Publications on investigation of
crush syndrome pathogenesis, particularly of enzymatic systems upon traumatic toxicosis are rather limited. Such investigations are necessary for opportune diagnosis and definition of a treatment tactic. To replenish this deficiency, the
adenosine deaminase level was studied in 12 rat tissues at experimental
crush syndrome in vivo.
RESULTS: The experimental model of
crush syndrome on white rats was induced by crush and
decompression of femoral muscle tissue. The
crush syndrome influence on activity of
adenosine deaminase isoenzymes was investigated in hemisphere, cerebellum, hypothalamus, pituitary body, heart, lung, liver, spleen, kidney, adrenal, as well as in crushed and native muscles. In 2 and 5 hours after compression, the
enzyme activity decreased in muscles, lung and heart; increased in hypothalamus; remains near the control value in kidney and spleen. In cerebellum the parameter practically does not vary during 2 hours compression, while increased in 5 hours. In adrenal, liver, pituitary body and hemisphere the data after 5 hours compression approximated the level of control value in account of compensating mechanism. In 48 hours
decompression after 2 hours crush, the
adenosine deaminase activity becomes higher than control value in hemisphere, hypothalamus, cerebellum, liver, heart, adrenal, intact muscle, lung and kidney; in the crushed muscle and spleen the activity is reduced down to 60% of control value. In 48 hours
decompression after 5 hours compression, the
enzyme activity is higher than control value in hypothalamus, pituitary body, hemisphere, cerebellum, kidney, adrenal, heart and lung. The activity is reduced in muscles, spleen and liver.
CONCLUSION: