Cerebral ischemia is a neurogenerative disoder that leads to partial or general paralysis and subsequent disability. The development of oxidative-nitrosative stress on the background of insufficient production of nitric oxide (NO) and hydrogen sulfide (H2S) are the main reasons behind the pathogenesis of focal ischemia-reperfusion and cerebrocardial syndrome. We studied the combined use of propargylglycine and L-cysteine as drugs that prevent oxidative and nitrosative stress and are activators of gasotransmitters - NO and H2S in the heart tissues of rats with focal ischemia. It was shown that focal ischemiareperfusion was accompanied by a significant increase in the heart of rats calcium-independent inducible synthesis of NO (iNOS) and an increase in markers of oxidative stress (superoxide anion radical, hydroxyl radical, diene conjugates) NO-synthase (cNOS). This caused disruption of nitric oxide synthesis due to the uncoupling state of cNOS in the rat heart. The use of a combination of DL-proparlgylglycine (11.31 mg/ kg) and L-cysteine (112.1 mg / kg) 40 min before the modeling of focal ischemia significantly reduced the activity of iNOS and the content of markers of oxidative metabolism in the heart of adult rats and increased the constitutive synthesis of NO, which led to restoration of the cNOS incoupling. We observed activation of endogenous synthesis of H2S, which interacts closely with the nitric oxide system and is a powerful antioxidant. It should also be noted an increase in animal survival after 24 h by 25%. Thus, the combined use of propargylglycine and Lcysteine in rats prevented disruption of NO and H2S synthesis in cardiac tissues in ishemia-reperfusion due to a slowing of the development of oxidative stress, which helped to restore cNOS coupling.