Linked Life Data

1998202

Source:http://linkedlifedata.com/resource/pubmed/id/1998202

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1991-4-1
pubmed:abstractText
The effects of HI-6 and pralidoxime chloride (2-PAM) on soman-induced lethality, time to death and several cholinergic parameters in rats were compared to understand the beneficial action of HI-6. Treatment with atropine sulfate (ATS) or HI-6 alone protected against 1.2 and 2.5 LD50s of soman respectively, whereas 2-PAM or methylated atropine (AMN) alone afforded no protection. Addition of ATS, but not AMN, to HI-6-treated rats enhanced the protection from 2.5 to 5.5 LD50s. HI-6 increased the time-to-death, while 2-PAM had no effect; a combination of HI-6 and ATS provided the most significant increase in time-to-death. Cholinesterase (ChE) activity was not altered in any tissue by ATS, HI-6 or 2-PAM treatment individually, but was markedly inhibited in all tissues by 100 micrograms/kg of soman. In soman-poisoned rats, the HI-6, but not the 2-PAM, group had significantly higher levels of ChE in blood and other peripheral tissues than did the group given soman alone. Neither HI-6 nor 2-PAM affected soman-inhibited ChE in the brain. Additional ATS treatment had no effect on ChE activity. HI-6 and 2-PAM neither modified baseline brain acetylcholine (ACh) or choline (Ch) levels nor protected against soman-induced ACh or Ch elevation. 2-PAM exhibited a 4-fold more potent in vitro inhibition of 3H-quinuclidinyl benzilate (3H-QNB) binding and sodium-dependent high-affinity Ch uptake (HACU) than did HI-6 in brain tissues. The findings that 2-PAM is a more potent in vitro inhibitor of muscarinic receptor binding and HACU than HI-6, and yet neither elevates ChE activity in the periphery nor protects rats against soman poisoning, indicate the importance of higher ChE activity in the periphery of HI-6-treated rats. Maintenance by HI-6 of a certain amount of active ChE in the periphery appears to be important for survival after soman exposure.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Acetylcholinesterase, http://linkedlifedata.com/resource/pubmed/chemical/Atropine, http://linkedlifedata.com/resource/pubmed/chemical/Cholinesterase Reactivators, http://linkedlifedata.com/resource/pubmed/chemical/Cholinesterases, http://linkedlifedata.com/resource/pubmed/chemical/HI 6, http://linkedlifedata.com/resource/pubmed/chemical/Oximes, http://linkedlifedata.com/resource/pubmed/chemical/Pralidoxime Compounds, http://linkedlifedata.com/resource/pubmed/chemical/Pyridinium Compounds, http://linkedlifedata.com/resource/pubmed/chemical/Quinuclidinyl Benzilate, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Muscarinic, http://linkedlifedata.com/resource/pubmed/chemical/Soman, http://linkedlifedata.com/resource/pubmed/chemical/pralidoxime
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0378-4274
pubmed:author
pubmed:issnType
Print
pubmed:volume
55
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
131-47
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
1991
pubmed:articleTitle
A comparison of cholinergic effects of HI-6 and pralidoxime-2-chloride (2-PAM) in soman poisoning.
pubmed:affiliation
U.S. Army Medical Research Institute of Chemical Defense Center, Aberdeen Proving Ground, MD.
pubmed:publicationType
Journal Article, Comparative Study