Biomedical subjects

Sonata Trumbeckaite

Publications and source records attributed to Sonata Trumbeckaite.

9 recordsLinked to original sources

PubMed2006

Influence of propolis water solution on heart mitochondrial function.

The effect of propolis water solution (PWS) on the respiration of rat heart mitochondria with NAD-linked (pyruvate + malate), FAD-linked (succinate) substrates and fatty acids (palmitoyl-L-carnitine) was investigated in this study. PWS at the lowest concentration of 4 microg mL(-1) of phenolic compounds (PC) had no effect on mitochondrial respiration with all investigated substrates. PWS at concentrations of 63 and 125 microg mL(-1) of PC caused a significant decrease of basal (24 and 54%) and maximal (58 and 70%) respiration rates with succinate as substrate. At these PWS concentrations the oxidation of pyruvate + malate and palmitoyl-L-carnitine was diminished to a lower degree: the basal respiration rate decreased by 13-18% and the maximal respiration rate by 15-28%. Succinate oxidation was affected, probably because of the inhibition of succinate dehydrogenase by the 1,2-benzenedicarboxylic acid esters found in PWS. The PWS-caused decrease in the mitochondrial respiration rate with pyruvate + malate and fatty acids could be due to diminished activities of respiratory chain complexes and/or ADP/ATP translocator.

Animals↗

PubMed2005

Myocardial protective effect of warm blood, tepid blood, and cold crystalloid cardioplegia in coronary artery bypass grafting surgery.

AIM: To compare the myocardial effects of cardioplegia by warm blood, tepid blood, and cold crystalloid during coronary artery bypass grafting (CABG). METHODS: Patients undergoing CABG surgery at Kaunas University Hospital between 2000 and 2004 were randomized into three groups (n=156), receiving a different method of cardioplegia. Intermittent antegrade warm blood cardioplegia was used in 51 patients, tepid blood cardioplegia in 50 patients, and cold crystalloid cardioplegia in 55 patients. Mitochondrial function, myocardial ultrastructure, troponin T, and hemodynamic and clinical data were analyzed after surgery. RESULTS: All cardioplegic methods similarly affected structural and functional properties of mitochondria and coupling of oxidative phosphorylation, and all lowered the capacity of mitochondria to synthesize ATP. Ultrastructure of myocytes showed slight to moderate injury in the cold crystalloid cardioplegia group. The concentration of troponin T was significantly lower in the warm blood cardioplegia group than in the tepid blood cardioplegia and cold crystalloid cardioplegia groups at 12 hours (0.8+/-0.1 ng/mL, 1.9+/-0.2 ng/mL, and 2.8+/-0.3 ng/mL, respectively; P<0.001) and 24 hours after surgery (1.0+/-0.1 ng/mL, 2.2+/-0.3 ng/mL, and 2.5+/-0.3 ng/mL, respectively; P<0.001). Echocardiographic examination after surgery revealed that the changes in the left ventricle diastolic function were similar in all groups, and that systolic function did not change. The warm blood cardioplegia group showed shorter duration of intubation and hospitalization. There were no differences in the need of catecholamine administration, incidence of complications, and duration of stay in the intensive care unit. CONCLUSIONS: Intermittent antegrade warm blood cardioplegia provides better myocardial protection during CABG surgery, as assessed by the lower release of troponin T, lower fluid balance, shorter duration of tracheal intubation and hospital stay.

Body Temperature↗

PubMed2004

[Investigation of chemical composition of propolis extract].

Propolis is a natural product, produced by bees and containing exudates from plants, mixed with bee wax. Propolis and its ethanolic extract are usually used for treatment and prevention of different diseases. Propolis has antibacterial, antiviral, antifungal, anti-inflammatory, anesthetic and immunomodulating properties. Till now there is no data about chemical composition of Lithuanian propolis. Thus, the aim of our work was to investigate the chemical composition of Lithuanian propolis and its ethanolic extract by using gas chromatography / mass spectrometry. We found, that the main structural types of compounds were terpenoids, aromatic and aliphatic acid esters. The most of terpenoids were mono- and sesquiterpens: azulene, alpha-bisabolol, citral, valerenol, etc. Thus, our data show, that the composition of propolis is various and depends on the origin of plants, from where propolis was collected.

Anti-Infective Agents↗

PubMed2003

Calpain inhibitor (BSF 409425) diminishes ischemia/reperfusion-induced damage of rabbit heart mitochondria.

Calpains are involved in ischemia/reperfusion-induced changes of myocard. To obtain information on the action of calpain on mitochondria, the effect of a new developed calpain inhibitor (CI) BSF 409425 on the ischemia/reperfusion-induced damage of rabbit heart mitochondria was investigated. Rabbit hearts were subjected to 45 min of global ischemia followed by 60 min of reperfusion in the presence or absence of 10nM CI. Mitochondrial properties were characterized by skinned fiber technique with pyruvate+malate as substrates. In the presence of CI, the decrease of state 3 respiration and the increase of state 4 respiration after ischemia and reperfusion were clearly smaller than without CI resulting in significantly smaller changes of respiratory control index, too. Ischemia/reperfusion-caused leaks in mitochondrial inner and outer membranes were diminished by CI. It is concluded that mitochondria are a target of calpain which reinforces the damage of oxidative phosphorylation and mitochondrial membranes during ischemia/reperfusion.

Animals↗

PubMed2003

A novel water-soluble and cell-permeable calpain inhibitor protects myocardial and mitochondrial function in postischemic reperfusion.

The effects of the novel calpain inhibitor A-705239 were studied in isolated perfused rabbit hearts subjected to 45 min of global ischemia, followed by 60 min of reperfusion. During 15 min of perfusion the inhibitor accumulated in myocardial tissue up to 16 times the concentration in the perfusate. Almost complete recovery and survival of heart function (90%) was seen with an inhibitor concentration of 10(-8) M in the perfusion fluid when the compound was administered prior to ischemia. Left ventricular pressure amplitude and coronary flow showed significantly higher values during reperfusion in the presence of the inhibitor. A-705239 significantly reduced the release of creatine kinase, from 166+/-49 U/l in untreated hearts to 44+/-10 U/l, and diminished the release of lactate dehydrogenase from 118+/-20 U/l in untreated hearts to 63+/-4 U/l. Mitochondrial dysfunction following ischemia and reperfusion was markedly attenuated by the inhibitor. Thus, the state 3 respiration rate only decreased to 4.2 in contrast to 2.6 nmol O2/(min x mg s.w.) in untreated hearts, reflecting a reduced damage of oxidative phosphorylation. Furthermore, in the presence of the inhibitor the inner mitochondrial membranes became less permeable as indicated by a smaller leak respiration. The excellent properties of A-705239 should make this compound a valuable tool for further pharmacological studies.

Adenosine Diphosphate↗

PubMed2002

Mitochondrial dysfunction in sepsis: evidence from bacteraemic baboons and endotoxaemic rabbits.

Mitochondria, that provide most of the ATP needed for cell work, and that play numerous specific functions in biosyntheses and degradations, as well as contributing to Ca2+ signaling, also play a key role in the pathway to cell death. Impairment of mitochondrial functions caused by mutations of mt-genome, and by acute processes, are responsible for numerous diseases. The involvement of impaired mitochondria in the pathogenesis of sepsis is discussed. By means of the skinned fiber technique and high resolution respirometry, we have detected significantly reduced rates of mitochondrial respiration in heart and skeletal muscle of endotoxaemic rabbits. Mitochondria from heart were more affected than those from skeletal muscle. Decreased respiration rates were accompanied by reduced activities of complex I + III of the respiratory chain. Endotoxin-caused impairment was also detectable at the level of the Langendorff perfused heart, where the coronary vascular resistance was significantly increased. For an investigation of the influence of bacteraemia on the mitochondrial respiratory chain, baboons were made septic by infusion of high and low amounts of E. coli. For complex I + III and II + III, a clear dose-dependent decrease was detectable and in animals which died in septic shock, a further decrease of enzyme activities in comparison to the controls were found. These results are discussed in the light of current knowledge on the role of mitochondria in cell pathology in respect to sepsis. In conclusion, we present evidence that mitochondrial function is disturbed during sepsis. Besides ischaemic and poison-induced disturbances of mitochondrial function, sepsis is a further example of an acute disease where impaired mitochondria have to be taken into account.

Animals↗

PubMedDate not supplied

Cytochrome C effect on respiration of heart mitochondria: influence of various factors.

The effect of exogenous cytochrome c on respiration rate of the rat and human heart mitochondria was assessed in situ, using permeabilized fibers. It was (i) much more pronounced in State 2 and 4 than in State 3 with all the respiratory substrates (pyruvate+malate, succinate, palmitoyl-CoA+carnitine and octanoyl-L-carnitine), (ii) different with different substrates, (iii) much higher after ischemia in both metabolic states, particularly in the case of succinate oxidation compared to pyruvate+malate, (iv) the highest in State 4 with succinate as a substrate. Similar results were obtained with the isolated rat and rabbit heart mitochondria. The differences in the degree of stimulation of mitochondrial respiration by cytochrome c and, thus, sensitivity of cytochrome c test in evaluation of the intactness/injury of outer mitochondrial membrane are probably determined by the differences in the cytochrome c role in the control of mitochondrial respiration in the above-described conditions.

Animals↗

PubMedDate not supplied

Energetic depression caused by mitochondrial dysfunction.

Mitochondria, providing most of ATP needed for cell work, realizing numerous specific functions as biosyntheses or degradations, contributing to Ca2+ signalling also play a key role in the pathways to cell death. Impairment of mitochondrial functions caused by mutations of mt-genome and by acute processes are responsible for numerous diseases. The relations between changes on the level of molecules and the clinical state are rather complex, and the prediction of thresholds is difficult. Therefore investigations on different levels of an organismus (genome, metabolites, enzymes, mitochondrial function in vivo and in vitro) are necessary (multi level approach). Metabolic control theory is a valuable tool for understanding the different effects of mutations on the level of enzyme activities and mitochondrial function. Decreased concentrations of adenine nucleotides, leaky outer and inner mitochondrial membranes, decreased rates of mitochondrial linked pathways and decreased activities of respiratory chain enzymes contribute to depression of cellular energy metabolism characterized by decreased cytosolic phosphorylation potentials as one of the most important consequences of mitochondrial impairments. This review regards classical bioenergetic mechanisms of mitochondrial impairment which contribute to energetic depression.

Animals↗

PubMedDate not supplied

Energetic depression caused by mitochondrial dysfunction.

Mitochondria not only provide most of the ATP needed for cell work and numerous specific anabolic and catabolic functions, they also contribute to Ca++ signalling and play a key role in the pathway to cell death. Impairment of mitochondrial functions caused by mutations of the mt-genome or by acute processes, is responsible for numerous diseases. Decreased concentrations of adenine nucleotides, leaky outer and inner mitochondrial membranes, and decreased activities of respiratory chain enzymes contribute to depression of cellular energy metabolism, one of the most important consequences of mitochondrial impairment as characterized by decreased cytosolic phosphorylation potentials.

Adenine Nucleotides↗