MORPHOHISTOCHEMICAL ANALYSIS OF CORTICAL STRUCTURES IN AN EXPERIMENTAL MODEL OF PROLONGED COMPRESSION SYNDROME OF THE HIND LIMB IN RATS.

Crush syndrome (CS) is a pathological shock-like condition that develops following prolonged compression of the trunk, extremities, or their segments by heavy objects, and is characterized by an inflammatory response that extends beyond the affected soft tissues and penetrates into complex brain structures. To investigate the dynamics of the morphological and functional state of rat brain cellular structures following hind limb compression, we employed a histochemical method for detecting the activity of Ca²⁺-dependent acid phosphatase. Experiments were performed on sexually mature albino rats. Experimental CS models were created using a custom apparatus that allowed 3-hour and 6-hour compression of the hind limb. Morphohistochemical analysis revealed that after 3 hours of compression, neurons in the sensorimotor cortex (SMC) largely retained their typical morphology, dendritic orientation, and moderate levels of cytoplasmic enzymatic activity. In a subset of neurons-predominantly in the granular layer-early signs of central chromatolysis were observed. After 6 hours of compression, the morphological profile of neurons in the studied SMC layers deteriorated markedly: alterations in cell shape and size, neuronal deformation, nuclear ectopia, and shortened or disrupted neurites indicated impaired intercellular connectivity. Notably, pyramidal neurons exhibited greater resilience compared with granular cells. An increase in nuclear acid phosphatase activity suggests the activation of early preventive mechanisms of the cellular damage response during the initial stages of injury. Thus, Ca²⁺-dependent acid phosphatase histochemistry demonstrated that crush syndrome is accompanied by progressive morphological impairments in SMC neurons, which become more pronounced with increasing compression duration. The observed morphological features of SMC neuronal injury following limb compression are characteristic of nonspecific neuronal damage and resemble acute neuronal swelling-a common, reversible form of cellular pathology. which is recognized as a reversible alteration.