Hyperammoniemia in rats with barbiturate coma.

Sodium thiopental in the comatogenic (but not soporogenic) dose caused hyperammoniemia in rats. Blood ammonium level increased 3-fold within 3 h and 5-fold within 18 h. Blood urea level increased by one-third within 18 h against the background of unchanged creatinine level and hematocrit.

Metabolic correction of gas exchange disturbances in rats with barbiturate coma.

Krebs cycle intermediates normalized gas exchange and decreased the mortality rate in rats with barbiturate coma. Treatment with other substrates including glucose and products of glycolysis was ineffective. Oxygen inhalation had no effect on oxygen consumption and indexes of external respiration.

Effect of sodium succinate on gas exchange in rats with barbiturate-induced coma.

Injection of sodium succinate in doses of 5 or 10 mmol/kg (but not 1 mmol/kg) intensified oxygen consumption in rats with sodium thiopental-induced coma. Injection of SDH inhibitor (sodium malonate) inhibited gas exchange and abolished the effect of sodium succinate. The effect of succinate on rat survival was positive, while that of malonate was negative, but manifested only as a trend.

[Gas exchange intensity: relation to the body radiation resistance].

In the absence of immobilization stress gas exchange in rats does not increase in response to exposure to 6 to 13 Gy. Oxygen uptake intensity by intact animals at room and low ambient temperature is a stable individual characteristic positively correlating with life span following acute bone marrow irradiation. It is hypothesized that high gas exchange in radioresistant animals is linked with high inherent DNA synthesis and reparation.

[Mechanisms of cerebral radiation syndrome].

Postradiation DNA breaks activate the repair enzyme, Adenosine diphosphoribosil transferase, which consumes NAD as a substrate and causes neuronal NAD and then ATP pool depletion; here this is considered to be the crucial links of the cerebral radiation syndrome (CRS) mechanism. Two ways of its metabolic correction were examined: (a) prevention of postradiation NAD depletion by administration of the enzyme inhibitor and (b) shunting NAD-dependent oxidative phosphorilation path of ATP resynthesis by administration of substrate of NAD-independent oxidation.

[Gas exchange as a factor of the body radiation resistance].

Cold-provoked intensification of oxygen consumption was correlated with individual radioresistance of mice. There was a positive correlation between the parameters in normoxia and hyperoxia, and a distinct negative correlation in hypoxia. Radiosensitizer of hypoxic cells, metronidasol, severed the correlation no matter what level of oxygenation in the course of irradiation.

[Rationale for social and hygienic methods of rehabilitation of the population of the areas exposed to radioactive contamination resulting from the Chernobyl accident].

The factors preventing the stabilization of life in the contaminated areas include sociopsychic epidemic of "victim's syndrome" among the population; unfavourable information environment; secondary negative action of contrameasures (obligatory behavioral limitations, privileges, compensations, etc.). The rehabilitation of the population's life is based on the activization of a personal position and initiative of individuals, stimulation of economic activity in the areas.

[ Multigeneration carcinogenesis in the evaluation and prognosis of delayed radiation effects].

Radiation multigeneration carcinogenesis' mechanisms are associated with inheritance of non-specific genome lesions. Evidence indicates that the effect is significantly enhanced by some chemical carcinogens action on the offspring of irradiated parents. Hereditary character of the phenomenon is a prerequisite to accumulation of these genetic determinants in the population.

[Protective reaction of brain cells during change in permeability of the blood-brain barrier].

General anesthesia carried out in neurosurgical operations caused liberation of neurospecific proteins into blood. High content of these antigens was maintained in biological fluids within 7 days, which occurred apparently due to activation of biosynthesis. Antibodies to the antigens were detected only within 21 days after the surgical intervention.

[Acute radiation cerebral disorders as an effect of neuronal DNA damage].

Early transient incapacity and cerebral radiation syndrome were shown to result from the de-energizing of the brain due to NAD and ATP neuron pools depletion since DNA breaks stimulate the repair enzyme, ADP-ribosyltransferase, that consumes NAD as a substrate. The phenomenology of syndromes, peculiarities of the CNS repair and neutron RBE might be attributed to this mechanism. DNA is thus a common target for stochastic, deterministic and physiological effects of radiation.

[An experimental assessment of the genetic effects of low doses of internal irradiation].

Genetic study of rats showed the possibility of registration of the minor doses of the inside and outside irradiation. The postmiosis mutations, number of reciprocal translocations in spermatogonia may be used for indexation of the effects.

[The radiation hygiene problems of multigenerational carcinogenesis].

This review deals with a phenomenon of multigeneration carcinogenesis; the carcinogenic risk for offsprings of irradiated persons can be estimated as 4.10(-3) Sv-1. Though some epidemiological findings in this area are contradictory, multigeneration carcinogenesis may present a part of a population risk (genetic load).

[A comparative evaluation of the genetic effects of uniform internal (137Cs) and local x-ray (testes) irradiation of rats].

In experiments with rats it was shown that with equal absorbed doses after single injection of 137Cs and local X-irradiation of testes the mutation yield in gametes was different when tested by the frequency of dominant lethals and half-lethals, reciprocal translocations, univalents, and chromosome fragments. A higher efficiency of whole-body irradiation as compared to local exposure of testes, with respect to genetic damages induction, and the statistically significant increase in the number of the damages during a long period of time after cessation of the absorbed dose formation indicated that indirect effects of whole-body irradiation contributed to the injury to hereditary structures and permitted to estimate approximately their contribution (up to 50%).

[Patterns in the formation of cerebral damage and recovery from supralethal irradiation].

In experiments with rats it has been shown that dose-rate and radiation fractionation influence the dose dependence of early transient incapacity (ETI) and the development of tolerance to ETI. The authors discuss the possibility of interpreting the tolerance to ETI as a form of the cerebral damage displayed by the impairment of the brain response to radiation. A correlation has been revealed between the cerebral damage and recovery and repair of radiogenic damages to DNA.

[The physical work capacity parameters of rodents studied by repeated high-speed swimming following uniform and nonuniform irradiation at high doses].

Physical fitness of irradiated (20-200 Gy) mice and rats was estimated by the method of repeated swimming at a fixed distance. Revealed was the reduction adequacy of the two indices, that is the starting time and the fatigue coefficient, the latter being changed more considerably. The dose of 80-100 Gy determined the threshold of the cerebral damage and caused an irreversible decrease in the physical fitness of rodents.

[Regulatory disorders of locomotor functions in dogs during prolonged irradiation in a wide range of dose rates].

A biphase pattern of the development of locomotor disturbances, connected with the primary response and cerebral radiation syndrome, was demonstrated in experiments with dogs subjected to prolonged irradiation, just as it was observed after acute exposure. Dose thresholds for the development of these states were somewhat higher with the prolonged irradiation. The time of the appearance of disturbances increased due to the delay of achievement the dose threshold increase with dose-rate decrease, the time interval needed for the development of the corresponding pathological process being unchanged.

[Physiological characteristics of posture maintenance by dogs during immediate reaction to irradiation].

The ability of dogs to maintain a vertical posture during the first hours after irradiation at a dose of 10 or 80 Gy was investigated. Two experiments were performed. In the first experiment, during 5 hours after irradiation the vector stabilogram area, peak muscle efforts and sensorimotor coordination were measured 10 times every 30 min.

[Postradiation motor disorders in rodents as the equivalent of the clinical manifestations of a primary radiation reaction].

In experiments with albino mice it was found that during the first hours following gamma irradiation with doses of 10-80 Gy stability of implementation of loading and coordination tests was impaired and hard work endurance decreased. With doses exceeding 100 Gy, cerebral damages were stably manifested. There was a similarity between the postirradiation motor disturbances in animals of various species.

[The mechanism of the neuromotor disorders in the period of the primary reaction to irradiation].

In experiments with dogs it was shown that the impairment of the capacity of fulfilling some actions (e. g. high jumping, equilibration, racing) was maximum 4h after gamma-irradiation with doses of 10 and 40 Gy and did not coincide with vomiting.

[The phasic structure of early disorders of functional capacity following irradiation in rats].

In experiments with rats it was shown that an early decrease in physical efficiency after irradiation involves some partially mutually superimposed phases. Phases of excitation, hypokinesia and neurological disorders are identified in early transient inefficiency followed by phases of an early transient diminution of efficiency and a reversible disturbance of the accomplishment of the known operations. Simultaneously, there is a phase of an irreversible decrease of the informational capacity of CNS as well as the tolerance to early transient in efficiency upon repeated exposure.

[The rate of repair of a radiation lesion of the central nervous system during protracted and fractionated irradiation].

In experiments with fractionated and prolonged irradiation of guinea pigs and dogs it was shown that the recovery of CNS from acute radiation affection may be approximated, for different animal species, by an exponential function at a rate of 0.02 h-1 and a half-life period of approximately 30 h.

[The dosage thresholds for disordered physical work capacity in mice and rats following irradiation].

Physical efficiency of mice and rats at early times following irradiation with doses of 35 to 200 Gy was estimated by the muscle endurance and motor coordination indices. A threshold nature of the effects was exhibited at high doses. For instance, as large as 40 Gy was the dose threshold at which stability in the accomplishment of the known operations was impaired; at 70-100 Gy, the accomplishment decreased down to 50% of the initial level, by the 2nd hour after irradiation, with the subsequent partial restoration; 200 Gy was the threshold dose at which the disturbances were irreversible.

[Various physiological characteristics of primary radiation reaction and its apomorphine model].

Experiments were performed on 52 dogs exposed to irradiation at a dose of 5-80 Gy or injected with 0.02-0.5 mg/kg apomorphine.

[Evaluation of toxemia and peripheral blood indices in dogs irradiated with large doses].

Toxemia and peripheral blood of dogs were studied after irradiation with doses of 2.9, 10, 40, and 80 Gy. Destructive changes were revealed in the blood part of which could not be counted by conventional methods.