I. G. Khaliulin

Learn More
A prolonged period of ischaemia followed by reperfusion irreversibly damages the heart. Such reperfusion injury (RI) involves opening of the mitochondrial permeability transition pore (MPTP) under the conditions of calcium overload and oxidative stress that accompany reperfusion. Protection from MPTP opening and hence RI can be mediated by ischaemic(More)
Urocortin (UCN) protects hearts against ischemia and reperfusion injury whether given before ischemia or at reperfusion. Here we investigate the roles of PKC, reactive oxygen species, and the mitochondrial permeability transition pore (MPTP) in mediating these effects. In Langendorff-perfused rat hearts, acute UCN treatment improved hemodynamic recovery(More)
We have recently shown that brief episodes of hypothermic perfusion interspersed with periods of normothermic perfusion, referred to as temperature preconditioning (TP), are cardioprotective and can be mimicked by consecutive isoproterenol/adenosine treatment. Here we investigate the optimal temperature for TP and whether TP further enhances protection(More)
AIMS Temperature preconditioning (TP) provides very powerful protection against ischaemia/reperfusion. Understanding the signalling pathways involved may enable the development of effective pharmacological cardioprotection. We investigated the interrelationship between activation of protein kinase A (PKA) and protein kinase C (PKC) in the signalling(More)
Consecutive treatment of normal heart with a high dose of isoproterenol and adenosine (Iso/Ade treatment), confers strong protection against ischaemia/reperfusion injury. In preparation for translation of this cardioprotective strategy into clinical practice during heart surgery, we further optimised conditions for this intervention using a(More)
It has now been demonstrated that the μ, δ1 , δ2 , and κ1 opioid receptor (OR) agonists represent the most promising group of opioids for the creation of drugs enhancing cardiac tolerance to the detrimental effects of ischemia/reperfusion (I/R). Opioids are able to prevent necrosis and apoptosis of cardiomyocytes during I/R and improve cardiac contractility(More)
Stimulation of CB1 receptors was found to mimic the phenomenon of preconditioning. As the cardioprotective effect of the cannabinoid HU-210 is seen in both in vivo experiments and in vitro studies, there are grounds for suggesting that the protective effects of HU-210 are mediated by activation of cardiac CB1 receptors. The cardioprotective effect of the(More)
CB receptor agonist HU-210 exhibits an infarction-limiting effect during in vitro reperfusion of the heart after focal ischemia. This effect is paralleled by a decrease in left-ventricular developed pressure and double product. In addition, HU-210 reduces end-diastolic pressure during the reperfusion period, which indirectly attests to reduced Ca2+ overload(More)
Analysis of published data provided evidence that the main candidates for the role of the end effector for ischemic postconditioning of the heart are: 1) BK-type K+ channels (big conductance K+ channels); 2) mitochondrial ATP-sensitive K+ channels; and 3) MPT pores (mitochondrial permeability transition pores). However, some investigators believe that(More)
MEK, PI3, p38, tyrosine, and mTOR kinases are not involved in the regulation of heart resistance to the arrhythmogenic action of short-term ischemia/reperfusion in non-adapted rats.