!! --> NOT GOOD. risk for HTN!

all this = malignant hyperthermia.

I think after you realize what malignant hyperthermia really is, how it develops, and then you just think of the drugs that can cause it. Just remember that HALOTHANES and SUCCINYLCHOLINE both have something in common...they can cause those ryanodine channels to release Calcium into the cell. And i suppose more importantly, not everyone who is administered Halothane or succinylcholine will get malignant hyperthermia...that's becuase this mechanism involves only those ryanodine channels, which are structurally mutated (autosomal dominant disorder)

But to answer your question in short, I don't think Nitrous Oxide can do what halothane's can (above mechanism). As far as N20 goes, pretty much causes Spontaneous abortions, and could cause diffusional hypoxia. other than that, not much Cardiovascular side effects.

Last edited by ReggieMiller; 07-07-2013 at 06:43 PM.
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Old 07-08-2013
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Thanks ReggieMiller for your great help
I have another question if you please,
why choline esterase inhibitors (e.g., neostigmine) are not effective in phase I of succinlycholine action? FA says it may increase the depolarization.
Why they only work in phase 2, not phase 1?
Thanks again dear
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