Factor released under heart reperfusion may be themarker of opening of the mitochondrial permeability transition pore
Sagach V.F., Shymanskaya T.V., Nadtochiy S.M
A.A. Bogomoletz Institute of Physiology National Academy ofSciences of Ukraine
Abstract
In experiments on isolated hearts of guinea-pigs, on a model
of ishaemia-reperfusion cardiac reperfusion has been shown
to result in a constriction of coronary vessels, arrhythmia, an
inhibition of the contractile activity of the myocardium, and
an increase in an oxygen cost of the myocardial work . Apart
from that, a stable agent was detected in a reperfusion solution
by spectrophotometry on the wave length of 250 nM.
Similar deterioration of the heart function and the availability
of the stable agent in the solution were observed under influence
of the known activators of mitochondrial permeability
transition pore-phenilarsine oxide and antimycin A. In anaesthetized
animals a release of the stable factor into the
blood was induced by either ishaemia - reperfusion or those
activators. Application of the known inhibitors of the mitochondrial
permeability transition pore cyclosporin A or trolox
(water-soluble vitamin E) decreased remarkably both the cardiodynamic
deterioration and a release of the stable factor
under heart reperfusion. Mitochondrial origin of the factor
was confirmed in experiments on isolated mitochondria. Thus,
the detected factor has been determined to be released from
mitochondria at the opening of mitochondrial permeability
transition pore and is thought to be the marker of its opening
in experiments in vitro and in vivo.
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