Reactive anxiety, immune system function, and metabolism were studied in healthy volunteers. Temperament characteristics, state of health, number of leukocytes and platelets, and concentration of glucose, albumin, and fibrinogen significantly differed in subjects with low, moderate, and high level of reactive anxiety.

The response of the blood system to injection of neutrophilokin, a secretory product of latex-stimulated neutrophils, is studied. Neutrophilokin is shown to induce neutrophilic leukocytosis, eosinopenia, and lymphocytopenia and to reduce the cell count in the spleen. The ability of neutrophilokin to increase spontaneous oxidation of lipids is noted in the rat brain. Key Words: neutrophilokin; stress; lipid peroxidationLatex-stimulated neutrophils have been found to secrete a group of new transmitters of the immune response, which have been termed neutrophilokins (NK). These compounds raise the number of antibody-producing cells in the spleen, stimulate the host-graft reaction, and increase the functional activity of phagocytes [5][6][7]. On the other hand, immunization with sheep erythrocytes has been demonstrated to trigger in the blood system and immunocompetent organs a reaction which is similar to the effects of the general adaptive syndrome resulting from hypodynamia and hyperthermia [10]. In addition, immunization and immobilization stress cause unidirectional shifts in the content of biogenic monoamines in brain structures and the adrenals [11]. It should also be mentioned that immunogenesis is thought by some to be a particular case of adaptogenesis [2]. In addition to their immunostimulating effect, NK also elicit systemic biological effects (psychotropic and actoprotective effects and stimulation of wound repair) [8,9].In the present study we investigated the role of NK in the induction of the general adaptive syndrome. MATERIALS AND METHODSThe study was caried out on 48 nonpedigree rats weighing 160-200 g. The animals were divided into three groups. The control group (lst) received physiological saline subcutaneously and the 2nd group was given NK in a dose of 7x10 -7 rag/rat, subcutaneously. NK is a substance of peptide nature, which is isolated from the supernatant of stimulated neutrophils, as was described previously [6]. The rats of the 3rd group were injected subcutaneously with physiological saline, after which they were immobilized in the supine position by fixing the four extremities for 60 rain. Two hours after the start of the procedure, blood was taken from the retroorbital sinus under ether anesthesia, and the animal was killed by transcervical dislocation. The leukocyte count in the blood and the karyocyte count in the spleen were determined routinely [4]. One day before the experiment the animals were deprived of food; water was available ad libitum. The effect of NK on lipid peroxidation (LPO) was assessed as the degree of spontaneous LPO of the rat brain homogenate in the presence of 0.9% NaC1 (control) and NK in different concentrations (experiment). LPO was assessed as the accumulation of 2-thiobarbituric acid (TBA)-reactive substances [3]. The data obtained were statistically processed using Student's t test and nonparametric methods.

Objective — To examine the morphometric parameters of neurons and the oxidative status of the Wistar rat brain tissues after administering proline-containing peptides, also known as glyprolines (Arg-Gly-Arg-Pro-Gly-Pro [RGRPGP] and Thr-Lys-Pro-Arg-Pro-Gly-Pro [WKPRPGP; Selank]), on a traumatic brain injury (TBI) model. Study subjects — Our study involved 26 mature male Wistar rats (2.5-3 mos. old, 220-300 g). The morphometric parameters of neurons and the oxidative status of animal brain tissues were studied. Material and Methods — Four experimental groups were formed. Group 1 included intact control animals. Animals in three other groups were subjected to TBI via free fall of a 50 g weight from a height of 50 cm on the second day of the experiment and received the following injections: 0.9% sodium chloride solution in Group 2; WKPRPGP peptide solution in Group 3; RGRPGP peptide solution in Group 4. Substances were administered intraperitoneally on a daily basis at a dose of 0.1 mg/kg from day 1 through day 5 of the experiment. Morphometric parameters of rat brain neurons were studied on paraffin sections stained with hematoxylin and eosin. The intensity of free radical processes in the brain tissue was investigated by chemiluminescence. Results — An analysis of morphometric parameters revealed significant increases in the neuronal cytoplasm area, nucleolar area, number of nucleoli, and nuclear-nucleolar index with the introduction of the RGRPGP peptide after TBI, compared with the WKPRPGP peptide under the same conditions. After TBI and peptide administration, we observed an oxidative stress in the neocortex of Wistar rats, and it was more pronounced in the group of animals treated with RGRPGP. Conclusion — After RGRPGP peptide administration, we observed an increase in the morphometric parameters of neurons in the closed TBI model: a larger area and a greater number of nucleoli. Chemiluminescence data implied that WKPRRPGP peptide better protected brain tissue in rats from the effects of oxidative stress caused by TBI.

The acute action of unfavorable environmental factors on the mammalian body, including humans, produces a stereotypical metabolic reaction consisting of hyperglycemia, accumulation of ketone bodies in the blood, secondary hyperlipidemia, increased lipolysis, glycogenolysis, gluconeogenesis, and increased oxygen consumption [5, 8]. These changes are considered as reflecting a stabilizing (hypercatabolic, calorigenic) strategy for adaptation, or as stress diabetes. This variation of the adaptation strategy is realized essentially through activation of/3-adrenoceptors and increased production of glucocorticoids by the adrenals [5, 8], accompanied by the development of insulin resistance [I, 12]. Along with the metabolic changes described above, insulin resistance suggests a similarity between stress diabetes and diabetes mellitus as a nosological condition. In addition, one-hour immobilization stress produced after one day of food deprivation is known to generate an insulin-sensitizing effect, leading to the development of hypoglycemia [1]. It has also been shown that chronic cold stress produces a staunch hypoglycemia with development of resistance to the diabetogenic action of alloxan [8, 11]. This contradiction in the literature does not allow an unambiguous conclusion to be made regarding the role of stress in the pathogenesis of diabetes mellitus. The prophylaxis of type II diabetes mellitus developing on a background of a continuous increase in stress during ontogenesis (hyperadaptation) is among the methods with potential for preventing geriatric pathology in general [12].The aims of the present work were to study the hypoglycemic effects of various forms of stress and to consider the possibility of using this effect for the prophylaxis of diabetes mellitus. MATERIALS AND METHODSA total of 303 white mongrel rats (180-220 g) were used. Animals were subjected to acute and chronic stress. Acute stress was produced by periods of immobilization lasting 1 and 9 h. Chronic stress was modeled using three sessions of immobilization (60 rain daily) and three s.c. doses of neutrophilokine (NK)* given at doses of 7-10 -7 mg. This substance is a secretory product of activated neutrophils [3], has pro-oxidant activity and induces a stress syndrome [4]. In another series of experiments, immobilization stress was modeled by a preliminary 24-h period of food deprivation and/or s.c. dosage with Obsidan (propranolol HCI, Arzneimittelwerk Dresden GmbH, Germany) at a dose of 0.45 mg/kg. Diabetes was induced by i.p. injection of alloxan trihydrate (Lachema, Czechoslovakia) at a dose of 200 mg/kg [9] and s.c. doses of the long-acting glucocorticoid kenalog (VEB Berlin-Chemic, Germany) at a dose of 2 mg/kg. Experimental diabetes was induced after one-day starvation after completion of chronic stress. Tests for diabetes were carried out three days after induction with aUoxan and four days after doses of kenalog. *A homogeneous preparation of NK produced by a collaboration of the Institute of Immunology, Ministry of Medical Industry o...

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