Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.9.3.1 (cytochrome oxidase)
 8,822 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a clinically applicable cat stroke model, 16 purpose-bred adult animals were used to evaluate the beneficial effects of two treatment regimens: isovolemic hemodilution with either a perfluorocarbon emulsion or dextran 40 (a glucose polymer). Animals that received these treatment regimens were then compared with a control group of untreated animals. Focal cerebral infarctions were produced by transorbital ligation of the left middle cerebral artery. The randomly allocated treatment arms of the study were instituted 3 hours after ligation of the middle cerebral artery, thereby simulating a human clinical situation. In vivo mitochondrial metabolic activity of the peri-infarct cerebral tissue was continually assessed by means of a multiwavelength near-infrared spectrophotometer. This allowed measurement of cellular oxygenation at the cytochrome aa3 level, the terminal member of the cytochrome chain. Sequential proton-based magnetic resonance imaging was used to measure intracerebral water in vivo. Cardiac output, oxygen consumption/delivery, chemical, histologic, and rheologic parameters were also assessed. The data collected were analyzed by group means and standard statistical analyses, which revealed that the group treated with the perfluorocarbon emulsion had both less brain edema in the early post-infarct period (p less than 0.05), as well as a higher level of oxidation of cytochrome aa3 (p less than or equal to 0.025). This evidence supports the premise that isovolemic hemodilution with an oxygen-carrying hemodiluent may be beneficial in the treatment of ischemic strokes.
 ...
PMID:Beneficial effects of isovolemic hemodilution using a perfluorocarbon emulsion in a stroke model. 171 44

Hyperglycemic, but not normoglycemic cats exposed to anoxia develop neurologic signs following reoxygenation including fasciculations, focal and tonic-clonic seizures and coma after a symptom-free period. These symptomatic hyperglycemic cats may develop brain edema and will show diffuse neuronal injury or brain infarction depending on length of survival. Brain mitochondria isolated from symptomatic but not asymptomatic cats have decreased ADP- and uncoupler-stimulated oxygen consumption rates. Since impaired respiration could result from altered electron transport chain function, we measured cytochrome c, b, and aa3 concentrations and the activities of the five electron transfer complexes in isolated brain mitochondria. In symptomatic cats marked alterations were present in particular in complex IV, cytochrome oxidase, with a 57% reduction in activity and a 45% reduction in prosthetic group (cytochrome aa3) concentrations. Less marked reductions in other segments of the chain included 27% and 41% decreases, respectively, in cytochrome c concentrations and in electron transfer complex II, succinate:ubiquinone oxidoreductase activity. Cytochrome b concentrations and complex I, II and V activities were unchanged. Small but significant decreases in cytochrome aa3 concentrations (18%) and cytochrome oxidase activity (20%) were also present in mitochondria from postanoxic hyperglycemic cats prior to appearance of neurologic signs. These results indicate that delayed decreases in the activities of specific electron transfer complexes are correlated with impaired mitochondrial respiration and neurologic deterioration in postanoxic hyperglycemic cats. However, it is presently unclear if these postanoxic brain mitochondrial alterations are primary or secondary events in the development of brain injury.
 ...
PMID:Delayed decreases in specific brain mitochondrial electron transfer complex activities and cytochrome concentrations following anoxia/ischemia. 208 31

Hydrocephalus induces interstitial brain edema, which causes neurological deficits, even if the intracranial pressure is maintained within the normal range, and the cerebral blood flow (CBF) does not decline to an ischemic level. The precise mechanisms underlying such edema-induced neuronal dysfunction remain unclear. In the present study, in an attempt to elucidate the metabolic derangements in brain tissue with interstitial edema, we evaluated the changes in CBF and oxidative/glucose metabolism using a rat model of kaolin-induced hydrocephalus. Hydrocephalus was produced in male Wistar rats by intrathecal injection of 0.1 ml aluminum silicate suspension (200 mg/ml) via the cisterna magna. CBF was determined by 14[C]-iodoantipyrine autoradiography. Oxidative metabolism was evaluated by cytochrome oxidase (CYO) histochemistry, and glucose metabolism by hexokinase (HK) histochemistry. CBF declined with the development of hydrocephalus, but did not reach an ischemic level. The CYO activity was diffusely depressed in both the cortex and hippocampus. The HK activity was preserved at the early stage of hydrocephalus. At the advanced stage, the HK activity was reduced in the hippocampal CA3 region first, and diffusely thereafter. In conclusion, interstitial brain edema impairs oxidative metabolism even at the early stage of hydrocephalus, and shifts the metabolism to anaerobic glycolysis despite a preserved CBF. Impairment of glucose metabolism was first observed in the CA3 region, suggesting that the CA3 is metabolically vulnerable, and CA3 dysfunction may contribute to the memory deficits seen in hydrocephalus.
 ...
PMID:Metabolic derangements in interstitial brain edema with preserved blood flow: selective vulnerability of the hippocampal CA3 region in rat hydrocephalus. 1475 3