Year : 2018  |  Volume : 9  |  Issue : 1  |  Page : 17-20

Effect of etoksidol against sulfur-containing gas induced reduction in bone marrow microcirculation in different stages of ontogenesis in rats

Department of Pathological Physiology of Astrakhan State Medical University, 414000, Astrakhan, Russia

Correspondence Address:
Olga A Ovsyannikova
Astrakhan State Medical University, 121 Bakinskaya St., Astrakhan, 414000
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jpp.JPP_196_16

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Objective: To investigate the state of femoral red bone marrow microvasculature of nonlinear white male rats in the course of an acute experiment. Materials and Methods: The ontogenesis of experimental animals were between 36 and 730 days: Intact ones, those subjected to the action of subtoxic doses of sulfur-bearing gas, and those receiving a protector-drug “Etoksidol”. The data on microcirculation were obtained using laser Doppler flowmetry. The industrial sulfur-containing natural gas of the Astrakhan gas condensate field was used as a toxic agent. It was revealed that the reducing intensity of blood microcirculation in the red bone marrow of intact rats is statistically more significance in the presenile period of ontogenesis compared with the earlier periods. Results: The use of “Etoksidol” along with the influence of sulfur-containing pollutant on the experimental animals of different age groups led to improvement of microcirculation in the bone marrow at all the studied stages of ontogeny. However, such improvement was statistically highly significant (P < 0.01) in the mature age I, very close to significant in the mature age II, and was not statistically significant in the young and presenile age. Conclusions: As a result, the following findings were obtained: The toxic effect greatly reduces the intensity of the microcirculation in the bone marrow, which is most pronounced in younger animals; the experimental results suggest that the drug “Etoksidol,” with an antihypoxic and antioxidant action, has a positive effect on red bone marrow microvasculature.

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