The experiments on random-bred male rats have established that 4 and 6 min clinical death of acute blood loss initiated lipid peroxidation processes (LPO), causing biomembrane damage, enhanced adenyl nucleotide catabolism, activated glycolysis and glycogenolysis in the heart muscle and caused cardiac arrhythmias. Carnosine at a dose 25 mg/kg administered together with pumped blood enhanced resuscitation efficacy and reduced considerably lethality in the early rehabilitation period. A favourable effect of carnosine is associated with its ability to restrict LPO processes, inhibit glycolysis and glycogenolysis and create optimal conditions for the functioning of membrane-located lipid-dependent enzymes.