Vol. 4, Issue 7 (2015)

Author(s):
Lyzogub VG, Zavalskaya TV, Zhornichenko DM, Bogdan VV, Merkulova IO, R Bhattacharya

Abstract:
The study involved 67 patients with unstable angina, aged from 59 to 74 years (average age of patients was 67.2 ± 5.2 years) and 18 healthy subjects between the ages of 50 to 65 years (average age was 56.2 ± 4.7 years). Object of study was amino acid (AA) of blood serum. We used the method of liquid-ion exchange column chromatography. The blood plasma was determined following AA: alanine, aspartic acid, glycine, glutamine, glutamic acid, ornithine, proline, serine, taurine, tyrosine, cysteine. We investigate patients before and after treatment (after 15-17 days). All patients received conventional antianginal therapy as following; beta-blocker (konkor or Bisoprolol - 5 mg), antiplatelet agents (Acetylsalicylic acid - 75 mg), statins (Atorvastatin 10 mg), ACE inhibitor (Enalapril 10 mg). In addition to these medicinal drugs patients were assigned intravenously 100 ml L -arginine (Tivortin) once a day. A total of 6 infusions. Patients with Unstable Angina compared with the control group (CG) showed a significant decrease in the vast majority of non-essential AA (glutamic acid, proline, serine, taurine, cysteine), which indicates an increase in its catabolism. In patients under the influence of antianginal therapy with L-arginine occurs a significant decrease of following serum AA: alanine, aspartic acid, glycine, glutamine, serine and tyrosine, which is probably due to the increased use of the AA for the synthesis of biologically active substances that generally possess protective features. Under the influence of therapy significantly increases the content of ornithine, which can be seen as a defensive response, as ornithine, participates in the ammonia neutralization cycle. On the background of treatment in patients with Unstable Angina significantly increases the content of taurine, which probably will facilitate the entering of the AA to the myocardium as a cardioprotector. Antianginal therapy including L-arginine resulted in a significant increase in the serum content of cysteine ​​as a substrate for the synthesis of hydrogen sulfide (H2S), which can be considered as a compensatory response to myocardial ischemia.