Morphological changes in the conditions of adrenaline myocardial dystrophy against the background of the introduction of the compound PC-66 and amiodarone to rats

  • O.V. Dzhyhaliuk National Pirogov Memorial Medical University, Vinnytsya, Ukraine
  • D.A. Lysenko National Pirogov Memorial Medical University, Vinnytsya, Ukraine
  • D.G. Smolko National Pirogov Memorial Medical University, Vinnytsya, Ukraine
  • I.M. Kyrychenko National Pirogov Memorial Medical University, Vinnytsya, Ukraine
  • S.V. Prokopenko National Pirogov Memorial Medical University, Vinnytsya, Ukraine
Keywords: cardioprotection, PC-66, amiodarone, myocardium, morphology.


Adrenaline damage to the myocardium is an important element in the pathogenesis of myocardial infarction in humans. Despite the use of modern methods of treatment of myocardial infarction, the issue of cardioprotection of reperfusion myocardial damage remains open. Promising in this direction is the use of quinazolone derivatives, which have already shown cardioprotective properties in other models of myocardial infarction. The aim of the study was to establish morphological changes in the conditions of adrenaline myocardiodystrophy (AMD) against the background of the introduction of the compound PC-66 and amiodarone in rats. The study was performed on 100 nonlinear rats of both sexes weighing 165-220 g, divided into four groups of 25 animals each: 1 – intact rats; 2 – rats with a model of adrenaline myocardial infarction without treatment (control); 3 – rats with AMD treated with amiodarone (10 mg/kg, intraperitoneally); 4 – rats with AMD treated with compound PC-66 (10 mg/kg, intraperitoneally). It was found that control rats under conditions of cardiotoxic dose of adrenaline in the left ventricular myocardium for up to 8 days of the experiment does not fully restore the myocardial structure, dystrophic and necrobiotic changes were found in both cardiomyocytes and walls of vessels of a blood microcirculatory channel of a myocardium. Course intraperitoneal administration to rats of the compound PC-66 in the conditions of adrenaline myocardial infarction as well as amiodarone, contributes to the attenuation of signs of dystrophic and destructive processes. The degree of protective effect on the myocardium under conditions of cardiotoxic dose of adrenaline compound PC-66 was not lower to the reference drug – amiodarone. Thus, it is morphologically confirmed that in adrenaline myocardial infarction the compound PC-66, similar to the action of amiodarone, has a cardioprotective effect.


[1] Álvarez-Diduk, R., & Galano, A. (2015). Adrenaline and noradrenaline: protectors against oxidative stress or molecular targets?. The Journal of Physical Chemistry B, 119(8), 3479-3491. doi: 10.1021/acs.jpcb.5b00052
[2] Boarescu, P. M., Boarescu, I., Bocșan, I. C., Pop, R. M., Gheban, D., Bulboacă, A. E., ... & Bolboacă, S. D. (2019). Experimental model of acute myocardial infarction for evaluation of prevention and rehabilitation strategies in cardiovascular diseases – A pilot study. Balneo Res. J, 10, 288-293. doi: 10.12680/balneo.2019.270
[3] Bøtker, H. E., Hausenloy, D., Andreadou, I., Antonucci, S., Boengler, K., Davidson, S. M., ... & Efentakis, P. (2018). Practical guidelines for rigor and reproducibility in preclinical and clinical studies on cardioprotection. Basic research in cardiology, 113(5), 39. doi: 10.1007/s00395-018-0696-8
[4] Buchholz, B., Donato, M., Perez, V., Deutsch, A. C. R., Höcht, C., Del Mauro, J. S., ... & Gelpi, R. J. (2015). Changes in the loading conditions induced by vagal stimulation modify the myocardial infarct size through sympathetic-parasympathetic interactions. Pflügers Archiv-European Journal of Physiology, 467(7), 1509-1522. doi: 10.1007/s00424-014-1591-2
[5] Davidson, S. M., Arjun, S., Basalay, M. V., Bell, R. M., Bromage, D. I., Bøtker, H. E., … Yellon, D. M. (2018). The 10th Biennial Hatter Cardiovascular Institute workshop: cellular protection-evaluating new directions in the setting of myocardial infarction, ischaemic stroke, and cardio-oncology. Basic Res. Cardiol., 113(6), 43. doi: 10.1007/s00395-018-0704-z
[6] Dzhyhaliuk, O. V., Stepanyuk, G. I., Shabelnik, K. P., Kovalenko, S. I., & Pashinskaya, O. S. (2019). Cardioprotective activity and screening in a series of N-substituted quinazolin-4 (3H) -ones. Zaporizhzhya Medical Journal, 21(1), 112-117. doi: 10.14739/2310-1210.2019.1.155852
[7] Eitel, I., Stiermaier, T., Rommel, K. P., Fuernau, G., Sandri, M., Mangner, N., ... Mende, M. (2015). Cardioprotection by combined intrahospital remote ischaemic perconditioning and postconditioning in ST-elevation myocardial infarction: the randomized LIPSIA CONDITIONING trial. European Heart Journal, 36(44), 3049-3057. doi: 10.1093/eurheartj/ehv463
[8] Hausenloy, D. J., Garcia-Dorado, D., Bøtker, H. E., Davidson, S. M., Downey, J., Engel, F. B., … Ferdinandy, P. (2017). Novel targets and future strategies for acute cardioprotection: Position Paper of the European Society of Cardiology Working Group on Cellular Biology of the Heart. Cardiovascular Research, 113(6), 564-585. doi: 10.1093/cvr/cvx049
[9] Heusch, G. (2015). Molecular basis of cardioprotection: signal transduction in ischemic pre-, post-, and remote conditioning. Circulation Research, 116(4), 674-699. doi: 10.1161/CIRCRESAHA.116.305348
[10] Johansson, P. I., Bro-Jeppesen, J., Kjaergaard, J., Wanscher, M., Hassager, C., & Ostrowski, S. R. (2015). Sympathoadrenal activation and endothelial damage are inter correlated and predict increased mortality in patients resuscitated after out-of-hospital cardiac arrest. a post Hoc sub-study of patients from the TTM-trial. PLoS One, 10(3), e0120914. doi: 10.1371/journal.pone.0120914
[11] Kapur, N. K., Alkhouli, M. A., DeMartini, T. J., Faraz, H., George, Z. H., Goodwin, M. J., ... Kaki, A. (2019). Unloading the left ventricle before reperfusion in patients with anterior ST-segment–elevation myocardial infarction: a pilot study using the Impella CP. Circulation, 139(3), 337-346. doi: 10.1161/CIRCULATIONAHA.118.038269
[12] Kim, Y. H., Nijst, P., Kiefer, K., & Tang, W. W. (2017). Endothelial glycocalyx as biomarker for cardiovascular diseases: mechanistic and clinical implications. Current heart failure reports, 14(2), 117-126. doi: 10.1007/s11897-017-0320-5
[13] Ko, B., Drakos, S. G., Ibrahim, H., Kang, T. S., Thodou, A., Bonios, M., ... Welt, F. G. (2020). Percutaneous mechanical unloading simultaneously with reperfusion induces increased myocardial salvage in experimental acute myocardial infarction. Circulation: Heart Failure, 13(1), e005893. doi: 10.1161/CIRCHEARTFAILURE.119.005893
[14] Kumar, M., Kasala, E. R., Bodduluru, L. N., Dahiya, V., Sharma, D., Kumar, V., & Lahkar, M. (2016). Animal models of myocardial infarction: mainstay in clinical translation. Regulatory Toxicology and Pharmacology, 76, 221-230. doi: 10.1016/j.yrtph.2016.03.005
[15] Lindsey, M. L., Bolli, R., Canty Jr, J. M., Du, X. J., Frangogiannis, N. G., Frantz, S., ... Lefer, D. J. (2018). Guidelines for experimental models of myocardial ischemia and infarction. American Journal of Physiology-Heart and Circulatory Physiology, 314(4), H812-H838. doi: 10.1152/ajpheart.00335.2017
[16] Liu, N. B., Wu, M., Chen, C., Fujino, M., Huang, J. S., Zhu, P., & Li, X. K. (2019). Novel molecular targets participating in myocardial ischemia-reperfusion injury and cardioprotection. Cardiol. Res. Pract., 2019, 1-16 6935147. doi: 10.1155/2019/6935147
[17] Michaud, K., Basso, C., d’Amati, G., Giordano, C., Kholová, I., Preston, S. D., … , van der Wal A. C. (2020). Diagnosis of myocardial infarction at autopsy: AECVP reappraisal in the light of the current clinical classification. Virchows Arch., 476(2), 179-194. doi: 10.1007/s00428-019-02662-1
[18] Ostrowski, S. R., Pedersen, S. H., Jensen, J. S., Mogelvang, R., & Johansson, P. I. (2013). Acute myocardial infarction is associated with endothelial glycocalyx and cell damage and a parallel increase in circulating catecholamines. Critical Care, 17(1), R32. doi: 10.1186/cc12532
[19] Parviz, Y., Waleed, M., Vijayan, S., Adlam, D., Lavi, S., Al Nooryani, A., ... Stone, G. W. (2019). Cellular and molecular approaches to enhance myocardial recovery after myocardial infarction. Cardiovascular Revascularization Medicine, 20(4), 351-364. doi: 10.1016/j.carrev.2018.05.021
[20] Takawale, A., Fan, D., Basu, R., Shen, M., Parajuli, N., Wang, W., ... Kassiri, Z. (2014). Myocardial recovery from ischemia-reperfusion is compromised in the absence of tissue inhibitor of metalloproteinase 4. Circulation: Heart Failure, 7(4), 652-662. doi: 10.1161/CIRCHEARTFAILURE.114.001113
[21] Valentin, J., Frobert, A., Ajalbert, G., Cook, S., & Giraud, M. N. (2016). Histological Quantification of Chronic Myocardial Infarct in Rats. JoVE (Journal of Visualized Experiments), (118), e54914. doi: 10.3791/54914
[22] Wang, J., Toan, S., & Zhou, H. (2020). New insights into the role of mitochondria in cardiac microvascular ischemia/reperfusion injury. Angiogenesis, 2020. doi: 10.1007/s10456-020-09720-2
[23] Zaidel, E. J. (2019). Amiodarone: updated review of its current usefulness. Arch. Clin. Exp. Cardiol., 1(1), 102.
How to Cite
Dzhyhaliuk, O., Lysenko, D., Smolko, D., Kyrychenko, I., & Prokopenko, S. (2020). Morphological changes in the conditions of adrenaline myocardial dystrophy against the background of the introduction of the compound PC-66 and amiodarone to rats. Reports of Morphology, 26(1), 48-53.