hgg-12 has been researched along with pralidoxime* in 3 studies
3 other study(ies) available for hgg-12 and pralidoxime
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Therapy of organophosphate poisoning in the rat by direct effects of oximes unrelated to ChE reactivation.
Isolated rat diaphragm preparations treated with soman or with the irreversible and oxime resistant cholinesterase (ChE) inhibitor S27 showed a considerable recovery of neuromuscular transmission (NMT) during incubation with the (bis)pyridinium oximes HI-6, HGG-12, P2S and obidoxime. In the soman-treated preparations this NMT recovery was predominantly caused by reactivation of acetylcholinesterase (AChE) but in the S27-treated preparations it was caused by a direct (pharmacological) effect unrelated to enzyme reactivation. Atropinized rats were artificially ventilated after injection with 3 x LD50 soman for 3 h and then treated with HI-6, i.e. at a time when oxime reactivation of soman inhibited ChE is no longer possible. Nevertheless, these rats started to breathe spontaneously and 50-60% survived more than 24 h, whereas all control animals (saline instead of HI-6) died within 10 min after artificial ventilation was terminated. In such animals no significant reactivation of ChE activity at various time intervals following HI-6 treatment was found, either in the diaphragms or in the brains. There was a significant amount of NMT (50%) in vitro in diaphragms obtained from these animals. This NMT did not improve in vitro in the presence of HI-6 and was not inhibited by soman administered to the medium. It is concluded that in this case the NMT found was based on synaptic adaptation to the continued inhibition of ChE and that the survival of the animals might be due to a combination of this synaptic adaptation and central direct effects of HI-6. Topics: Animals; Antidotes; Blood-Brain Barrier; Cholinesterase Reactivators; Diaphragm; In Vitro Techniques; Male; Neuromuscular Junction; Obidoxime Chloride; Organophosphate Poisoning; Oximes; Pralidoxime Compounds; Pyridinium Compounds; Rats; Respiratory Insufficiency; Synaptic Transmission | 1991 |
Effect of PAM-2 Cl, HI-6, and HGG-12 in poisoning by tabun and its thiocholine-like analog in the rat.
It has been shown that HI-6 was the most potent oxime so far known in poisoning by sarin, VX , and soman, but its protective effect in tabun poisoning, allegedly due to poor reactivation of inhibited ChE, was much less pronounced. We have found that the thiocholine-like analog of tabun , O-ethyl, N-N- dimethyamino -S-(2-diethylaminoethyl)- thiophosphatemethylsul fomethylate (Ta-S-N+), was very useful in resolving this problem and established the relationship between reactivating and protective effects of PAM-2 Cl, HI-6, and HGG-12 in rats. PAM-2 Cl (protective ratio (PR) = 22.1) and HI-6 (PR = 24.8), combined with atropine, were very effective against Ta-S-N+ poisoning and reactivating inhibited RBC AChE in vitro and rat blood ChE in vivo. The inefficiency of PAM-2 Cl (PR = 1.6) and HI-6 (PR = 2) in tabun poisoning was due to their inadequacy to reactive tabun -inhibited ChEs . The protective effects of HGG-12 in tabun (PR = 2.8) and Ta-S-N+ poisoning (PR = 2.6) were low, and in the absence of any reactivation of inhibited ChEs , have been attributed to its direct pharmacological effects, which were much more potent in the comparison with PAM-2 Cl or HI-6. It is concluded that the reactivation of inhibited ChE is of decisive importance in the efficient protection in poisoning by tabun and other known chemical warfare nerve agents, whereas their direct pharmacological effects are of limited value, allowing survival of animals only against a few LD50s . Topics: Animals; Atropine; Choline; Cholinesterase Reactivators; Cholinesterases; Female; Guinea Pigs; Heart; Humans; Lethal Dose 50; Male; Muscle Contraction; Muscle, Smooth; Organophosphate Poisoning; Organophosphates; Oximes; Phrenic Nerve; Pralidoxime Compounds; Pyridinium Compounds; Rats; Thiocholine | 1984 |
PAM-2 Cl, HI-6, and HGG-12 in soman and tabun poisoning.
Acute sc toxicity of soman increased in the order, mice----rats----guinea pigs----dogs, being 12.6 times more toxic to dogs (LD50 = 0.05 mumol/kg) than to mice. It was 2.8 times more toxic than tabun to mice and 35 times more toxic to dogs. HI-6 was the least toxic and had similar toxicity values to the four animal species studied and HGG-12 the most toxic of the three oximes used. HGG-12 has shown the greatest interspecies variation (rats:dogs = 1:19.5). HI-6, HGG-12, and PAM-2 Cl (in conjunction with atropine and diazepam) revealed the best protective effect in soman-poisoned dogs, with the respective protective indices of 9, 6.3, and 3.5, followed by guinea pigs. In tabun poisoning the best, but relatively low, protective effect was found only in guinea pigs. The introduction of diazepam increased the protective effects of atropine-oxime combination in soman and tabun poisoning by 10 to 80%. We suggest that the high toxicity of soman and low toxicity of HI-6 may be anticipated in man. The inefficiency of HI-6, HGG-12, and PAM-2 Cl in tabun poisoning points either to the search of new compounds or to the use of the mixture of the oximes found to be effective against the known chemical warfare nerve agents. Topics: Acetylcholinesterase; Animals; Antidotes; Atropine; Cholinesterase Inhibitors; Cholinesterase Reactivators; Diazepam; Dogs; Guinea Pigs; Lethal Dose 50; Male; Mice; Organophosphate Poisoning; Organophosphates; Oximes; Pralidoxime Compounds; Pyridinium Compounds; Rats; Soman; Species Specificity | 1984 |