[Severe contusion of the eyeball as a risk factor for the development of proliferative vitreoretinopathy]. / Kontuziya glaznogo yabloka tyazheloi stepeni kak faktor riska razvitiya proliferativnoi vitreoretinopatii.

The article is devoted to the problem of proliferative vitreoretinopathy (PVR) developing after severe contusions of the eyeball. Some experts doubt the possibility of developing such a severe complication after a closed eye injury, however, the accumulated literature data and research by scientists demonstrate a high probability of developing PVR in such cases, which could lead to adverse outcomes. The article presents the views of different authors and systematizes information about the frequency and the risk factors of developing PVR after different types of closed eye injury. The main purpose of this review is to demonstrate a high probability of developing PVR after a closed eye injury, which should alert specialists at the first stages of treatment in such patients and stimulate timely prevention and treatment of this complication.

Possibility of usage of aminostigmine structural analogue for the treatment of toxic cognitive disorders.

We studied the effects of 2-(hexyl(methyl)amino)methyl)pyridyl-3-dimethyl carbamate (OPDC), a structural analogue of aminostigmine oxalate, on memory formation in rats with toxic scopolamine-induced amnesia. It was shown that OPDC in non-toxic doses ((1)/215 LD50) has significant anti-amnesic action. Ipidacrine and galantamine in the doses similar to toxic doses ((1)/17 and (1)/6 of LD50, respectively) induced the retention of memory trace. Administration of aminostigmine ((1)/11 of LD50) induced unstable anti-amnesic effect in the model of scopolamine-induced amnesia.

Prospects of using benzodiazepines in complex therapy of poisonings with anticholinesterase agents.

The efficiency of benzodiazepines on mouse model of anticholinesterase poisoning was shown. The protective effects of clonazepam and midazolam were observed at high (1 TD50, incoordination) and medium (0.3 TD50) doses and the effects of phenazepam and diazepam were found only at high doses. Midazolam produced the most pronounced protective effect: administration of this drug significantly increased the protective index of atropine+HI-6 combination during poisoning.

[Specific features of the anticonvulsant effect of memantine in mice intoxicated with a model organic phosphate].

The effect of memantine administration has been studied on the model of mice poisoning with an anticholinesterase compound. It is established that the memantine action is due to its influence on the cholinesterase activity in the brain, blood plasma, and erythrocytes in addition to its NMDA-blocking action. Memantine promotes oxime-induced erythrocyte enzyme reactivation on the model of mice poisoning with anticholinesterase compound (0.8 LD50).

[Study of tolerance of central muscarinic receptor blockers].

The tolerance of five central muscarinic receptor antagonists has been studied in experimental animals. According to the effect on orientation-exploratory reaction, drugs were arranged in the following order of increasing toxicity: procyclidine < trihexiphenidyl < benactizine < atropine < scopolamine. For the same therapeutic index, trihexiphenidyl and benactizine were characterized by the maximum tolerance (TD50/ED50 > 10) in mice. Scopolamine and atropine exhibited anticonvulsant activity at doses exceeding the threshold values by a factor of 6.3 and 3.9, respectively. For procyclidine, the average anticonvulsant dose was threefold lower than the threshold value. Benactizine and procyclidine had maximum tolerance levels in rats. The TD50/ED50 ratio for these drugs was greater than 3 (against 0.5 - 0.7 in groups treated with trihexiphenidyl, atropine and scopolamine).