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Hripsime L. Hayrapetyan, Hranush F. Khachatryan, Sona S. Mardanyan, Guevork A. Kevorkian
Med Sci Monit 2000; 6(5): BR845-852
Background: 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.
Conclusions: 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.