[Effect of strophanthin and digoxin on the activity of succinate and lactate dehydrogenases and membrane Na+, K+-ATPase in the heart of rats with experimental myocarditis]. / Vliianie strofantina i digoksina na aktivnost' suktsinat-laktatdegidrogenaz i membrannoi Na+, K+-ATFazy v serdtse krys s éksperimental'nym miokarditom.

In rats with adrenaline-induced myocarditis conditionally therapeutic doses of strophanthin (2.7 mg/kg) and digoxin (0.89 mg/kg) were chosen according to performance of the test of swimming until the complete fatigue. The influence of drugs in these doses on enzymatic activity was evaluated by histochemical methods in heart of control and myocarditis rats. It was found out that both of cardiac glycosides decreased lactate dehydrogenase and membrane Na+, K+-ATPase activity and increased succinate dehydrogenase activity in rats with experimental myocarditis.

[Allopurinol in the combined therapy of severe forms of epilepsy in children]. / Allopurinol v kompleksnoi terapii tiazhelykh form épilepsii u detei.

Allopurinol was tested as an antiepileptic drug (AED) in children with progressive history of the disease, frequent severe seizures and ineffective conventional AED treatment. A total of 38 children aged 4 months to 10 years were given allopurinol at daily doses of 4 to 5 mg/kg body weight. The drug had positive effects in 10 out of 28 patients having frequent seizures. Complications were not observed. Allopurinol increased serotonin content in platelets. Biochemical investigations proved the therapy with allopurinol alone or combined with other AEDs to be effective.

[Pharmaco-dynamic mechanisms for reducing the activity of an epileptogenic focus with allopurinol]. / Farmako-dinamicheskie mekhanizmy umen'sheniia aktivnosti épileptogennogo ochaga pod vliianiem allopurinola.

Experiments on 73 rats with electrochemotrodes implanted into the dorsal portion of the left hippocamp showed that allopurinol (A) injected intraperitoneally in a dose of 25 and 50 mg/kg decreased the activity of the penicillin-induced epileptogenic foci in the hippocamp and significantly increased the content of serotonin (S) in their area at the 40th minute of the epileptogenesis. Thus, all this provided evidence in favour of a shift in tryptophan metabolism toward an elevated S production that inhibited the development of the epileptic process. A is suggested for clinical use in treating patients with epilepsy, especially in those cases that are resistant to common therapy.