cytochrome oxidase/hypoxia

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Transient hypoxia-ischemia in rats: changes in diffusion-sensitive MR imaging findings, extracellular space, and Na+-K+ -adenosine triphosphatase and cytochrome oxidase activity.

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OBJECTIVE To investigate the correlation between diffusion-weighted (DW) magnetic resonance (MR) image changes with alterations in extracellular volume and changes in cytochrome oxidase and Na(+)-K(+)-adenosine triphosphatase (ATPase) activity at various times during and after cerebral

Determination of oxygen dosage effects on cytochrome oxidase after anoxia in brain.

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Recent evidence reports that high doses of O(2) administered via hyperbaric oxygen therapy (HBOT) improve the return of spontaneous circulation (ROSC), and the outcome of damage to the heart following a 25 min normothermic cardiac arrest. However, excessive O(2) during HBOT can be toxic. Near

Delayed onset of neurologic deterioration following anoxia/ischemia coincides with appearance of impaired brain mitochondrial respiration and decreased cytochrome oxidase activity.

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We previously demonstrated markedly inhibited brain mitochondrial respiration only in cats that (a) were hyperglycemic at anoxia and (b) had neurologic signs, i.e., fasciculations in tongue or facial muscles or focal seizures following reoxygenation. However, since the relationship between time of

Cytochrome oxidase is decreased in piglet hippocampus following hypoxia-ischemia.

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We assessed cytochrome oxidase (CytOx) staining in sham-operated control piglets and in piglets subjected to 30 minutes of cerebral hypoxia-ischemia (H-I) plus 4 hours of reperfusion (REP). The 1-day-old piglets were sedated, anesthetized, and ventilated. Cerebral blood flows (CBFs) were quantitated

Chronic hypoxia impairs cytochrome oxidase activity via oxidative stress in selected fetal Guinea pig organs.

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We hypothesized that chronic hypoxia disrupts mitochondrial function via oxidative stress in fetal organs. Pregnant guinea pig sows were exposed to either normoxia or hypoxia (10.5% O2, 14 days) in the presence or absence of the antioxidant, N-acetylcysteine (NAC). Near-term anesthetized fetuses

The effects of hyperoxia, hypoxia, and ischemia/reperfusion on the activity of cytochrome oxidase from the rat retina.

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Cytochrome oxidase activity from the retina can be enhanced or depressed by free radical-mediated reactions both in positive and negative aspect. The greatest effect was exerted by ischemia/reperfusion, which significantly increased the fluorescent products of lipid peroxidation (358 %, P < 0.01)

Ambient temperature of hypoxia: a differential study of liver catalase and cytochrome oxidase in guinea pig.

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The activities of liver catalase and cytochrome oxidase have been determined in sea-level and high-altitude native guinea pigs exposed to different ambient temperatures. The activities of both of these enzymatic systems have been found to increase as ambient temperature is reduced, and this occurs

c-fos expression and redox state of cytochrome oxidase of rat brain in hypoxia.

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Hypoxic induction of c-fos was studied in rat brains as a function of the cerebral oxygenation state using near-infrared spectroscopy by which the hemoglobin oxygenation state and redox state of mitochondrial cytochrome oxidase could be monitored noninvasively. Following reoxygenation after hypoxia,

Nitric oxide from neuronal nitric oxide synthase sensitises neurons to hypoxia-induced death via competitive inhibition of cytochrome oxidase.

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Hypoxia/ischaemia is known to trigger neuronal death, but the role of neuronal nitric oxide synthase (nNOS) in this process is controversial. Nitric oxide (NO) inhibits cytochrome oxidase in competition with oxygen. We tested whether NO derived from nNOS synergises with hypoxia to induce neuronal

Effect of a short-term fasting and altitude hypoxia on the cytochrome oxidase activity of rat brain mitochondria.

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The effect of short-term fasting and thirst, prolonged fasting and hypoxic hypoxia upon the activity of cytochrome oxidase was studied in mitochondrial fractions obtained from the brain and the liver. The investigation was carried out in two groups of rats, 5 and 60 days old. a) The activity of

Cellular respiration during hypoxia. Role of cytochrome oxidase as the oxygen sensor in hepatocytes.

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We previously reported that hepatocytes exhibit a reversible suppression of respiration during prolonged hypoxia (PO2 = 20 torr for 3-5 h). Also, isolated bovine heart cytochrome c oxidase undergoes a reversible decrease in apparent Vmax when incubated under similar conditions. This study sought to

Decreased rat brain cytochrome oxidase activity after prolonged hypoxia.

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Three weeks of hypoxic exposure results in a spectrum of systemic physiological and local brain tissue adaptations. Cytochrome oxidase histochemistry was used as an indicator of changes in energy demand in response to hypoxia. We found overall cytochrome oxidase activity decreased in hypoxic adapted

Nitric oxide does not inhibit cerebral cytochrome oxidase in vivo or in the reactive hyperemic phase after brief anoxia in the adult rat.

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In this study, near-infrared spectroscopy was applied to examine whether cytochrome oxidase in the rat brain is inhibited by nitric oxide in vivo. During normoxia, intravenous N(G)-nitro-L-arginine methyl ester (L-NAME) administration significantly decreased the cerebral saturation of hemoglobin

Chronic hypoxemia increases myocardial cytochrome oxidase.

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OBJECTIVE Cyanotic patients have potentially decreased tissue oxygen tension. Cytochrome oxidase catalyzes the reduction of oxygen and is integral to adenosine triphosphate production. Cytochrome oxidase subunit I, the active site, is encoded by mitochondrial DNA. Using a newborn swine model of

Daily acute intermittent hypoxia induced dynamic changes in dendritic mitochondrial ultrastructure and cytochrome oxidase activity in the pre-Bötzinger complex of rats.

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Mitochondria, as primary energy generators and Ca²⁺ biosensor, are dynamically coupled to neuronal activities, and thus play a role in neuroplasticity. Here we report that respiratory neuroplasticity induced by daily acute intermittent hypoxia (dAIH) evoked adaptive changes in the

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