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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Under effects of myocardial ischemia (30 min), the activities of the intermembrane enzymes of rabbit heart mitochondria, i.e., adenylate kinase and creatine kinase, are inhibited by 20% and 23%, respectively. Consequently, the creatine- and AMP-activated respiration of mitochondria diminishes by 52% and 39%, respectively. An inhibitory analysis of ADP-, AMP- and creatine-activated mitochondrial respiration performed in the presence of atractyloside has demonstrated that ischemia (30 min), adriblastin (0.688 mM) and succinate (10 mM) cause alterations in the functional coupling of adenylate kinase and creatine kinase with the adenine nucleotide translocator. These alterations lead to the diminution of the rate and efficiency of energy transfer from mitochondria to hexokinase, as an arbitrary site of energy consumption. An addition of cytochrome c to ischemic heart mitochondria results in an increase in the rate of ATP synthesis; however, the efficiency of this process is lowered. The toxic effect of the anticancer drug--adriblastin on heart mitochondria respiration is enhanced in the presence of creatine in the bathing solution.
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PMID:[Functional changes in the mitochondrial site of adenylate kinase and creatine kinase systems of energy transport induced by myocardial ischemia and adriablastin]. 284 Jan 29

Under conditions of perfusion of isolated rabbit heart in aerobic medium and, especially, during ischemia, cytochrome c was liberated from heart cells into perfusate, thus indicating that integrity of mitochondrial outer membrane and of cell membrane was impaired. In situ developed deficiency of cytochrome c was distinctly less as compared with isolated mitochondria (50%, 3 hrs perfusion in ischemia), which appears to occur in response to ultrastructural impairments of mitochondria arising during their isolation and to other reasons.
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PMID:[The state of membrane structures of heart cells during ischemia]. 285 Dec 12

Antioxidant activity of exogenous cytochrome c was investigated in vitro using the whole brain homogenate, mitochondrial fraction and postmitochondrial supernatant containing microsomes prepared from rat brains. Increments in the amount of lipid peroxides were observed in each fraction when incubated at 30 degrees C, while the addition of cytochrome c (200 mM) effectively suppressed the production of peroxides. This depressive effect of cytochrome c was more prominent in the supernatant than in the mitochondrial fraction. Although the peroxidation was enhanced markedly by the addition of NADPH (2 mM), particularly in the mitochondrial fraction, cytochrome c was able to prevent its acceleration. This inhibitory mechanism might be explained by the fact that cytochrome c deprived superoxide radicals of electrons generated in ischemic insult. The results of the present study suggest that exogenous cytochrome c has free radical scavenging or antioxidant activity, which might be responsible in part for its cerebral protective action during ischemia.
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PMID:Effect of cytochrome c on formation of lipid peroxides in rat brain in vitro. 285 20

The structural and functional heterogeneity of mitochondria isolated from intact and ischemic (after 60 min exposure at 37 degrees C) rabbit myocardium was evaluated. In the presence of cytochrome c. a relatively high (260 +/- 26 ng at O/min . mg of protein) rate of rotenone-sensitive NADH oxidation was observed, which was increased in ischemia. Cytochrome c stimulated the increase of NADH oxidation in mitochondria of normal and ischemic myocardium by the factors of 3.5 and 3.4, respectively. Succinate oxidation in the presence of bromthymol blue in normal and ischemic myocardium mitochondria was activated by cytochrome c 3.3- and 2.9-fold, respectively. The percentage of mitochondria with both structurally damaged membranes was 15% and 25% in normal and ischemic myocardium preparations, respectively. In the absence of ADP, cytochrome c contributed to the increase of the succinate oxidase activity in ischemic mitochondria; that in the 3rd state was inhibited in ischemia and normalized by cytochrome c. A principle was proposed for estimating the percentage of mitochondria with damaged outer membranes, the indices being equal to 34% in control and to 56% in ischemic myocardium. Evidence was obtained suggesting that this mitochondrial fraction was characterized by lowered coupling and absence of rotenone-sensitive NADH: oxidase activity. The percentage of intact mitochondria, in which succinate oxidation is inhibited by bromthymol blue and does not need exogenous cytochrome c, is 51% in control and 19% in ischemic myocardium mitochondria.
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PMID:[Evaluation of structuro-functional heterogeneity of isolated mitochondria from the normal and the ischemic myocardium]. 300 Apr 62

The influence of malate and cytochrome c on fatty acid oxidation under control and ischemic conditions was investigated. In the medium without malate, cytochrome did not make fatty acid oxidation decreased during ischemia return to normal. Oxidation in the media containing malate and cytochrome did not differ from control only when it was measured after preliminary oxidation of endogenous substrates. The ratio of palmitoyl-CoA and palmitoyl carnitine to the respiration rates at state 3 was unchanged at 60 min ischemia. Apparently, no changes in carnitine acyltransferase playing a role in oxidation of palmitoyl-CoA took place. Thus, the decrease of fatty acid oxidation at early periods of ischemia is largely caused by a reduction in the content of cytochrome c and intermediates of Krebs cycle in the mitochondria.
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PMID:[Reasons for disorders of fatty acid oxidation in isolated heart mitochondria during ischemia]. 398 34

The relationships among isometric tension development, the oxidation-reduction states of pyridine nucleotides and cytochrome c, and the oxygenation state of myoglobin have been assessed using the arterially perfused rabbit interventricular septum under different conditions of contraction rate, perfusate [Ca2+] and pH, catecholamine stress, and hypoxia. Hypoxia was produced either by decreasing oxygen availability with maintained flow (high-flow hypoxia) or by decreasing the flow rate (ischemia). Under normoxic conditions, increased work caused a fall of the cytosolic adenine nucleotide phosphorylation potential, delta G(ATP)c, an oxidation of the pyridine nucleotides, and a reduction of cytochrome c; the opposite occurred with decreased work. Thus, the redox potential span from NADH to cytochrome c, delta Eh, varied with the energy demand such that delta Eh and delta G(ATP)c changed in the same direction. Under hypoxic conditions, all respiratory components became more reduced, and myoglobin was partially deoxygenated. The percentage change of developed tension under hypoxic conditions was approximately proportional to the percentage change of oxidized cytochrome c. When high-flow hypoxia and ischemia were compared at the same rates of oxygen delivery, the developed tension at any level of cytochrome c reduction was always lower with ischemia than with high-flow hypoxia. This difference was attributed to the low intracellular pH of ischemic tissue. Myoglobin deoxygenation was linearly related to cytochrome c reduction under all conditions of hypoxia, indicating steep oxygen gradients. The results support the concept of heterogeneous oxygenation of the tissue with mixed populations of aerobic and anaerobic mitochondria in the hypoxic state. In the full aerobic state, the control of mitochondrial respiration in situ appears similar to that of isolated mitochondria.
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PMID:Mitochondrial function in normal and hypoxic states of the myocardium. 630 29

Polarographic measurements show that activity of cytochrome oxidase (CO), assayed as ascorbate plus TMPD oxidase, is decreased in the mitochondria (M) from postischemic areas of rabbit heart 1, 6, and 9 days after temporary (1-hr) coronary artery occlusion (CAO). This effect is observable only in the absence of added cytochrome c. Cytochrome oxidase activity in the cytochrome c-containing medium was not different from the control level. Levels of cytochromes c + c1 and a were substantially lower in tissue from postischemic areas and elevated in the intact tissue 1 and 6 days after temporary CAO as compared with control hearts. Stoichiometry of the cytochromes was not changed. After 1 or 4 hr of permanent CAO, CO activity (plus cytochrome c) of ischemic M was equal to that of M from intact area; CO activity (with or without cytochrome c) was reduced after 0.5 and 1 hr but elevated after 3 or 4 hr of in vitro ischemia as compared with control. The changes of CO activity in infarcted human heart M were similar to those in rabbits after temporary CAO; CO activity was restored after addition of cytochrome c. The data suggest that leakage of cytochrome c occurs during isolation of M and is more pronounced in ischemia-damaged M.
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PMID:Cytochrome oxidase activity of mitochondria from ischemic and reperfused myocardium. 630 31

Differential cytochrome spectra and their fourth degree derivatives were recorded at 77 degrees K temperature. During myocardial ischemia (2-h autolysis), only cytochrome c content was found to be decreased in isolated mitochondria. According to these data mitochondrial state 3 respiration with succinate decreased only in a medium without cytochrome c. Before ADP addition mitochondrial respiration increased but in a medium with cytochrome c. This was followed by an increase in the respiration rate minimized by bromthymole blue, an inhibitor of dicarboxylate transport. It is inferred that these alterations seen in ischemia are linked with increased permeability of mitochondrial membranes: external for cytochrome c, and internal for inorganic ions and low-molecular compounds.
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PMID:[Changes in the quantitative composition of cytochromes and the functional activity of heart mitochondria during ischemia]. 631 61

Effect of ischemia and cytochrome c on oxidation of pyruvate and malate as well as of 3-hydroxybutyrate, succinate and exogenous NADH was studied. Respiration of mitochondria at the state 3 was markedly decreased in presence of the mixtures free of cytochrome c and containing pyruvate and malate, 3-hydroxybutyrate and succinate. In the same mixtures, but containing cytochrome c, oxidation of NAD-dependent substrates was decreased less distinctly and oxidation of succinate was similar to the control values. The rate of rhothenone-sensitive oxidation of NADH as well as the activating effect of cytochrome c on oxidation of all the substrates studied, except of NADH, were increased in ischemia. The data obtained suggest that alterations in the mitochondria functional activity in ischemia occur due to an increase in penetration of pyridine nucleotides across the inner membrane and of cytochrome c across the outer layer. Heterogeneity of mitochondria is discussed.
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PMID:[Effect of ischemia on the functional activity and membrane permeability of heart mitochondria]. 633 Oct 1

Synaptosomes isolated on isosmotic Ficoll density gradients are an effective model for some aspects of neuronal function. They maintain metabolic energy levels ([ATP]/[ADP] [Pi]) and transplasma membrane electrical potentials very similar to those of neurons in the intact brain. The concentration of K+ in the external medium (K+-sensitive electrode), O2 uptake, and cytochrome c reduction (550 nm minus 540 nm) were simultaneously monitored in synaptosomal suspensions. Oxidative metabolism is the primary source of intrasynaptosomal ATP and at pH 7.4 anaerobiosis results in K+ leakage at 4.5 +/- 0.8 nmol/min/mg protein with glucose as substrate and 10.7 +/- 1.9 nmol/min/mg protein with lactate plus pyruvate (10:1) as substrate. Reintroduction of oxygen initiates complete (ouabain-sensitive) reuptake of K+ at initial rates of 35.4 +/- 3.2 nmol/min/mg protein and 18 +/- 1.7 nmol K+/min/mg protein, respectively. The rates of K+ leakage and reuptake fall when the pH is lowered from 7.4 to 6.0 but recover fully if the pH is raised to the original value. The rates of K+ release and uptake decrease when the Na+ concentration in the medium is decreased and increase when the Ca2+ concentration is decreased. The intrasynaptosomal [K+] under aerobic conditions was 77.3 +/- 3 mM and the calculated K+ diffusion potential was -72 mV. Anaerobic incubation of the synaptosomes from up to 20 min and at pH values from 7.4 to 6.0 did not produce irreversible impairment of any of the measured variables. These results suggest that permanent loss of brain function following prolonged hypoxia and ischemia is not due to irreversible damage to the synapses with respect to these parameters but rather to impairment of some other neuronal functions.
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PMID:Effects of in vitro hypoxia and lowered pH on potassium fluxes and energy metabolism in rat brain synaptosomes. 746 41


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