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

A study was made of the effect of cervical sympathectomy (SE) on the time course in the content of prostaglandins (PG) (E + A) and F2 alpha under normoxia and circulatory hypoxia. The sympathectomized rats manifested a biphasic change in the content of PG (E + A). The content of PG (E + A) rose by days 1 and 7. It returned to normal by day 14 and increased again by day 40 after SE. The content of PG F2 alpha drastically increased 7 days after SE and then returned to normal. Brain ischemia induced by bilateral ligation of the common carotid arteries led to an increase in the content of PG (E + A) and in that of PGF2 alpha, in particular. Preliminary SE resulted in the absence of differences in the content of PG (E + A) caused by brain ischemia. It is assumed that PGF2 is largely implicated in the regulation of the tone of the bran vessels and in the regulation of metabolism during ischemia with disordered sympathetic control.
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PMID:[Dynamics of the change in the prostaglandin content of brain tissue in upper cervical sympathectomy and circulatory hypoxia]. 708 97

Two groups of changes in the cerebral substance were revealed by histological examinations of the central nervous system in a case of clinical death followed by respiratory resuscitation for 12 days. Changes of the 1st group consisted in foci of incomplete necrosis in the stage of organization in the cortex and dentate nuclei of the cerebellum, lower olives of the medulla, Zommer sector of the Ammon horn, and caudate nuclei. Their development is due to ischemia and circulatory hypoxia in the early resuscitation period. Changes of the 2nd group included acute disorders of microcirculation and extensive protein and carbohydrate dystrophy of nerve cells of the cortex and subcortical ganglia in the form of hyperchromatosis hydropic degeneration. "alzheimerization", accumulation of glycogen in the cytoplasm of neurons and astrocytes. The degenerative changes were combined with signs of gradual death of neurons and pseudolaminar losses in the cerebral cortex. Changes of the 2nd group may be classified as the so-called secondary nor delayed cerebral hypoxia in the development of which microcirculatory disorders are of importance. The observed morphological changes in the brain after clinical death and prolonged respiratory resuscitation represent morphological expression of "resuscitation-conditioned encephalopathy".
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PMID:[Morphology of "resuscitation-induced encephalopathy"]. 727 11

During short-term (3.7 and 15 min) circulatory hypoxia (ischemia) pronounced ultrastructural changes, having an obvious focal character, were observed in the rabbit cerebral cortex. In some regions, the extracellular space was widened; in the neurons, changes are seen both in the nucleus (appearance of polymorphic vacuoles and deep invaginations of nuclear envelope, aggregation of chromatin) and cytoplasmic organelles (mitochondrial swelling, swelling of profiles of endoplasmic reticulum, dislocation of ribosomes). Most striking reactions were observable in synapses - the number of synaptic vesicles was sharply reduced, its location in the axon terminal changed, the dense material associated with pre- and postsynaptic membranes was enlarged, mitochondria were swollen. The degree of the above alterations was proportional to the duration of ischemia.
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PMID:[Ultrastruct characteristics of neurons and synapses in the central cortex during circulatory hypoxia]. 738 56

Ischemia of the rat brain led to permanent increase in oxygen consumption, sharp phasic changes of oxydative phosphorylation, and fall of the P/O coefficient in the brain mitochodria which indicates a dissociation between respiration and phosphorylation. During the postischemic period all the parameters become normal. Oxygen consumption in the cardiac mitochondria is only enhanced in the early (15 min of circulatory hypoxia--CH) and late (72 hrs of CH) periods of CH. The oxydative phosphorylation is particularly low at 15 min and at 24-hr duration of CH. During the posthypoxic period the oxygen consumption is significantly enhanced but it drops lower than control level after 24-hr CH. The changes of oxydative phosphorylation occur in phases. The P/O coefficient is minimal in the posthypoxic period after the 15-min CH. Disturbances of oxydative metabolism seem lesser in the cardiac mitochondria. The changes occurring in the cardiac muscle during cerebral CH seem to underlie different signs of the cerebro-cardiac syndrome in brain pathology.
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PMID:[Heart and brain tissue mitochondrial respiration and oxidative phosphorylation during cerebral circulatory hypoxia and in the posthypoxic period]. 739 34

The aim of this study was to detect structural, spatial and quantitative changes of cellular elements of midbrain paranigral nucleus (PNN) and telencephalic anterior cingulate area (ACA) under different conditions of circulatory hypoxia. PNN anteriormedial part and ACA layers V-VI were examined in adult rats 7 days (n=4) after an occlusion of both common carotid arteries as well as in intact (1st control, n=4) and sham-operated animals (2nd control, n=4). In histological the sections, stained with Nissl cresyl violet, and using the methods of glial fibrillary acidic protein and an Ibal-protein detection, the proportions of unmodified, hypochromic, pyknomorphic neurons and ghost cells were determined as well as the numbers of astrocytes, oligodendrocytes, microgliocytes and endotheliocytes. Cell body area of neurons and gliocytes, and the distance between cell bodies and capillaries were measured, a gliocyte-neuronal index was calculated. It was found that brain cellular elements that survive different conditions of a circulatory hypoxia underwent a range of pathological changes. Neurons were in process of nuclear pyknosis, lysis and transformation into the ghost cells. The cells within the hypoxia nuclear zone were prone to death or pyknosis. The neurons located outside the area of hypoxia which were affected only by a humoral impact of reactions of the glutamate-calcium cascade, frequently underwent acute swelling. Microgliocyte reaction in the form of poorly expressed increase in their number and structural signs of activation was an early diffuse manifestation of a prosencephalic focal hypoxia. Endotheliocyte proliferation 7 days after of ischemic challenge was not associated with a chain of cascade reactions and was observed only in the hypoxia focus. Concentration of viable neurons and astrocytes near blood capillaries, as well as an increase in the number of satellite form gliocytes is an adaptation mechanism and a condition for the survival of cells during various types of brain exposure to ischemia.
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PMID:[Reactive changes of the rat brain cellular elements under different conditions of circulatory hypoxia]. 2402 Jan 78