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Download Brain Ischemia by Eugene I. Gusev, Veronika I. Skvortsova PDF

By Eugene I. Gusev, Veronika I. Skvortsova

Ischemia is localized tissue anemia as a result of obstruction of the influx of arterial blood, hence mind ischemia is the situation the place inadequate blood is dropped at the mind. Many physiological procedures happening within the mind significantly rely on the country of its power metabolism. The nation of mind power metabolism in flip depends upon the supply of oxygen and glucose to the mind through the bloodstream. even though it includes merely 2% of the entire bodyweight, the human mind consumes 20-25% of the oxygen and as much as 70% of the unfastened glucose taken in through the physique. The mind respires extra intensively than the other organ of the physique. The depth of oxygen intake by means of cortical mind tissue a lot exceeds the calls for of alternative tissues (5.43 mmol 02/g in step with h as opposed to 3.06 and 4.02 mmol for center at leisure and intensively operating, respectively, 2.4 mmol for kidneys, and 1.8 mmol for liver). Oxidative phosphorylation in mitochondria generates ninety five% of the adenosine triphosphate (ATP) that's shaped within the mind. therefore, it truly is transparent why insufficiency of oxygen supply to mind cells adversely impacts mind functionality. Glucose is the most energy-providing substrate within the mind. the elemental pathway of its metabolism in neural tissue is cardio glycolysis.

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Moscow, pp. 5-44 (in Russian). 25. Lukyanova, L. , 1991, Advances in Science and Technology. Pharmacology and Therapeutic Agents. Moscow, 27: 5-25 (in Russian). 26. Lukjyanova, L. , 1996, In Adaptation Biology and Medicine (Shanina, B. , Ganguly, N. ) New Delhi. I: 261-279 (in Russian). 27. Lukyanova, L. , 1997, Bull Exp Bioi Med. 9: 244-254 (in Russian). 28. Lukyanova, L. , Balmukhanov, B. , Ugolev, A. , 1982, In Oxygen-Dependent Events in Cell and Cellular Functions. 30 I. 29. Lukyanova, L. , Chemobayeva, G.

This opens ci+ channels allowing Ca 2+ to enter the postsynaptic cell. Under ischemic conditions, this process becomes excessive-the "glutamate-calcium cascade". Fast reactions of the glutamate-calcium cascade underlie the formation of a focal ischemic necrotic lesion. These reactions develop in the first minutes and hours after a vascular event and are the borders of the therapeutic window period [32, 144, 145, 166, 167]. 1). 1. The induction stage: energy-dependent ion pump failure and glutamate excitotoxicity Decrease in ATP content in the ischemized brain area and compensatory activation of anaerobic glycolysis in response to hypoxia cause inorganic phosphate content as well as lactate production and H' generation to increase.

After an hour, one can observe in neurons a heterochromatin fraction, enlargement of endoplasmic reticulum, and vacuolization and swelling of the internal mitochondrial matrix [22, 24, 30). These potentially reversible changes last for approximately 6 h. Ten to twelve hours later in the ischemic core one can observe features of irreversible cell damage such as destruction of cytosolic and nuclear membranes and deposition of calcium-rich salts in the internal mitochondrial membrane [22, 24], whereas the reversible changes in the penumbra do last longer.

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