CHANGES IN THE MORPHOLOGICAL AND FUNCTIONAL STATE OF HYPOTHALAMUS NUCLEI NEURONS IN LONG-TERM CRUSHING SYNDROME.

Abstract

Crush syndrome (CS) is a severe stress-induced condition that leads to systemic metabolic and neuroendocrine disturbances. The hypothalamus, serving as a central integrator of neuroendocrine and autonomic regulation, is particularly sensitive to prolonged stress. In this context, we examined neuronal changes in the supraoptic (SON) and paraventricular (PVN) nuclei of the hypothalamus in rats subjected to prolonged hind limb compression. To assess the dynamics of the morphological and functional state of hypothalamic neurons after limb compression, we employed histochemical detection of Ca²⁺-dependent acid phosphatase activity. Animals were randomly assigned to three groups: control (Co), compression for 3 hours (CS3), and compression for 6 hours (CS6). Experimental CS models were created using a specialized apparatus to apply hind limb compression for the designated durations. Brain tissue samples containing the SON and PVN were collected one hour after compression. The results demonstrated differential morphological responses in the SON and PVN following 3 hours of compression. SON neurons largely preserved their structural integrity, showing increased phosphatase activity in the neuron cytoplasm. In contrast, PVN neurons displayed pronounced cytoplasmic rarefaction and central chromatolysis. After 6 hours of compression, degenerative changes were observed in neurons of both nuclei, accompanied by a sharp rise in phosphatase activity in the neuron cytoplasm. This increase indicates enhanced metabolic processes that may support cellular regeneration and survival, reflecting the activation of neuroprotective mechanisms. Overall, these findings suggest that hypothalamic nuclei undergo distinct, time-dependent morphological and functional responses to crush syndrome, encompassing both compensatory and maladaptive processes.