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ISSN 2522-9028 (Print)
ISSN 2522-9036 (Online)

Fiziologichnyi Zhurnal

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. 2018; 64(5): 7-15


Y.V. Goshovska1, R.A. Fedichkina1, O.I. Korneliuk2, V.F. Sagach1

  1. Bogomoletz Institute of Physiology, NAS of Ukraine
  2. Institute of Molecular Biology and Genetics, NAS of Ukraine


Endothelial Monocyte-Activating Polypeptide II (EMAPII) was showed to decrease oxidative stress and restore cNOS coupling in rat model of genetically determined hypertension. We hypothesized that EMAPII is able to prevent oxidative stress induced by ischemia-reperfusion. Wistar rats were pretreated with EMAPII (30mkg/kg) or its precursor proEMAPII/ p43 (10 mkg/kg) injected i.v. 30 min before the experiment. Isolated hearts were subjected to 20 min total ischemia and 40 min reperfusion. EMAPII as well as p43 greatly diminished ischemia-reperfusion induced disturbances of heart function and prevented non-effective oxygen utilization by reperfuzed myocardium. In particular, in the control group at the 40th min of reperfusion, the left ventricular pressure was only 43.8%, while in groups with EMAPII and p43 - 61.5 (P <0.01) and 82 % (P <0.001), respectively. At the 5th min of reperfusion, the oxygen cost of myocardial work was 9×10-7 mmol O2 min-1 per g of tissue in control which is 5.6 times higher than that observed before ischemia, while EMAPII and p43 completely prevented an increase of this parameter at reperfusion. Additionally, p43 and EMAPII prevented the release of mitochondrial factor from ischemized heart indicating at least partial inhibition of mitochondrial permeability transition pore opening. Thus, we have found the cardioprotective effect of exogenous p43 and EMAPII.

Keywords: heart; ischemia; cardioprotection; EMAPII; proEMAP/p43; mitochondrial permeability transition pore


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