Contribution of the gasotransmitter nitric oxide to the structural and functional organization of erythrocytes under conditions of hypoxia/reoxygenation.

Hypoxia is accompanied by changes in metabolism and cell functioning. Erythrocyte hemoglobin can be involved in adaptation to hypoxia by acting as an oxygen sensor, providing a link between oxygen content and blood circulation. The mechanisms providing this function have not been completely established. The purpose of this study was to evaluate the effect of the gasotransmitter nitric oxide on the structural and functional organization of erythrocytes under conditions of hypoxia/reoxygenation. NO participated in adaptive reactions under hypoxia/reoxygenation conditions by changing hemoglobin conformation, followed by changes in hemoprotein spectral characteristics and hemoglobin affinity to oxygen together with increasing anisocytosis, volume and cell surface. The increase in intracellular NO concentrations under hypoxic conditions was provided by extracellular fluid nitrites. Molsidomine (a NO donor) induced a higher NO increase without involvement of the nitrite reductase mechanism, it caused an increase in the average erythrocyte volume, anisocytosis, and an increase in the cell surface.

[The fatty acids and fatty aldehydes of blood as a biochemical of multiple organ failure].

The article presents the results of analysis of fatty acids and fatty aldehydes of plasma and blood erythrocytes in patients with the syndrome of multiple organ failure. The increase of relative level of mono-unsaturated fatty acids and decrease of poly-saturated fatty acids and saturated stearic acid in blood plasma is demonstrated. The reliable alterations in erythrocytes concerning the content of saturated palmitic and poly-saturated linoleic fatty acids are detected. In patients with multiple organ failure the decrease of level of fatty aldehydes and cholesterol in blood plasma is established too. The conclusion is made about significant role of mono non-saturated fatty acids in disorders of systemic haemodynamics and evaluation of degree of disorder of lipid metabolism between cells and blood plasma lipoproteins.

[Nitrogen monoxide and nociceptive processes]. / Monooksid azota i notsitseptivnye protsessy.

Experiments on conscious rats studied the effects of systemic or central application of a nitric oxide (NO) donor or NO-synthase inhibitor on the pain sensitivity threshold. Injection of SNAP in doses of 0.2, 2.0, and 20.0 micrograms into the subarachnoidal space of the ventral medulla through a preimplanted steel cannula was accompanied by a dose-dependent change in tail-flick latency. Intraperitoneal injection of 30 mg L-NAME also increased pain sensitivity threshold levels. The findings suggest that the decrease in pain sensitivity after systemic NO-synthase inhibitor administration is due to the modulation of NO-dependent processes at both the central and peripheral levels.

First and second phases of biphasic fever: two sequential stages of the sickness syndrome?

We hypothesized that the systemic inflammatory response undergoes two consecutive stages, each characterized by different nonspecific sickness patterns. To test this hypothesis, we studied thermal, nociceptive, and motor responses to lipopolysaccharide (LPS) in 43 unanesthetized, habituated, and lightly restrained male Wistar rats previously implanted with a catheter in the jugular vein. Escherichia coli LPS was injected intravenously in a dose of 0, 0.1, 1, 10, 100, or 1,000 micrograms/kg. Colonic temperature (Tc) was measured with a thermocouple. Changes in nociception were assessed by tail flick latency (TFL) to a noxious heat stimulus. Motor activity was evaluated using an observation-based activity score (AS). The two lowest doses were apyrogenic. The next dose induced a monophasic fever with a maximal Tc rise of 0.9 +/- 0.2 degrees C at 108 +/- 11 min post-LPS. The next two higher doses caused biphasic fevers with the first and second peaks of 0.7 +/- 0.1 and 1.4 +/- 0.1 degrees C (10 micrograms/kg) and 0.7 +/- 0.1 and 1.4 +/- 0.2 degrees C (100 micrograms/kg) occurring at 60 +/- 6 and 165 +/- 17 min and at 45 +/- 3 and 141 +/- 6 min, respectively. The highest dose of LPS resulted in a Tc fall (nadir, -0.6 +/- 0.1 degree C at 83 +/- 6 min). Two different sickness patterns were exhibited. The first (high Tc, low TFL and high AS) occurred during the monophasic fever and the first (early) phase of the biphasic fevers, and it was termed the early phase syndrome. The second pattern (high or low Tc, high TFL, and low AS) developed during the second (late) phase of the biphasic fevers and LPS-hypothermia (endotoxin shock), and it was termed the late phase syndrome. Occurring at different stages of the systemic inflammatory response and developing through different coping patterns [fight/flight (energy expenditure) vs. depression/withdrawal (energy conservation)], the two syndromes represent two different types of adaptation to infection and have different biological significance. Viewing sickness as a dynamic entity is justified clinically. Such a dynamic approach to the problem resolves several contradictions in the current concept of sickness.