Abstract
The number of publications on the investigation of crush syndrome (CS) pathogenesis at traumatic toxicosis is rather limited. The influence of some pharmacological preparations on the development of CS pathogenesis is not very well clarified. Proline-rich peptide (PRP) is a fragment of a glycopeptide comprising the carboxyterminus of the neurohypophyseal vasopressin-neurophysin precursor isolated from the bovine neurohypophysis neurosecretory granules. The polypeptide possesses stimulating activity on differentiation and proliferation of T-lymphocytes and Interleukin-2 (Il-2) biosynthesis. The experimental model of CS of white rats was induced by 2-h of compression followed by 2, 24, and 48-h of decompression of femoral muscle tissue. The influence of PRP on [14C]glucose utilization was investigated in brain, heart, and kidney tissues. The level of [14C]glucose utilization decreased in brain during compression followed by 2-h and 24-h of decompression, while it increased under the influence of PRP at all decompression periods. The influence of PRP on the myocardium and kidneys differs, depending on its nature and on the periods of decompression.
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