http://en.wikipedia.org/wiki/4-Aminopyridine#Medical_use
DISCLAIMER : LEGAL
THE INFORMATION HEREIN IS BY NO MEANS INTENDED AS A REPLACEMENT FOR PROFESSIONAL MEDICAL ADVICE, IT IS FOR
RESEARCH AND EDUCATIONAL PURPOSES ONLY
1.) 4-Aminopyridine (4-AP, INN fampridine, USAN dalfampridine)
Fampridine is also marketed as Ampyra (pronounced "am-PEER-ah," according to the maker's website) in the United States by Acorda Therapeutics[5][6] and as Fampyra in Europe. In Canada, the medication has been approved for use by Health Canada since February 10, 2012.[7]
Toxicon. 1998 Apr;36(4):571-88.Recovery from the lethal effects of saxitoxin: a therapeutic window for 4-aminopyridine (4-AP).
Abstract
We have shown that saxitoxin (STX) induced lethality can be reversed by 4-AP when it is administered at the time of respiratory arrest [Benton, B. J., Spriggs, D. L., Capacio, B. R. and Chang, F.-C. T. (1995) 4-Aminopyridine antagonizes the lethal effects of saxitoxin (STX) and tetrodotoxin (TTX). International Society of Toxicology, 5th Pan American Symposium on Animal, Plant and Microbial Toxins, Frederick, MD. July/August 1995, p. 217]. The purpose of this study was to determine whether 4-AP's efficacy could be enhanced further when administered at different times relative to STX intoxication. The animals used in this study were chronically instrumented for concurrent recordings of diaphragm electromyogram (DEMG), neck skeletal muscle electromyogram, Lead II electrocardiogram, and electrocorticogram (ECoG). There were five groups of unanesthetized guinea pigs. The first group served as 4-AP controls and received a 2 mg/kg i.m. dose of 4-AP. The four remaining groups were given a lethal dose of STX (5 microg/kg i.m.); the second group, STX controls, received no 4-AP; the third group, the 4-AP treatment group, received 4-AP immediately following cardiorespiratory collapse; the fourth group was the 4-AP/STX co-administration group and 4-AP was given concurrently with STX; and the fifth group was the 4-AP pretreatment group in which 4-AP was given 10 min before STX. At the point of STX-induced cardiorespiratory collapse, the guinea pigs were ventilated and given an i.p. injection of sodium bicarbonate. Results showed that 4-AP prevented cardiorespiratory collapse in 3/7 animals in the 4-AP pretreatment group. Also, 4-AP in conjunction with artificial ventilation and sodium bicarbonate accelerated recovery from STX-induced cardiorespiratory collapse in all the treatment groups compared to the STX controls.
- PMID:
- 9643470
- [PubMed - indexed for MEDLINE]
2.) ATP; Adenosine Tri-Phosphate (injection)
Br J Pharmacol. 1984 Feb;81(2):277-82.Antagonism of tetrodotoxin- and procaine-induced axonal blockade by adenine nucleotides in the frog sciatic nerve.
Abstract
The effects of adenosine triphosphate (ATP), adenosine diphosphate (ADP), adenosine monophosphate (AMP), and adenosine on compound action potentials were investigated in de-sheathed frog-sciatic nerve preparations. ATP and ADP but not adenosine antagonized the inhibitory action of tetrodotoxin (TTX) on nerve conduction. AMP had little or no antagonistic effect on TTX-induced axonal block. ATP was more effective than ADP. The effects of the nucleotides were related to the degree of the TTX-induced inhibition and were more evident where the blockade was more intense. ATP and ADP but not adenosine antagonized the procaine-induced axonal blockade which, in some experiments, was completely reversed by these nucleotides. ATP and ADP were of similar potency. The axonal blockade induced by pentobarbitone was not antagonized by ATP, ADP, AMP or adenosine. The possibility that ATP stimulates a TTX-sensitive sodium channel is discussed. Free PMC Article
- PMID:
- 6704590
- [PubMed - indexed for MEDLINE]
- PMCID:
- PMC1986875
**OTHER SOURCES**
http://www.ctrl-c.liu.se/~ingvar/methods/poison.html
http://www.sott.net/article/232912-Assassinations-by-induced-heart-attack-and-cancer
http://www.ncbi.nlm.nih.gov/pubmed/6704590
http://www.sott.net/article/232912-Assassinations-by-induced-heart-attack-and-cancer
http://www.ncbi.nlm.nih.gov/pubmed/6704590
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