Published Oct 23, 2003
g8rlimey
171 Posts
Just wondering if any of you knowledgeable folks out there can give me simple explanation for this one:
Presence of fade w/ NDNMB during tetany/TOF vs absence of fade w/ DNMB (Phase I) during tetany/TOF.
The only good explanations I have found for this action are as follows:
1. Fade is present during tetany/TOF w/ NDNMB b/c of the depletion of Ach at presynapse.
2. Fade is present during tetany/TOF w/ NDNMB b/c of presynapse receptor inhibition of Ach release--much like the presynaptic alpha-receptor inhibition of NE release at the sympathetic terminal?
3. Fade is absent in the DNMB during tetany/TOF b/c of the inhibition of repolarization produced by sux.
Does this sound reasonable?
My other question is this---if there are available receptors at both inhibited nicotinic cholinergic post-junctional receptors, why can't sux have fade like panc or roc?
I would really like to understand the physiology behind these differences, so any help would be appreciated.
THX---Sam
---Post edited for clarification
charles-thor
153 Posts
Any takers?
Athlein
88 Posts
Sam,
I'm not following your line of thinking, but...
Barash has a good explanation of the neuromuscular pharmacology phenomenon going forward from page 387 in 3rd edition. Did you look there?
Athlein:
Thx for the reference. I understand now. For those of you lurking on this question, the answer is as follows:
Barash, Cullen, and Stoelting, Clinical Anesthesia, 2nd edition, pp. 483-487
"The blocking effect of succinlycholine at the NMJ is probably due to desensitization. Prolonged exposure to an agonist leads to a state characterized by a lack of responsiveness of the receptors.
Nondepolarizing NMB drugs bind to the postsynaptic receptor in a competitive fashion. An excess of Ach can tilt the balance in favor of neuromuscular transmission. There are good reasons to believe that Ach release is maintained during high frequency stimulation under physiologic conditions through presynaptic Ach receptors that regulate transmitter release. These positive feedback receptors are blocked by small doses of nondepolarizing relaxants."