The Influence of Hypothalamic Cytokine PRP on Protein Synthesis in Brain Subcellular Compartments in Crush Syndrome

The effect of hypothalamic peptides, neurohormone C and proline-rich peptide-1on the Ca2+-handling system in heartin pathophysiological conditions

“…We found histomorphological changes in the heart in early period of decompression (2-48 h), which are accompanied by a decrease in calcium-binding ability of membrane proteins in SR of cardiomyocytes, including CSQ2, and these processes are strikingly similar to those observed with pancreatic necrosis [40]. An effective dose of PRP-1 (10 À6 M), administered at the end of compression and after an hour, significantly ameliorates the heart damage caused by pancreatic necrosis and/or crush syndrome and protects against harmful processes, sufficiently modulating the calcium-binding properties of Ca 2þ -binding proteins in the cardiomyocytes, and also destroying MDF, nonapeptide and other toxic peptides derived from myoglobin [44]. It can be assumed that there is a possible interaction between NC and PRP-1, since they use similar mechanisms of heart protection for the same pathologies, but this requires further study (Figure 2).…”

“…The combination of peritoneal dialysis and massive fluid resuscitation is used to reduce lactic acidosis, serum levels of myoglobin and K þ and myoglobin-derived toxic peptides, which protect against tissue damage increasing the survival of animals with long-term crush injuries [43]. We revealed four toxic peptides resulting from anaerobic cleavage of muscle myoglobin after long-term compression (more than 2-5 h), accompanied by ischemia and necrosis, resulting in MI and cardiac arrest [44]. One of these peptides is nonapeptide, which completely coincides with MDF except additional C-terminal L-arginine, which enhances penetration of the peptide into the tissues, in particular, the myocardium [45].…”

Alterations in Calcium-Binding Properties of Sarcoplasmic Reticulum Membrane Proteins Following Cardiac Injury

“…Interestingly, CS and experimental CS animal model induces the total intoxication, myocardium damage, and multiple organ failure mirrored the picture occurred following NP, at that changes are observed at the early stage of decompression but not at compression -the most dangerous period of cardiomyocyte injury was at the 12th hour of decompression [9][10][11]. We established the experimental rat model of CS in which deep myocardial injury and acute intoxication cause a typical myocardial infarction ischemic damage and subsequent death of the animals in decompression period [12]. However, whether cardiomyocyte injury is induced after both CS and NP has not been investigated.…”

“…Model of CS was induced by application of a standardized mechanical pressure (10 kg/100 g body weight) applied to the femoral muscle section of rat for two hours [12]. Thereafter rats were sacrificed at 2, 4, 24, and 48 h decompression stages.…”