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Mitochondria have emerged as key players in cardioprotection against ischemia/reperfusion (I/R) injury. Diazoxide (Dx) has been shown to reduce infarct size in several experimental models through the opening of mitochondrial ATP-dependent... more
Mitochondria have emerged as key players in cardioprotection against ischemia/reperfusion (I/R) injury. Diazoxide (Dx) has been shown to reduce infarct size in several experimental models through the opening of mitochondrial ATP-dependent potassium channels (mKATP) and ...
Research Interests: Calcium, Apoptosis, Hemodynamics, Permeability, Blood Pressure, and 15 moreAnimals, Male, Cell Death, Heart, Cyclosporine, Acute Myocardial Infarction, Myocardial Infarction, Myocardium, Mitochondrial Permeability Transition Pore, Rabbits, Infarct Size, Reperfusion injury, Preconditioning, Ischemia–reperfusion, and Ischemic Preconditioning
A possible role of palmitic acid/Ca2+ (PA/Ca2+) complexes in the cyclosporin-insensitive permeability transition in mitochondria has been studied. It has been shown that in the presence of Ca2+, PA induces a swelling of mitochondria,... more
A possible role of palmitic acid/Ca2+ (PA/Ca2+) complexes in the cyclosporin-insensitive permeability transition in mitochondria has been studied. It has been shown that in the presence of Ca2+, PA induces a swelling of mitochondria, which is not inhibited by cyclosporin A. The swelling is accompanied by a drop in membrane potential, which cannot be explained only by a work of the Ca2+ uniporter. With time, the potential is restored. Evidence has been obtained indicating that the specific content of mitochondrial lipids would favor the PA/Ca2+-induced permeabilization of the membrane. In experiments with liposomes, the PA/Ca2+-induced membrane permeabilization was larger for liposomes formed from the mitochondrial lipids, as compared to the azolectin liposomes. Additionally, it has been found that in mitochondria of the TNF (tumor necrosis factor)-sensitive cells (WEHI-164 line), the content of PA is larger than in mitochondria of the TNF-insensitive cells (C6 line), with this difference being mainly provided by PA incorporated in phosphatidylethanolamine and especially, cardiolipin. The PA/Ca2+-dependent mechanism of permeability transition in mitochondria might be related to some pathologies, e.g. myocardial ischemia. The heaviness of myocardial infarction of ischemic patients has been demonstrated to correlate directly with the content of PA in the human blood serum.
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Recent investigations have focused on the pivotal role of the mitochondria in the underlying mechanisms volatile anesthetic-induced myocardial preconditioning. This study aimed at examining the effect of anesthetic preconditioning on... more
Recent investigations have focused on the pivotal role of the mitochondria in the underlying mechanisms volatile anesthetic-induced myocardial preconditioning. This study aimed at examining the effect of anesthetic preconditioning on mitochondrial permeability transition (MPT) pore opening. Anesthetized open chest rabbits were randomized to one of four groups and underwent 10 min of ischemia, except for the sham 1 group (n = 12). Before this, they underwent a treatment period consisting of (1) no intervention (ischemic group; n = 12), (2) 30 min of desflurane inhalation (8.9% end-tidal concentration) followed by a 15-min washout period (desflurane group; n = 12), or (3) ischemic preconditioning (IPC group; n = 12). A second set of experiments was performed to evaluate the effect of a putative mitochondrial adenosine triphosphate-sensitive potassium channel antagonist, 5-hydroxydecanoate (5-HD). The animals underwent the same protocol as previously, plus pretreatment with 5 mg/kg 5-HD. They were randomized to one of five groups: the sham 2 group, receiving no 5-HD (n = 12); the sham 5-HD group (n = 12); the ischemic 5-HD group (n = 12), the desflurane 5-HD group (n = 12), and the IPC 5-HD group (n = 12). At the end of the protocol, the hearts were excised, and mitochondria were isolated. MPT pore opening was assessed by measuring the amount of calcium required to trigger a massive calcium release indicative of MPT pore opening. Desflurane and IPC group mitochondria needed a higher calcium load than ischemic group mitochondria (362 +/- 84, 372 +/- 74, and 268 +/- 110 microM calcium, respectively; P < 0.05) to induce MPT pore opening. The sham 1 and sham 2 groups needed a similar amount of calcium to trigger mitochondrial calcium release (472 +/- 70 and 458 +/- 90 microM calcium, respectively). 5-HD preadministration had no effect on sham animals (458 +/- 90 and 440 +/- 128 microM calcium without and with 5-HD, respectively) and ischemic group animals (268 +/- 110 and 292 +/- 102 microM calcium without and with 5-HD, respectively) but abolished the effects of desflurane on calcium-induced MPT pore opening (362 +/- 84 microM calcium without 5-HD vs. 238 +/- 96 microM calcium with 5-HD; P < 0.05) and IPC (372 +/- 74 microM calcium without 5-HD vs. 270 +/- 104 microM calcium with 5-HD; P < 0.05). Like ischemic preconditioning, desflurane improved the resistance of the transition pore to calcium-induced opening. This effect was inhibited by 5-HD, suggesting a link between mitochondrial adenosine triphosphate-sensitive potassium and MPT.
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Research Interests: Obstetrics, Kinetics, Nuclear medicine, Ultrasound, Cardiovascular Risk, and 37 moreNuclear, Pregnancy, Humans, Female, Clinical, Male, Endothelial dysfunction, Artery, Clinical Sciences, Aged, Middle Aged, C reactive protein, Single Photon Emission Computed Tomography, Adult, Cardiac Imaging, Myocardium, Analysis of Variance, Cardiovascular Risk Factor, Doppler, Group, Technetium, Internal medicine Doppler ultrasonography, Coronary Circulation, The Carotid Artery Intima Media Thickness, Radiopharmaceuticals, Low Risk, Risk Evaluation, Carotid Artery, Cross Sectional Studies, Blood Flow Velocity, Enzyme Linked Immunosorbent Assay, Peripheral artery disease, Pre Eclampsia, Systolic blood pressure, Coronary Flow Reserve, Brachial artery, and Pulmonary Artery
Journal of Electrocardiology, Volume 44, Issue 2, Pages e32, March 2011, Authors:Ioana Mozos; Mircea Hancu; Camelia Costea; Danina Muntean; Alexandru Cristescu. Advertisement. Journal Home, Register or Login: Password: Auto-Login... more
Journal of Electrocardiology, Volume 44, Issue 2, Pages e32, March 2011, Authors:Ioana Mozos; Mircea Hancu; Camelia Costea; Danina Muntean; Alexandru Cristescu. Advertisement. Journal Home, Register or Login: Password: Auto-Login [Reminder]. ...