Nitrergic response to Clostridium perfringens infection in the rat brain regions: effect of red light irradiation.

A single intraperitoneal injection of a gram-positive pathogen Clostridium perfringens (Cp) causes a remarkable down-regulation the constitutive nitric oxide synthase (cNOS) with a simultaneous increase in the activity of inducible NOS (iNOS) and the level of reactive nitrogen species in the rat brain major regions (cortex, striatum, hippocampus and hypothalamus) at 48 h post-administration of Cp. Treatment by both a semiconductor laser (SCL) and/or a light-emitting diode (LED) with same wavelength, energy density and time exposure (continuous wave, λ=654 nm, fluence=1.27 J/cm(2), time exposure=600 s) could modulate brain nitrergic response following Cp-infection. Besides, unlike the LED, the SCL-irradiation prevents the cNOS inhibition in all the studied brain regions and might be useful in restoring its function in neurotransmission and cerebral blood flow, along with providing a protective effect against nitrosative stress-induced iNOS-mediated injury in the brain regions.

Vitamin B-complex initiates growth and development of human embryonic brain cells in vitro.

We studied a combined effect of subcomponents of vitamin B complex on the growth, development, and death of human embryonic brain-derived cells (E90) cultured using a modified method of Matson. Cell death was detected by trypan blue staining. According to our results, vitamin B-complex in low-doses promote the development, maturation, and enlargement of human embryonic brain cells, on the one hand, and increases the percent of cell death, which attests to accelerated maturation and metabolism, on the other.

Influence of hypothalamic proline-rich peptide on the level of [14C]glucose utilization during crush syndrome.

The number of publications on the investigation of crush syndrome (CS) pathogenesis at traumatic toxicosis is rather limited. The influence of some pharmacological preparations on the development of CS pathogenesis is not very well clarified. Proline-rich peptide (PRP) is a fragment of a glycopeptide comprising the carboxyterminus of the neurohypophyseal vasopressin-neurophysin precursor isolated from the bovine neurohypophysis neurosecretory granules. The polypeptide possesses stimulating activity on differentiation and proliferation of T-lymphocytes and Interleukin-2 (Il-2) biosynthesis. The experimental model of CS of white rats was induced by 2-h of compression followed by 2, 24, and 48-h of decompression of femoral muscle tissue. The influence of PRP on [14C]glucose utilization was investigated in brain, heart, and kidney tissues. The level of [14C]glucose utilization decreased in brain during compression followed by 2-h and 24-h of decompression, while it increased under the influence of PRP at all decompression periods. The influence of PRP on the myocardium and kidneys differs, depending on its nature and on the periods of decompression.

Activity of enzymes of adenyline compounds metabolism during crush and decompression of muscle tissue. Part I. Adenylate deaminase activity at experimental crush syndrome.

INTRODUCTION: The number of works on investigation of crush syndrome (CS) pathogenesis, of organs and enzymatic systems at traumatic toxicosis is rather limited. While the clinical current of trauma and the lethality prognosis depend on a degree of violations in them. Such investigations are necessary for opportune diagnosis and definition of a treatment tactic. To complete this deficiency, adenylate deaminase (AMPD) level was studied in twelve tissues at experimental CS in vivo. RESULTS: The experimental model of CS on white rats was caused by crush and decompression of femoral muscle tissue. The CS influence on AMPD activity was investigated in hemisphere, cerebellum, hypothalamus, pituitary body, heart, lung, liver, spleen, kidney, adrenal, crushed and not crushed muscles. In muscles, kidney, pituitary body and adrenal the activity decreased in 2 hours crush but the compensation of effect is observed after 5 hours crush. In cerebellum, hemisphere, heart, liver and lung it decreased during both of crush times. After 2 and 5 hours crush in hypothalamus and in spleen AMPD activity appeared much higher than in control. After 2 hours crush at the end of 48 hours decompression, the activity in muscles, kidney, adrenal and pituitary body was lower, in cerebellum, hypothalamus, hemisphere and heart--higher than, in lung, spleen and liver--close to control. After 5 hours crush in the majority of studied tissues at the end of decompression, the activity was below of control. The greatest deviance was observed in muscles. As to brain in cerebellum and hemisphere the parameter was close to, in pituitary body and in hypothalamus it was 1,5-fold of control. CONCLUSION: AMPD level in the most of studied tissues differs from the control at definite time of crush and decompression. These results mean the possibility of nucleotides pool balance distortion and intermediates accumulation.

Neurohormonal regulation of calcium in the cell.

Neurohormone C (NC) is a glycopeptide isolated from bovine hypothalamus, which inhibits Ca-calmodulin (CaM)-dependent cAMP and cGMP phosphodiesterase (PDE) and is a regulator of Ca in the cell. Distribution of [45Ca]CaCl2 in the mitochondria and reticulum (SR) of heart and brain mitochondria and changes of Ca-binding proteins in these organelles under NC influence have been studied in the myocardium before and after isoproterenol-induced necrosis. Intraperitoneal administration of 80-100 mU of PDE inhibitory activity of NC to rats did not cause any noticeable changes in the protein content of intracellular organelles, but altered the affinity of certain proteins to 45Ca2+. This property of NC was especially noticeable after isoproterenol necrosis. Necrotic injury of the myocardium induced Ca2+ storage in the mitochondria and SR of brain, and decreased the Ca2+ concentration in myocardial mitochondria. NC injection to the animals with necrosis was followed by Ca2+ release from all the studied organelles.