PubMed Health⌕ Search

Biomedical subjects

A A Timoshin

Publications and source records attributed to A A Timoshin.

At least 19 recordsLinked to original sources
PubMed2005

[Protection of rat heart myocardium with a selective Na(+)/H(+) exchange inhibitor and ischemic preconditioning].

Aim of this study was to compare effects of BIIB-722, a novel Na(+)/H(+) exchanger-1 inhibitor, and ischemic preconditioning (IP) on infarct size and metabolism of area at risk in rats. Regional ischemia was induced by 40-min occlusion of a diagonal branch of left anterior descending coronary artery (LAD); it was followed by 60-min reperfusion. Intravenous bolus injection of BIIB-722 (3 mg/kg) dissolved in 280 mM xylitol was performed before regional ischemia or during the first minute of reperfusion. In the control group 280 mM xylitol was infused before ischemia or at the beginning of reperfusion at the same mode. IP was initiated by two cycles of 5-min LAD occlusion followed by 5-min reperfusion prior to sustained regional ischemia. Microdialysis technique was used to monitor pH and inorganic phosphate (P(i)) in the interstitial fluid of the area at risk. Metabolic state of the area at risk was assessed by ATP, phosphocreatine (PCr) and lactate levels; cellular membrane damage was evaluated by total creatine (SigmaCr=PCr+Cr) tissue content. Myocardial infarct size was determined by computer planimetry after staining of left ventricular slices with 2,3,5-triphenyltetrazolium chloride. BIIB-722 administration before or after ischemia, as well as IP, had no effect on cardiac hemodynamics and acid-base indices of arterial blood throughout the experiments. The infarct size/area at risk ratio was 43.5+/-5.2% in control and was reduced to 11.4+/-3.1% with IP, and to 17.0+/-3.6% and 25.8+/-2.6% with BIIB-722 infused on early reperfusion and before ischemia, respectively. BIIB-722 administration during the first minute of reperfusion as well as IP significantly augmented ATP and PCr contents, reduced lactate level and decreased ECr loss at the area at risk by the end of reperfusion as compared with values in control. Additionally significantly higher rates of pH recovery and reduction of P(i) concentration in the interstitial fluid were observed during reperfusion compared with these indices in control. BIIB-722 administration before ischemia had much effects on contents of energy and carbohydrate metabolites at area at risk. The results obtained indicate that ability of BIIB-722 to limit infarct size and improve metabolism in the area at risk is comparable to cardioprotective effects of IP. Therefore this study substantiates a possibility of application of a novel Na(+)/H(+) exchange inhibitor for clinical investigations.

Adenosine Triphosphate↗
PubMed2004

[Protective effect of hydrophilic ubiquinone on cardiac muscle during oxidative stress].

AIM: To assess effects of long term administration of a natural antioxidant ubiquinone on isoproterenol induced myocardial injury. METHODS: Rats were given hydrophilic ubiquinone with water for 8 weeks. RESULTS: Long term use of ubiquinone did not affect myocardial ultrastructure and relative myocardial weight. The dose of isoproterenol used in this study exerted moderate damaging action evidenced by disappearance of glycogen from sarcoplasm, development of edema, and partial destruction of mitochondrial cristae. These effects were associated with lowering of maximal magnitude of contractile function of the isolated heart and augmentation of superoxide radicals release in perfusate. These changes (except disappearance of glycogen) were not present in hearts of ubiquinone fed rats. Compared with controls mitochondria isolated from hearts of ubiquinone fed rats had higher respiratory control and more than twice lower rate of superoxide generation. CONCLUSION: As damaging effects of isoproterenol are mediated by augmented generation of active forms of oxygen the results obtained allow to suggest that myocardium of ubiquinone fed animals is characterized by elevated power of the antioxidant system.

Animals↗
PubMed2004

[Aspartic Acid and mannitol enhance protective efficiency of asanquineous cardioplegic solution].

The aim of this work was to assess effects of a novel asanquineous cardioplegic solution (CP-5), buffered with trisamine (pH 7.6+/-0.1 at 22 degrees C) and containing 21.5 mM aspartic acid and 20.0 mM mannitol, on postischemic functional and metabolic recovery of isolated rat heart. A modified Ringer solution with 25 mM KCl (pH 7.6+/-0.1 at 22 degrees C) and the St. Thomas' cardioplegic solution (pH 7.8+/-0.1 at 22 degrees C) were used as controls. Osmolarity of all cardioplegic solutions were 340+/-5. After 20-min initial perfusion according to Neely (steady state) the hearts were subjected to 40-min normothermal total ischemia followed by 30-min antegrade reperfusion. Cardioplegic solutions were infused prior to ischemia at rate of the initial coronary flow for 5 min at room temperature. During reperfusion the hearts of CP-5 group completely recovered coronary flow and significantly enhanced restoration of the majority functional indices compared to the hearts in both control groups. This effect was combined with less lactate accumulation and preservation of higher ATP and phosphocreatine (PCr) levels in the heart tissue by the end of ischemia and, probably was induced by inclusion of aspartic acid into composition of CP-5. By the end of reperfusion the hearts treated with CP-5 completely recovered PCr content and restored ATP level up to 65.2+/-4.6% of initial one. A better energy state of reperfused hearts in CP-5 group was accompanied by reduction of myocardial lactate tissue to the preischemic value. Restoration of ATP, PCr and lactate content was significantly poor in both control groups during reperfusion. The least formation of a spin adduct of the short life oxygen radicals was found in the myocardial effluent of the hearts of CP-5 group at the early reperfusion using EPR technique. These data suggest a reduced release of oxygen radical generating systems from postischemic myocardium into perfusate due to antioxidant effect of mannitol. The obtained results substantiate addition of aspartic acid and mannitol to the asanquineous cardioplegic solution, buffered with trisamine, to enhance efficacy of myocardial protection against ischemia and reperfusion injury.

Animals↗
PubMed2003

Protective effect of phenyl-t-butylnitrone in rats with focal cerebral ischemia.

Phenyl-t-butylnitrone produces a potent neuroprotective effect in rats with focal cerebral ischemia modeled by distal occlusion of the middle cerebral artery. The infarction area markedly decreased after treatment with phenyl-t-butylnitrone. The content of phenyl-t-butylnitrone in the brain, liver, and kidneys was measured by the method of electron paramagnetic resonance.

Animals↗
PubMed2003

[Effects of Na(+)/H(+)-exchanger inhibition on metabolism of area at risk and myocardial infarct size in dogs].

The aim of this work was to study cardioprotective effects of BIIB 722, a novel Na(+)/H(+) exchanger-1 inhibitor, during regional ischemia and reperfusion in canine myocardium. The experiments were carried out on anaesthetized dogs intubated and artificially ventilated with room air enriched with oxygen. Regional ischemia was induced by 30-min occlusion of a diagonal branch of left anterior descending coronary artery (LAD), which was followed by 60-min reperfusion. BIIB 722, dissolved in 280 mM xylitol, was infused intracoronary for 10 min prior to LAD occlusion and at the beginning of reperfusion at the rate of 1 ml/min (30 microg/g myocardial tissue). In the control group, 280 mM xylitol was used for intracoronary administration with the same regimen. Microdialysis probes were implanted in the region of LAD occlusion to monitor interstitial pH, inorganic phosphate (Pi) and hydroxyl radical adduct. Energy state of the area at risk was evaluated by ATP and phosphocreatine (PCr) contents, cell membrane damage was assessed by total creatine (SigmaCr=PCr+Cr) tissue content. Myocardial infarct size was determined by staining with Evans Blue dye and further incubation of left ventricular slices in 2,3,5-triphenyltetrazolium chloride. The percentage ratio of infarct size to area at risk was calculated by computer planimetry. BIIB 722 administration had no effect on cardiac hemodynamics and acid-base indices of arterial blood throughout the experiments but induced 1.8-fold reduction of myocardial infarct size comparing with control. Treatment with BIIB 722 decreased acidification of the interstitial fluid following ischemia and facilitated recovery of pH to initial value on reperfusion. This effect was combined with significantly less Pi formation in the area at risk during LAD occlusion and reduction of this index to the initial value during reperfusion. At the end of reperfusion, the treated group showed augmented recovery of ATP and PCr tissue levels and higher content of SigmaCr comparing with the control. Additionally, BIIB 722 treatment markedly decreased generation of free oxygen radicals following LAD occlusion and completely avoided their formation on early reperfusion. The results indicate that BIIB 722 ability to limit myocardial infarct size in dogs is tightly connected with its influence on energy metabolism and oxygen radical generation.

Animals↗
PubMed2002

[The protective action of ubiquinone at ischemia and reperfusion].

Effects of prolonged consumption of ubiquinone on myocardial injury caused by ischemia and reperfusion were studied in reperfused rat hearts. Wistar rats received lipophylic or hydrophilic forms of ubiquinone for 6-8 weeks with chow or water, respectively. Isolated isovolumic hearts with a constant volume latex balloon in the left ventricular cavity were subjected to total normothermic ischemia (25 min) and subsequent reperfusion (50 min). Time course of ischemic contracture and its level in both groups of ubiquinone treated animals were similar to those in controls. However recovery of left ventricular developed pressure after reperfusion was significantly better in both ubiquinone groups (54-/+9, 65-/+7, and 24-/+4 mm Hg in animals treated with lipophylic and hydrophylic ubiquinone and controls, respectively, p<0.01). As a result the developed pressure and heart rate product reflecting maximal aerobic capacity of the heart was also better restored. Both ubiquinone groups demonstrated absence of increased coronary tone that was characteristic for control animals. Mitochondria isolated from reperfused hearts of ubiquinone treated rats showed better preservation of structure and respiratory control. Rate of succinate-dependent generation of superoxide radicals determined with a spin trap TIRON in mitochondria from hearts of rats treated with hydrophylic ubiquinone (35-/+8 mmol O(2) /min/g) was approximately twice lower (p<0.05) than in control group (74-/+12 mmol O(2) /min/g) while the value in lipophylic ubiquinone group (48-/+9 mmol O(2) /min/g) did not differ significantly from the control. The results evidence that prolonged consumption of water-soluble ubiquinone increases resistance of rat myocardium to injuring action of reperfusion.

Animals↗
PubMed2000

Effect of a polymeric surfactant on electron transport in HL-60 cells.

To assess the effect of a polymeric surfactant, Pluronic P-105 on the activity of electron transport chains in the mitochondria of HL-60 cells, the bioreduction rates of two membrane-localized lipophilic spin probes, 16-doxylstearic acid methyl ester (16-DSME) and 5-doxylstearic acid (5-DS), were studied. In addition, the effect of Pluronic on the bioreduction rate of the DNA-intercalating spin-labeled anthracyclin drug, Ruboxyl (Rb) was evaluated. For 16-DSME, the bioreduction kinetics was zero order with regard to the nitroxide concentration, indicating that the rate was controlled by the concentration of the reducing enzyme(s), which depends on the activity of the electron transport chains. The introduction of Pluronic at concentrations higher than 0.01% resulted in the decrease of the 16-DSME bioreduction rate. The data suggested that short-term cell incubation with Pluronic resulted in reduced activity of the electron transport chains in the mitochondria of HL-60 cells. This was corroborated by the results of an MTT assay. For 5-DS, the bioreduction kinetics was first order in the absence of Pluronic, but did not follow any simple kinetic law after a short-term cell incubation with Pluronic. For Rb, the degree of nitroxide bioreduction dropped progressively with increasing Pluronic concentration. Thus, incubating cells with polymeric surfactants modulates the intracellular energy metabolism, which can affect the rates of energy-dependent intracellular processes.

Anthracyclines↗
PubMed1999

Bioreduction of Tempone and spin-labeled gentamicin by gram-negative bacteria: kinetics and effect of ultrasound.

The primary objective of this study is the investigation of bioreduction kinetics of hydrophilic spin probes, 2,2,6,6, -tetramethyl-4-oxo-piperidinyl-1-oxyl (Tempone), and spin-labeled antibiotic gentamicin by gram-negative bacteria maintained at various oxygen tensions, with emphasis on the effect of probe penetration rate. This information was used to evaluate the effect of ultrasound on the penetration of hydrophilic compounds, including antibiotics, into Pseudomonas aeruginosa and Escherichia coli cells. Penetration of spin-labeled compounds into the cells was assessed by the reduction rate of the nitroxyl moiety measured by EPR. In cell suspensions, both Tempone and spin-labeled gentamicin were localized predominantly in the aqueous phase surrounding the cells. However, a gradual reduction of the probes in contact with the cells indicated that the probes penetrated through the outer membrane and periplasmic space into the cytoplasmic membrane, where the electron transport chains and other metabolic activities of gram-negative bacteria are localized. The kinetics of probe reduction depended on oxygen tension and presence of electron transport chain blockers. It was found that probe penetration rate through the outer cell membrane affected the rate of probe reduction; damaging the permeability barrier by cell incubation with EDTA or by powerful insonation above the cavitation threshold increased the rate of probe reduction. In contrast, insonation below the cavitation threshold did not affect the rate of probe reduction. These findings imply that the recently observed synergistic effect between hydrophilic antibiotics and low frequency ultrasound in killing gram-negative bacteria did not result from the enhanced antibiotic penetration through bacterial cell walls.

Cell Membrane↗
PubMed1997

Metabolic and antioxidant effects of R(+/-)-N6-(2-phenylisopropyl)-adenosine following regional ischemia and reperfusion in canine myocardium.

Recent studies have indicated that activation of A1/A2-receptors may mediate metabolic adaptation of the heart to ischemia/reperfusion stress. This study tests whether pretreatment with A1-selective agonist R(-)-N6-(2-phenylisopropyl) adenosine (R-PIA) might mimic effects of a brief period of coronary occlusion (ischemic preconditioning, IP) on energy metabolism and hydroxyl radical (OH.) formation in canine myocardium following subsequent prolonged ischemia and reperfusion. Anaesthetized dogs were randomized to a control group subjected to 40-min occlusion of a diagonal branch of left anterior descending coronary artery (LAD) followed by 1-h reperfusion, or a preconditioned group (PC) in which the same period of sustained ischemia and reperfusion was preceded by a single cycle of IP (5-min occlusion of the same LAD branch and 10-min reperfusion), or to PIA group in which R-PIA infusion into the same branch of LAD (0.4 microg/kg per min during 5 min) was followed by 10 min of perfusion prior to sustained ischemia-reperfusion. Pretreatment with R-PIA similarly to IP reduced lactate (Lac), creatine (Cr) and inorganic phosphate (Pi) release from myocytes into the interstitial fluid during sustained ischemia compared to these indices in control. By the end of reperfusion, both IP and R-PIA infusion enhanced recovery of myocardial ATP and phosphocreatine (PCr) and attenuated the total creatine (sigmaCr = PCr + Cr) loss, an index of cell membrane damage. A1-receptor activation by R-PIA, as IP, led to a significant reduction in OH. radical generation following reperfusion assessed by a spin trap 5,5'-dimethyl-1-pyrroline-N-oxide (DMPO) using cardiac microdialysis. R-PIA pretreatment did not affect systemic and cardiac hemodynamic parameters. We conclude that (1) adaptive mechanisms of IP involve A1-receptor activation that contributes to the overall metabolic response and (2) R-PIA acts as a useful preconditioning-mimetic and anti-ischemic agent in dogs.

Adenosine↗
PubMed1997

The redox state of coenzyme Q10 in mitochondrial respiratory chain and oxygen-derived free radical generation in cardiac cells.

The aim of this study was to relate changes in the redox state of mitocondrial electron carriers to the 'burst' of oxyradicals in postischemic myocardium. The free radical EPR signals of control and re-oxygenated rat hearts were mainly due to coenzyme Q10, the line width was 0.81 +/- 0.02 mT, and the intensities (1.58 +/- 0.12) x 10(16) and (1.41 +/- 0.13) x 10(16) spins/g. The low-temperature spectra of oxygenated myocardium contained a predominant signal from a S3 Fe-S center and weak signals from N1b, N2, N3, N4 and S1 centers. Global ischemia caused cardinal changes in the redox state of the mitochondrial respiratory chain. The low-temperature EPR spectrum now contained intensive signals from most Fe-S centers. The amount of coenzyme Q10 semiquinones decreased during global ischemia, but the content of flavosemiquinones increased. The line width of the signal of the ischemic heart was 1.28 +/- 0.03 mT, and its intensity corresponded (3.16 +/- 0.94) x 10(16) spins/g. The spin-trapping experiments with TEMPONE-H showed that the rate of oxyradical generation in isolated cardiomyocytes essentially increased after hypoxia or on adding rotenone and antimycin A. It became equal to 4.2 +/- 0.3, 8.2 +/- 0.6 and 7.1 +/- 0.5 nmol/min mg-1 mitochondrial protein, respectively. The maximal stimulatory effect was observed in the presence of both inhibitors. The addition of superoxide dismutase, but not catalase, suppressed the formation of oxyradicals.

Animals↗
PubMed1997

Tertiary ammonium ion induces contraction of rat aorta segments and increases the mobility of lipids in the membrane of rat aorta smooth muscle cells.

The effects of tertiary ammonium ion--IEM-1194 (decyldiisopropylammonium bromide)--on smooth muscle cells (SMC) isolated from rat aorta were investigated. Using the patch-clamp technique in the cell-attached configuration, two types of effects on the Ca(2+)-activated K+ channels were recorded after application of IEM-1194: an increase in the number of fast transition bursts in open channels and the prolongation of the burst. The removal of the agonist led to the activation of these channels. Mechanical responses of aortic rings were recorded using the method of isometric tension measurements. IEM-1194 (100-400 microM) caused contractions consisting of two phases. The first phase emerged immediately after application of the agonist. The second phase was observed 10-15 min after application. The contraction of the aorta was followed by the relaxation for over 1.5 h. The same results were obtained in the Ca(2+)-free external solution. Measurements of SMC membrane fluidity by the EPR method showed that IEM-1194 induced an increase in the mobility of membrane lipids. Based on these results, we suggest a mechanism of IEM-1194 action on the Ca(2+)-activated K+ channels.

Animals↗
PubMed1994

Microdialysis study of ischemia-induced hydroxyl radicals in the canine heart.

A new experimental approach for spin-trapping of oxygen radicals in a selected region of the heart in situ is described. This approach is based on microdialysis, and it permits the detection of oxygen radicals in conditions of local ischemia and restoration of normal blood flow. Increased hydroxyl radical generation in an ischemic area of canine myocardium, as a result of 40 min local occlusion, has been studied.

Animals↗
PubMed1994

Allopurinol-enhanced postischemic recovery in the isolated rat heart involves repletion of high-energy phosphates.

The effects of allopurinol (AP) on functional and metabolic recovery of the isolated rat heart after global ischemia were studied. Hearts were subjected to aerobic perfusion (30 min), cardioplegic infusion (5 min), normothermic ischemia (37 min), and reperfusion (50 min) which was started with secondary cardioplegic infusion (10 min). AP was injected into rats (44 mg/kg body wt ip 2 h before heart excision) and added to cardioplegic solution (2 mM) prior and after ischemia. AP treatment significantly improved postischemic recovery of the function and reduced the leakage of lactate dehydrogenase from reperfused hearts. These beneficial effects were accompanied by a better preservation of tissue content of ATP, the total adenine nucleotides, phosphocreatine, and the total creatine at the end of reperfusion. Inhibition of xanthine oxidase by AP substantially decreased pre- and postischemic release of xanthine and uric acid and increased postischemic release of hypoxanthine into the coronary effluent. Despite this, AP-treated hearts did not exhibit a reduction in hydroxyl radical adduct formation in the effluents at reperfusion assessed by the spin-trap measurements. The results suggest that AP may protect the heart from ischemia/reperfusion injury due to enhanced energy provision rather than by prevention of oxygen-derived free radical formation.

Adenosine Diphosphate↗
PubMed1994

Human recombinant extracellular-superoxide dismutase type C improves cardioplegic protection against ischemia/reperfusion injury in isolated rat heart.

The cardioprotective effects of human recombinant extracellular-superoxide dismutase type C (hr-EC-SOD C) were compared with those of bovine Cu,Zn-SOD in isolated working rat heart subjected to 35-min global normothermic ischemia followed by 55-min reperfusion. hr-EC-SOD C or bovine Cu,Zn-SOD (3 x 10(4) and 6 x 10(4) IU/L, respectively) was added to St. Thomas' Hospital (STH) cardioplegic solution infused 5 min before and 10 min after the ischemic period. Control hearts were treated with STH cardioplegic solution without SOD. By the end of reperfusion, hr-EC-SOD C-treated hearts recovered left ventricular systolic pressure (LVSP), aortic flow (AF) and cardiac output (CO) to 95 +/- 4, 60 +/- 4, 69 +/- 6% of preischemic value, respectively, as compared with 86 +/- 3, 44 +/- 5, and 52 +/- 6% in the control (p < 0.05). Cardioplegia with hr-EC-SOD C significantly reduced lactate dehydrogenase (LDH) release into myocardial effluent during reperfusion (p < 0.05) and increased ATP, AMP, and total creatine (Cr) tissue contents in reperfused hearts (by 21 +/- 3, 42 +/- 4, and 34 +/- 3%, respectively, as compared with control hearts, p < 0.05). The effects of bovine SOD on functional and biochemical indexes were similar but not statistically significant as compared with control. Treatment with hr-EC-SOD C, but not with bovine SOD, resulted in reduction in hydroxyl radical formation assessed by 5-5-dimethy-1-pyrroline-N-oxide spin trap (DMPO) in coronary effluent at early reperfusion with electron spin resonance (ESR) technique. The results suggest that enhanced myocardial protection against ischemia/reperfusion injury afforded by hr-EC-SOD C is related to scavenging of oxygen-derived free radicals.

Animals↗
PubMed1993

Fumarate reductase activity of bovine heart succinate-ubiquinone reductase. New assay system and overall properties of the reaction.

A simple system for aerobic assay of the quinol-fumarate reductase reaction catalyzed by purified soluble bovine heart succinate-ubiquinone reductase in the presence of NADH, NAD(P)H-quinone reductase (DT-diaphorase) and an appropriate quinone is described. The reaction is inhibited by carboxin, suggesting that the same quinone/quinol binding site is involved in electron transfer from succinate to ubiquinone and from ubiquinol to fumarate. The kinetic properties of the reaction in both directions and comparative affinities of the substrate binding sites of the enzyme to substrates (products) and competitive inhibitors are reported. Considerable difference in affinity of the substrates binding site to oxaloacetate was demonstrated when the enzyme was assayed in the direct and reverse directions. These results were taken to indicate that the oxidized dicarboxylate-free enzyme is an intermediate during the steady-state succinate-ubiquinone reductase reaction, whereas the reduced dicarboxylate-free enzyme is an intermediate of the steady-state ubiquinol-fumarate reductase reaction. No difference in the reactivity of the substrate-protected cysteine and arginine residues was found when the pseudo-first-order rate constants for N-ethylmaleimide and phenylglyoxal inhibition were determined for oxidized and quinol-reduced enzyme. Quinol-fumarate reductase activity was reconstituted from the soluble succinate dehydrogenase and low-molecular-mass ubiquinone reactivity conferring protein(s). No reduction of cytochrome b was observed in the presence of quinol generating system, whereas S-3 low temperature EPR-detectable iron-sulfur center was completely reduced by quinol under equilibrium (without fumarate) or steady-state (in the presence of fumarate). No significant reduction of ferredoxin type iron-sulfur centers was detected during the steady-state quinol-fumarate oxidoreductase reaction. The data obtained eliminate participation of cytochrome b in the quinol-fumarate reductase reaction and show that the rate limiting step of the overall reaction lies between iron-sulfur center S-3 and lower midpoint potential redox components of the enzyme.

Animals↗
PubMedDate not supplied

[Effect of ischemic preconditioning on free radical centers of the isolated rat heart during ischemia and early reperfusion].

The effect of ischemic preconditioning on the free-radical state of isolated rat myocardium fixed by rapid freezing at the 25th min of normothermic total ischemia and the 3rd min of reperfusion was studied by the EPR method. It was shown that EPR spectra registered at -40 degrees C consist of two free-radical signals: of the semireduced forms of ubiquinone and flavine coynzymes. It was found that during ischemia and at the beginning of reperfusion, the preconditioning results in a narrowing of the spectra (as compared with control) due to an increase in the narrow ubisemiquinone EPR signal portion, and a decrease in the total concentration of free-radical centers: by 16% in the case of ischemia, and 23% in the case of reperfusion. It was concluded that in both cases the changes were due to a decrease in the concentration of myocardial flavosemiquinones as a result of ischemic preconditioning. We registered the microvawe power saturation curves for these two stages, which corresponded to control and ischemic preconditioning. In the case of ischemia these dependences had similar shapes; however, in the case of reperfusion they differ from each other due to changes in the relative intensities of the EPR signals from ubisemiquinone and flavosemiquinones in the integral myocardial free-radical spectra.

Animals↗
PubMedDate not supplied

[Free radical centers in the dog myocardial tissue in regional ischemia].

The effect of regional ischemia on canine myocardial in situ free radical species was studied by the EPR method. Rapid fixation of heart muscle samples by freezeclamping was performed at the following physiological states: native myocardial blood circulation, regional ischemia with the presence of collateral circulation, total ischemia, and postischemic reperfusion. EPR spectra of the samples at -40 degrees C exhibited two free radical signals from the semireduced forms of ubiquinone and flavine coenzymes. Upon transition from normal blood supply to regional ischemia, an increase in the contribution of the flavine signal was registered, but reperfusion resulted in the recovery of the characteristics of EPR signals. It was found that the increase in the intensity of collateral circulation in the ischemic area led to an increase in the portion of ubisemiquinone in the integral EPR signal, whereas in total ischemia this signal was not registered. It was shown that the changes in spectral characteristics of integral free radical signals are accompanied by changes in their relaxation parameters.

Animals↗