Hayrapetyan H L, Khachatryan H F, Mardanyan S S, Sargisova Y G, Kevorkyan G A
H. Buniatian Institute of Biochemistry of Armenian NAS, Yerevan, Republic of Armenia.
Med Sci Monit. 2000 Nov-Dec;6(6):1068-76.
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.
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.
The level of adenosine deaminase in most of studied tissues differs from the control value depending on compression and decompression time. It is worthy of note that namely during decompression, the enzyme level deviates from the control in the majority of tissues.
关于挤压综合征发病机制的研究文献，尤其是创伤性中毒时酶系统的研究相当有限。此类研究对于及时诊断和确定治疗策略是必要的。为了弥补这一不足，我们在体内实验性挤压综合征模型中研究了12种大鼠组织中的腺苷脱氨酶水平。
通过对股部肌肉组织进行挤压和减压建立了大鼠挤压综合征实验模型。研究了挤压综合征对半球、小脑、下丘脑、垂体、心脏、肺、肝脏、脾脏、肾脏、肾上腺以及挤压和未挤压肌肉中腺苷脱氨酶同工酶活性的影响。挤压后2小时和5小时，肌肉、肺和心脏中的酶活性降低；下丘脑中酶活性增加；肾脏和脾脏中的酶活性接近对照值。在挤压2小时期间，小脑的该参数实际无变化，而在挤压5小时时增加。由于代偿机制，挤压5小时后肾上腺、肝脏、垂体和半球的数据接近对照值水平。在挤压2小时后48小时减压时，半球、下丘脑、小脑、肝脏、心脏、肾上腺、未挤压肌肉、肺和肾脏中的腺苷脱氨酶活性高于对照值；在挤压肌肉和脾脏中，活性降至对照值的60%。在挤压5小时后48小时减压时，下丘脑、垂体、半球、小脑、肾脏、肾上腺、心脏和肺中的酶活性高于对照值。肌肉、脾脏和肝脏中的活性降低。
大多数研究组织中的腺苷脱氨酶水平因挤压和减压时间不同而与对照值存在差异。值得注意的是，即在减压期间，大多数组织中的酶水平偏离对照值。
