N1gg3r4tic
Member
In my I noted dramatic cessation of after an intravenous MC. The MC was 1% . Given that I've taken all the nutrients in the MC in high supplementary oral doses during my strongest twitching period without effect, the one item I've not taken prior to the MC stands out as the leading candidate for my twitch allevation. And sure enough, there is published research showing that procaine is anti-fasciculatory. Note that lidocaine was found to be stronger.
This may be the first time this abstract has been made available online since the citation for it in PubMed does not include its abstract, as is the case with most older studies. So without further ado, please note that in 1968 Usubiaga and Standaert reported in
The effects of local anesthetics on motor nerve terminals. The effects of four local anesthetics, procaine, lidocaine, tetracaine and dibucaine, were studied on the soleus neuromuscular preparation of the cat in vivo. All local anesthetics injected i.a. or i.v. depressed the posttetanic potentiation of the soleus muscle and abolished the neural repetitive afterdischarge of the motor nerve terminals. In addition, local anesthetics modified the pattern of tetanic muscle contraction. Lidocaine was 1.5, tetracaine was 10 and dibucaine was 15 times more potent than procaine in depressing posttetanic potentiation. Recovery of posttetanic potentiation (PTP) was rapid following procaine and lidocaine, but it was prolonged after tetracaine and dibucaine administration. Since PTP and posttetanic repetitive activity are neural events and local anesthetics depressed them without depressing the transmission of single twitches, it is concluded that local anesthetics act by selective depression of the motor nerve terminal. The correlation between drug potencies for PTP suppression and local anesthetic potency for blocking conduction in peripheral nerves and the agreement between doses depressing PTP and those affecting central nervous system neurons also support a neural locus of action. The possibility of a postjunctional effect of local anesthetics is considered, but, according to the dose-response relationship, it only occurs after the injection of larger doses.
This may be the first time this abstract has been made available online since the citation for it in PubMed does not include its abstract, as is the case with most older studies. So without further ado, please note that in 1968 Usubiaga and Standaert reported in
The effects of local anesthetics on motor nerve terminals. The effects of four local anesthetics, procaine, lidocaine, tetracaine and dibucaine, were studied on the soleus neuromuscular preparation of the cat in vivo. All local anesthetics injected i.a. or i.v. depressed the posttetanic potentiation of the soleus muscle and abolished the neural repetitive afterdischarge of the motor nerve terminals. In addition, local anesthetics modified the pattern of tetanic muscle contraction. Lidocaine was 1.5, tetracaine was 10 and dibucaine was 15 times more potent than procaine in depressing posttetanic potentiation. Recovery of posttetanic potentiation (PTP) was rapid following procaine and lidocaine, but it was prolonged after tetracaine and dibucaine administration. Since PTP and posttetanic repetitive activity are neural events and local anesthetics depressed them without depressing the transmission of single twitches, it is concluded that local anesthetics act by selective depression of the motor nerve terminal. The correlation between drug potencies for PTP suppression and local anesthetic potency for blocking conduction in peripheral nerves and the agreement between doses depressing PTP and those affecting central nervous system neurons also support a neural locus of action. The possibility of a postjunctional effect of local anesthetics is considered, but, according to the dose-response relationship, it only occurs after the injection of larger doses.
