Formation of the “setting” level of body temperature regulation during endotoxin fever

The experiments on rats and rabbits using modern physiological, biochemical research methods and the pharmacological approach established that in the body, the action of bacterial endotoxin, accompanied by fever, leads to a significant decrease in blood plasma and in CSF of the arginine content. In rabbits after 30 min intravenous administration of carbon-labeled arginine hydrochloride (25 μCi/kg) at the endotoxin fever peak (after the 60 min injection of endotoxine E. coli), the radioactivity level in the blood plasma decreases and significantly increases in the cerebrospinal fluid and the hypothalamus tissue. It was revealed that although the content and speed of norepinephrine turnover in the hypothalamus after the introduction of L-arginine hydrochloride (100 μg) into the ventricles of the rats does not change in comparison with control animals, however, the chemoreactive properties of the thermoregulatory structures of the brain have changed, which manifests itself in the change in the expression and duration of thermoregulatory effects of the central action of norepinephrine and acetylcholine. It was established that the administration of L-arginine hydrochloride into the brain ventricles at a dose of 100 μg per animal or in the blood flow at a dose of 20 mg/kg caused the pronounced antipyretic effect. It was found that L-arginine hydrochloride (100 μg), after it has been introduced into the ventricles of the brain, increases the impulse activity of heat-sensitive neurons of the medial preoptic region of the anterior hypothalamus in rabbits due to a brain temperature growth when the animal’s body is overheated. Apparently, CSF arginine can be considered as an important factor in the changes in the excitability thresholds of cold and heat-sensitive neurons in the hypothalamus and in the formation of the “setpoint” of body temperature regulation during endotoxin fever.