NITRIC OXIDE–PRODUCING ENZYMES AND SERUM CORTISOL LEVELS IN PATIENTS WITH Q-WAVE MYOCARDIAL INFARCTION DURING TREATMENT DYNAMICS

Honchar O. O.

NITRIC OXIDE–PRODUCING ENZYMES AND SERUM CORTISOL LEVELS IN PATIENTS WITH Q-WAVE MYOCARDIAL INFARCTION DURING TREATMENT DYNAMICS


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About the author:

Honchar O. O.

Heading:

CLINICAL AND EXPERIMENTAL MEDICINE

Type of article:

Scientific article

Annotation:

The search for new pharmacological strategies to mitigate ischemic myocardial injury remains one of the most critical challenges in modern cardiology. Particular focus is directed toward endothelial dysfunction, dysregulation of the nitric oxide (NO) system, and neurohumoral imbalance –specifically alterations in serum cortisol levels. A promising therapeutic direction involves evaluating the cardioprotective properties of anxiolytics, specifically temgicoluril, as a component of comprehensive targeted management for acute Q-wave myocardial infarction. This study aimed to evaluate the effect of incorporating temgicoluril into standard treatment protocols for patients with Q-wave myocardial infarction on the activity of nitric oxide synthase isoforms, serum concentrations of nitrites and peroxynitrites, and serum cortisol levels. The study evaluated 80 patients with acute myocardial infarction, stratified into groups based on the presence or absence of a Q wave, and further divided into subgroups according to the administration of temgicoluril at a dose of 500 mg three times daily for one month alongside guideline-based medical therapy and multidisciplinary cardiac rehabilitation. The control group comprised 20 healthy individuals. Serum activities of inducible (iNOS), endothelial (eNOS), and neuronal (nNOS) nitric oxide synthases were quantified spectrophotometrically by measuring the rate of L-citrulline accumulation. Serum levels of nitrites, peroxynitrites, and cortisol were likewise determined using spectrophotometric assays. Statistical analysis was performed using Microsoft Office Excel equipped with the Real Statistics 2019 add-in package (Charles Zaiontz; License CC BY 4.0). The results demonstrated that standard therapy for Q-wave myocardial infarction is accompanied by a significant suppression of excessive nitric oxide production alongside a reduction in serum cortisol levels. Concurrently, the addition of temgicoluril to the treatment protocol preserves total NO production through a more moderate modulation of inducible isoform (iNOS) activity and maintains optimal adaptive serum cortisol concentrations. Thus, the incorporation of temgicoluril into standard management protocols for patients with Q-wave myocardial infarction exerts a pathogenetically grounded modulating effect on the nitric oxide system and serum cortisol levels, offering new avenues to enhance myocardial cytoprotection and patient rehabilitation.

Tags:

cortisol, nitric oxide (NO), NO-producing enzymes, Q-wave myocardial infarction, temgicoluril

Bibliography:

  1. MOZ Ukrainy. Haluzevi standarty ta klinichni nastanovy. Kyiv: Derzhavnyi ekspernyi tsentr MOZ Ukrainy. Dostupno: [in Ukrainian].
  2. Lu Z, Chai Q, Dai W, Yu B, Lv Q, Qiu F, et al. Mitochondrial homeostasis restoring peptide-drug conjugates with ROS-responsive NO releasing ability for targeted therapy of myocardial infarction. J Nanobiotechnology. 2025;23(1):496. DOI: https://doi.org/10.1186/s12951-025-03578-6
  3. Wang Z, Yang N, Hou Y, Li Y, Yin C, Yang E, et al. L-Arginine-Loaded Gold Nanocages Ameliorate Myocardial Ischemia/Reperfusion Injury by Promoting Nitric Oxide Production and Maintaining Mitochondrial Function. Adv Sci (Weinh). 2023;10(26):e2302123. DOI: https://doi.org/10.1002/advs.202302123
  4. Zhu D, Hou J, Qian M, Jin D, Hao T, Pan Y, et al. Nitrate-functionalized patch confers cardioprotection and improves heart repair after myocardial infarction via local nitric oxide delivery. Nat Commun. 2021;12(1):4501. DOI: https://doi.org/10.1038/s41467-021-24804-3
  5. Roy R, Wilcox J, Webb AJ, O’Gallagher K. Dysfunctional and Dysregulated Nitric Oxide Synthases in Cardiovascular Disease: Mechanisms and Therapeutic Potential. Int J Mol Sci. 2023;24(20):15200. DOI: https://doi.org/10.3390/ijms242015200
  6. Pautz A, Li H, Kleinert H. Regulation of NOS expression in vascular diseases. Front Biosci (Landmark Ed). 2021;26(5):85-101. DOI: https://doi.org/10.52586/4926
  7. Abdelmonaem AA, Abdel-Aziz AM, Ibrahim YF, Abdelzaher WY, Amgad Mohammed N, Marey H, et al. Cardioprotective effect of tofisopam against isoprenaline-induced myocardial infarction in rats via modulation of NLRP3\IL-1β\caspase-1 pathway. Immunopharmacol Immunotoxicol. 2024;46(6):902-911. DOI: https://doi.org/10.1080/08923973.2024.2421528
  8. Wu B, Cao Y, Meng M, Jiang Y, Tao H, Zhang Y, et al. Gabapentin alleviates myocardial ischemia-reperfusion injury by increasing the protein expression of GABAARδ. Eur J Pharmacol. 2023;944:175585. DOI: https://doi.org/10.1016/j.ejphar.2023.175585
  9. Moibenko OO, Yuzkiv MIa, Korotsiuba AV, Bukhanevych OM, Tumanovska LV. Zminy systemy oksydu azotu pry hostrii ishemii ta reperfuzii miokardu. Fiziolohichnyi zhurnal. 2000;46(6):3-11. [in Ukrainian].
  10. Akimov OY, Kostenko VO. Role of NF-κB transcriptional factor activation during chronic fluoride intoxication in development of oxidativenitrosative stress in rat’s gastric mucosa. J Trace Elem Med Biol. 2020;61:126535. DOI: https://doi.org/10.1016/j.jtemb.2020.126535
  11. Tu E, Pearlmutter P, Tiangco M, Derose G, Begdache L, Koh A. Comparison of Colorimetric Analyses to Determine Cortisol in Human Sweat. ACS Omega. 2020;5(14):8211-8218. DOI: https://doi.org/10.1021/acsomega.0c00498
  12. Schaffter N, Ledermann K, Pazhenkottil AP, Barth J, Schnyder U, Znoj H, et al. Serum cortisol as a predictor for posttraumatic stress disorder symptoms in post-myocardial infarction patients. J Affect Disord. 2021;292:687-694. DOI: https://doi.org/10.1016/j.jad.2021.05.065
  13. Zhu Y, Chai Y, Su Z, Qi W, Yin M, Li L, et al. Danlou Tablet Protects Against Myocardial Infarction Through Promoting eNOS-Dependent Endothelial Protection and Angiogenesis. J Cardiovasc Transl Res. 2024;17(2):403-416. DOI: https://doi.org/10.1007/s12265-023-10437-y
  14. Kaul S, Methner C, Cao Z, Mishra A. Mechanisms of the «No-Reflow» Phenomenon After Acute Myocardial Infarction: Potential Role of Pericytes. JACC Basic Transl Sci. 2022;8(2):204-220. DOI: https://doi.org/10.1016/j.jacbts.2022.06.008
  15. Ebrahimi R, Rahmani M, Fallahtafti P, Ghaseminejad-Raeini A, Azarboo A, Jalali A, et al. Predicting the no-reflow phenomenon in STelevation myocardial infarction patients undergoing primary percutaneous coronary intervention: a systematic review of clinical prediction models. Ther Adv Cardiovasc Dis. 2024;18:17539447241290438. DOI: https://doi.org/10.1177/17539447241290438
  16. Jääskeläinen J, Renko M, Kuitunen I. Corticosteroids to prevent renal scarring in children with pyelonephritis: a systematic review and meta-analysis. J Nephrol. 2023;36(6):1509-1518. DOI: https://doi.org/10.1007/s40620-022-01552-1
  17. Liu X, Shui G, Wang Y, Chen T, Zhang P, Liu L, et al. Remimazolam alleviates myocardial ischemia/reperfusion injury and inflammation via inhibition of the NLRP3/IL‑1β pathway in mice. Int J Mol Med. 2025;55(4):57. DOI: https://doi.org/10.3892/ijmm.2025.5498
  18. Li Z, Yu Z, Cui S, Hu S, Li B, Chen T, et al. AMPA receptor inhibition alleviates inflammatory response and myocardial apoptosis after myocardial infarction by inhibiting TLR4/NF-κB signaling pathway. Int Immunopharmacol. 2024;133:112080. DOI: https://doi.org/10.1016/j.intimp.2024.112080
  19. Wang Y, He L, Du D, Cheng Z, Qin C. A Metabolomics-Based Study on NMDAR-Mediated Mitochondrial Damage through Calcium Overload and ROS Accumulation in Myocardial Infarction. Front Biosci (Landmark Ed). 2023;28(7):140. DOI: https://doi.org/10.31083/j.fbl2807140

Publication of the article:

«Bulletin of problems biology and medicine», 2026 Issue 3, 182, 253-258 pages, index UDC 616.127-005.8-085

DOI:

10.29254/2077-4214-2026-3-182-253-258

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