Soman

04/01/1993 - "The direct action does not correlate well with protection against soman poisoning in vivo, however, which suggests that additional non-reactivating properties of these compounds, at sites other than the neuromuscular junction, may also be important for their therapeutic effectiveness."
04/20/2007 - "On a mole basis, both the recombinant AChE and its PEGylated form provide higher levels of protection against soman poisoning than the native serum-derived HuBChE. "
10/01/1993 - "The combination of lower and medium PEG was somewhat less efficient, while the formulation consisting of mostly lower PEG exerted protective effects only in soman poisoning."
07/01/1985 - "However, they were only marginally effective in preventing the consequences of soman poisoning in mice (these data have been published elsewhere). "
07/01/1983 - "None of the compounds was effective against poisoning by soman. "

03/01/1999 - "Antimuscarinic compounds were extremely effective in blocking (pretreatment) or terminating soman seizures when given 5 min after seizure onset. "
09/01/1991 - "The results indicate that tertiary anticholinergic compounds afford protection against soman-induced convulsions and hypersecretions and that the beneficial anticonvulsant effects are mediated through the central cholinergic system. "
01/01/1983 - "This study reveals that TAB is effective in protecting against Soman-induced seizures, but only at the expense of a severe decrease in LCGU after Soman exposure."
04/15/2003 - "The dose of a given drug that was an effective anticonvulsant against a 2x LD50 challenge of soman was equally effective against seizures induced by a 5x LD50 challenge. "
12/01/2010 - "In some recent studies, it was shown that lesion of the area tempestas (AT), medial septum (MS), perirhinal cortex (PRC), or posterior piriform cortex (PPC) produces anticonvulsant effects (prevention of convulsions or delayed onset of convulsions) in rats exposed to soman, whereas damage to nucleus accumbens, nucleus basalis magnocellularis, amygdala, hippocampus, or entorhinal cortex does not cause anticonvulsant impact. "

01/12/2010 - "In the present study, we thus evaluated these changes in a murine model of soman-induced status epilepticus up to 7 days after intoxication. "
09/05/2007 - "In conclusion, the present study indicates a quick neuro-inflammatory gene response that does not subside over 7 days suggesting a potential role in the neurological consequences of soman-induced status epilepticus."
09/01/2014 - "Despite the loss of both interneurons and principal cells after soman-induced status epilepticus, the frequency of sEPSCs was increased in the soman-exposed rats. "
09/01/2014 - "Rats were exposed to soman, at a dose that induced prolonged status epilepticus. "
07/01/2014 - "The progression of epileptiform activity following soman (GD) exposure is characterized by a period of excessive cholinergic activity followed by excessive glutamatergic activity resulting in status epilepticus, which may lead to neuropathological damage and behavioral deficits. "

09/01/1993 - "The results of this study suggest that the soman-induced respiratory depression is primarily caused at the central nervous level and that a significant peripheral neuromuscular block develops only at very high soman doses. "
02/01/1990 - "These findings not only support the notion of a relatively more important involvement of central respiratory mechanisms in soman-induced respiratory failure, but also identify a state of functional dissociation of central respiratory timing mechanisms as being a significant component in soman intoxication."
02/01/1990 - "Soman-induced respiratory failure was investigated in awake, behaving guinea pigs chronically instrumented to allow concurrent recordings of medullary respiratory-related unit (RRU) activity, diaphragm electromyogram (DEMG), and electrocorticogram. "
02/01/1990 - "Neurophysiological concomitants of soman-induced respiratory depression in awake, behaving guinea pigs."
03/30/1987 - "This dose of soman produced severe respiratory depression and transient hypertension, but no significant changes in the cardiac output or heart rate of anesthetized rats. "

09/01/2014 - "Galantamine, a drug currently approved for the treatment of Alzheimer's disease, has recently emerged as an effective pretreatment against the acute toxicity and delayed cognitive deficits induced by organophosphorus (OP) nerve agents, including soman. "
12/01/2011 - "Galantamine, a drug used to treat Alzheimer's disease, protects guinea pigs against the acute toxicity and lethality of organophosphorus (OP) compounds, including soman. "
01/01/2010 - "Galantamine, a drug used to treat Alzheimer's disease, has recently emerged as a potential medical countermeasure against the toxicity of organophosphorus (OP) compounds, including the nerve agent soman. "
12/01/2009 - "Galantamine, a centrally acting cholinesterase (ChE) inhibitor and a nicotinic allosteric potentiating ligand used to treat Alzheimer's disease, is an effective and safe antidote against poisoning with nerve agents, including soman. "
01/01/2010 - "We reported recently that galantamine, a drug used to treat Alzheimer's disease, administered before (up to 3 h) or soon after (up to 5 min) an exposure of guinea pigs to 1.5-2 x LD50 soman or sarin effectively counteracted the acute toxicity and lethality of the nerve agents provided that the animals were also post-treated with atropine. "