Українська English

ISSN 2522-9028 (Print)
ISSN 2522-9036 (Online)
DOI: https://doi.org/10.15407/fz

Fiziologichnyi Zhurnal

(English title: Physiological Journal)

is a scientific journal issued by the

Bogomoletz Institute of Physiology
National Academy of Sciences of Ukraine

Editor-in-chief: V.F. Sagach

The journal was founded in 1955 as
1955 – 1977 "Fiziolohichnyi zhurnal" (ISSN 0015 – 3311)
1978 – 1993 "Fiziologicheskii zhurnal" (ISSN 0201 – 8489)
1994 – 2016 "Fiziolohichnyi zhurnal" (ISSN 0201 – 8489)
2017 – "Fiziolohichnyi zhurnal" (ISSN 2522-9028)

Fiziol. Zh. 2009; 55(1): 12-18

EARLY DIAGNOSTICS OF ISCHEMIC DAMAGES OF THE MYOCARDIUM BY MEANS OF THE MARKER OF OPENING THE MITOCHONDRIAL PORE

V. F. Sagach1, A.V. Dmitrieva1, J.A. Bubnova1, V.B. Maksimenko2, G.V. Knyshov2

  1. O.O. Bogomoletz Institute of Physiology National Academy Sciences of Ukraine, Kyiv, Ukraine
  2. M.M. Amosov Institute Surgery Academy Medical Sciencesof Ukraine, Kyiv, Ukraine
DOI: https://doi.org/10.15407/fz55.01.012


Abstract

In the article a possibility of definition of level of the mitochon-drial factor (MF) for early diagnostics of the myocardial is chemic damages at patients during heart surgery was investigated. The reperfusion damages of heart were manifested by MPTP activation and MF release. The rising of MF level during a cardioplegia is comparable to level, which has been noted at patients with angina before operation of aorto-coronary shunting. The beginning of reperfusion, practically did not change MF level, but 5 minutes after restoration of a blood flow and warm reductions it increased to the maximum values. Thus, it closely correlated with a level of a myocardial contractility de­pression and data of biochemical researches, which are tradi­tionally used in clinic for diagnostics of damages of a heart. It allows to confirm, what exactly reperfusion is a major factor damaging of a myocardium. Its important that, change of MF level we registered at first minutes of heart reperfusion, those are much earlier, than by means of other markers. It seems to us, that investigation of a MF is very perspective for early find­ing of an ischemic damages of different tissues and organs.

Full text: (PDF, in Ukrainian)

References

  1. Dmitrieva AV, Sagach VF, Boguslavsky A.Yu. Study of the participation of mitochondrial pores in the development of disorders of the contractile activity of the myocardium and blood vessels. Fiziol Zh. 2005. 51, N 3. P.18-24.
  2. Dmitrieva AV, Sagach VF, Boguslavsky A.Yu. Stable mitochondrial factor, which is released during reperfusion a study of the nature and effects on the myocardium and blood vessels . Wedge. and experiment. pathology. 2004. 3, N 2 (1). P.20-22.
  3. Kartashev DI, Mitofanova LB, Rubinchik VE et al. Comparative efficiency of operations of direct myocardial revascularization in the conditions of artificial blood circulation and on the working heart . Cardiovascular. surgery. 2006. Vip. 14. P. 93-96.
  4. Nadtochiy SN, Boguslavsky A.Yu., Sagach VF Determination of a stable factor of mitochondrial origin in vivo . Physiol. magazine. 2003. 49, N 5. p. 25-31.
    5. Sagach VF, Vavilova GL, Strutynska NA, Akopova OV Influence of inducers and inhibitors of mitochondrial pores on its formation and on release of unidentified mitochondrial factor . Ibid. 2003. 49, N 1. p. 3-12
  5. Sagach VF, Dmitrieva AV, Bubnova YO etc. Method for diagnosis of ischemic-reperfusion myocardial damage and opening of mitochondrial pore . Patent for utility model N 26385-2007.
  6. Sagach VF, Szymanska TV, Nadtochiy SN Prevention of postperfusion disorders of heart function and inefficient use of oxygen with inhibitors of mitochondrial pore opening . Physiol. magazine. 2002. 48, N 6. p. 3-12.
  7. Trifonov IR Biochemical markers of myocardial necrosis. Part 1. General characteristics of biomarkers. Their use for the diagnosis of myocardial infarction: a review of modern recommendations . Cardiology. 2001. N 11. P. 93-95.
  8. 9. Borutaite V., Jekabsone A., Morkuniene R., Brown G.C. Inhibition of mitochondrial permiability transion prevent mitochondrial dysfunction, cytochrom c release and apoptosis inuced by heart ischemia . J.Mol. Cell.Cardiol. 2003. 35. P. 357-366. CrossRef.1016/S0022-2828(03)00005-1
  9. 10. Crompton M. Mitochondrial intermembrane junctional complexes and their role in cell deth . J. Physiol. 2000. 29,N 1. P.11-21. CrossRef PubMed PubMedCentral
  10. Dimond G., Forrester J.S. Effect of coronary artery desease and acute myocardial infarction on left ven­tricular compliance in man . Circulation. 1972. 45. P. 115-118. CrossRef PubMed
  11. Donnely R., Millar-Craig M.W. Cardiac troponin: IT upgrade for the heart . Lancet. 1998. 351. P. 537-539. CrossRef.1016/S0140-6736(05)78549-4
  12. Halestrap A., Mcstay G., Clarke S. The permeability transition pore complex: another view . Biochimie. 2002. 84. P.153-166. CrossRef.1016/S0300-9084(02)01375-5
  13. Murphy A. Mitochondria in human desease . Biochem­ist. 2000. 4. P.139-184.
  14. Roberts R., Godwa K., Ludbrook P. et al. Specificity of elevated serum MB creatine phosphokinase activity in the diagnosis of acute myocardial infarction . Amer. J. Cardiol. 1975. 36. P. 433-437. CrossRef.1016/0002-9149(75)90890-5
  15. Sastre J., Pallardo F.V., Vina J. Mitochondrial oxidative stress play a key role in aging and apoptosis . Life. 2000. 49. P. 427-435. CrossRef PubMed
  16. Skulachev V.H. Mitochondrial physiology and pathol­ogy. Concepts of programmed deth of organelles, cells and organisms . Mol. Aspects Med. 1999. 20. P. 139-184. CrossRef.1016/S0098-2997(99)00008-4
  17. Vasudevan G., Mercer D., Varat M. Lactic dehydroge­nase isoenzyme determination in the diagnosis of acute myocardial infarction . Circulation. 1978. 57. P. 1055-1067. CrossRef PubMed
  18. Wu A., Apple F., Gibler B. et al. Use of cardiac marker in coronary artery disease. NACB SOLP Recom­mendations. National meeting American Association of Clinical Chemistry. Chicago, 1998. P. 148 152.
© National Academy of Sciences of Ukraine, Bogomoletz Institute of Physiology, 2014-2025.