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cytochrome oxidase/крварење

Врската е зачувана во таблата со исечоци
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Gene damages of mitochondrial DNA encoding cytochrome oxidase of intestinal epithelial cells in hemorrhagic shock rats.

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OBJECTIVE To investigate the detrimental effects of hemorrhagic shock on the structure and function of mitochondria DNA (mtDNA) encoding cytochrome oxidase genes in intestinal epithelial cells. METHODS Wistar rats were used and divided into two groups: hemorrhagic shock group and control group.

An in vitro model of aneurysmal subarachnoid hemorrhage: oxidation of unconjugated bilirubin by cytochrome oxidase.

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Aneurysmal subarachnoid hemorrhage is a stroke subtype with high rates of mortality and morbidity. Cerebral vasospasm can lead to ischemic injury or death and is a common complication of aneurysmal subarachnoid hemorrhage, usually occurring 3-9 days afterwards. The cause of vasospasm is not known.

[Non-invasive assessment of mitochondrial function in rat brain during and after hemorrhagic shock].

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Brain oxygen metabolism was studied noninvasively by the simultaneous measurement of hemoglobin (Hb) oxygenation, and cytochrome oxidase (aa3) redox state in the brain of a rat, using our near-infrared (NIR) transmission spectrophotometer. Redox state of cyt. aa3 was measured using a wavelength pair

[Bioenergetic processes in the cerebral cortex and diensephalon during hyperbaric oxygenation therapy of acute blood loss].

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It has been demonstrated in experiments on 134 cats that during acute blood loss (24 +/- 0.8 ml/kg), hyperbaric oxygen therapy (3039 hPa, 60 min) stimulates cytochrome oxidase, eliminates compensatory activation of mitochondrial creatine kinase and maintains the hyperactivity of cytoplasmic creatine

[Structural-metabolic characteristics of the myocardium in acute hemorrhage and hyperbaric oxygenation].

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Histochemical and pathomorphological changes in the myocardium in acute loss of blood and hyperbaric oxygenation were investigated in experiments on 130 white rats. It was established that acute loss of blood brought about an activation of phosphorylase, a decrease in the content of glycogen, an

Bioenergetics of different brain areas after experimental subarachnoid hemorrhage in rats.

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We studied energy metabolism after experimental subarachnoid hemorrhage in rats. Four different cerebral areas were tested: frontal cortex, occipital cortex, hippocampus, and brainstem. Vmax of the following enzymatic activities was evaluated: in the homogenate: hexokinase, phosphofructokinase, and

Pentobarbital fails to reduce cerebral oxygen consumption early after non-hemorrhagic closed head injury in rats.

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It is unknown whether barbiturates suppress cerebral oxygen metabolism after cerebral trauma as they do in normal individuals. We evaluated the influence of pentobarbital on cerebral oxygen handling of normal rats and rats subjected to non-hemorrhagic closed head injury (CHI). Oxygen delivery was

Detection of macrophages in atherosclerotic lesions with cytochrome oxidase.

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The anaerobic metabolism of the arterial wall allows macrophages to be demonstrated therein by the cytochrome oxidase histochemical method. Monocytes (macrophages) in human fatty streaks (WHO grade I) or fibrofatty (WHO grade II) human atherosclerotic lesions are normally confined to subendothelial

[Tissue respiratory enzymes in the rat liver in acute blood loss].

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An increase in activity of several dehydrogenases of tricarboxylic acid cycle (NADP-dependent malate dehydrogenase, alpha-ketoglutarate dehydrogenase) was observed in rat liver tissue under conditions of acute hemorrhage. The enzymatic activity was slightly higher in the group of animals with

[The state of energy metabolism in the rat liver after a single acute hemorrhage].

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A system of adenine nucleotides and redox state of liver cells as well as activities of dehydrogenases of the tricarbonic acid cycle and of cytochrome oxidase in liver cell homogenates were not altered after an acute single hemorrhage in rats even though the process run into the step of circulation

[Mitochondrial oxidation in the rat liver during acute blood loss].

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Acute hemorrhage was accompanied by impairments in electron transport and energy functions of rabbit liver mitochondria as well as by a decrease in activity of multienzyme systems responsible for electron transfer via redox chain. The impairments observed correlated distinctly with the rate of

Subarachnoid hemorrhage induces dynamic changes in regional cerebral metabolism in rats.

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Following a subarachnoid hemorrhage (SAH), adult rats exhibit dynamic regional changes in cerebral glucose metabolism characterized by an increase in metabolic rates and a subsequent upregulation of cytochrome oxidase (CO). We evaluated both local cerebral metabolic rates for glucose (ICMRglc:

Experimental isobaric subarachnoid hemorrhage: regional mitochondrial function during the acute and late phase.

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Patients treated for aneurysmal subarachnoid hemorrhage show, in the long-term follow up, an elevated rate of cognitive disturbances that are mainly related to the impact of the initial bleeding: the neurotoxic effects of blood deposition in subarachnoidal spaces may result in a diffuse
Specimens described as Rhadinorhynchus niloticus Meyer, 1932 (Rhadinorhynchidae) from two male specimens collected from Heterotis niloticus (Cuvier) in the Egyptian Nile were later redescribed in the genus Tenuisentis Van Cleave, 1936 (Tenuisentidae) based on 12 specimens collected from the same

Ischemic vasoconstriction and tissue energy metabolism during global cerebral ischemia in gerbils.

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Vasoconstriction is known to occur in cerebral arterioles during ischemia and considered to be distinct from vasospasm seen after subarachnoid hemorrhage. To elucidate the mechanism and functional significance underlying ischemic vasoconstriction, we investigated the relationship between arteriolar
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