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.