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Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Local cerebral ischemia was produced in rats by internal carotid artery injection of 35 mu carbon microspheres, and brain norepinephrine (NE), dopamine, and cyclic adenosine 3, 5-monophosphate (cAMP) were measured in embolized and intact hemispheres at intervals up to four hours. Sham-operated animals were controls. There was an instantaneous increase of cAMP. Norepinephrine was reduced within two minutes after embolization and remained low for four hours. Dopamine increased by five minutes after embolization and returned to normal after four hours. Results were qualitatively similar, but less, in the nonembolized hemisphere. Accumulation of cAMP is thought to be due to a direct effect of ischemic hypoxia and may be the initiating factor in increased glycolysis that occurs in ischemia. Decrease in NE may be secondary to its generalized release from presynaptic terminals throughout the brain and could be a factor in cortical vasocontriction that follows embolization. Dopamine changes are a reflection of alterations in energy metabolism.
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PMID:Catecholamines in experimental brain ischemia. 23 32

Cerebral ischemia was induced in normothermic, artificially ventilated rats, anesthetized with 70% N2O or 150 mg/kg of phenobarbitone, by bilateral occlusion of the common carotid arteries and by simultaneous depression of the mean arterial blood pressure to 50 mm Hg. The levels of tyrosine, dopamine (DA), noradrenaline (NA), tryptophan, 5-hydroxytryptamine (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) were measured after 15 min of ischemia as well as after 30 min of recirculation. In separate experiments (70% N2O) the rate of accumulation of DOPA and 5-hydroxytryptophan (5-HTP) was determined in three different brain regions (striatum, limbic forebrain and hemispheres) during recirculation. During ischemia, the monoamine pattern was unaffected. Following recirculation, increases in DA, 5-HIAA, tyrosine and tryptophan were found irrespective of the type of anesthesia used. Pronounced postischemic decreases in NA and 5-HT were observed in animals anesthetized with nitrous oxide but not in those given phenobarbitone. During recirculation the rate of tyrosine hydroxylation increased in all three brain regions while tryptophan hydroxylation was reduced. It is tentatively concluded that following transient, global cerebral ischemia, neuronal activity is low or eliminated in dopaminergic and serotoninergic neurons and high in noradrenergic neurons.
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PMID:Influence of transient ischemia on monoamine metabolism in the rat brain during nitrous oxide and phenobarbitone anaesthesia. 30 81

Time-compressed Fourier analysis of the electroencephalogram has proven to be a useful analytical procedure during anesthesia and surgery which simplifies data interpretation by presenting the EEG in a time-compressed frequency domain rather than the conventional time domain. This method of data analysis graphically accentuates the electroencephalographic correlates of ischemia-induced cerebral dysfunction and other cerebral oxygen consumption abnormalities. The ability to accentuate trends in frequency and power is derived from sequential plotting of spectra to produce a graph with three dimensional axes of frequency, time, and power. In carotid endarterectomies the system has proven more useful than the conventional EEG in assessing the need for a vascular shunt to maintain internal carotid flow during endarterectomy. In open-heart surgery time-compressed EEG spectral analysis has allowed early recognition of cerebral ischemia resulting from arterial hypotension and venous hypertension. Five cases are presented which demonstrate the ability of our system to reflect developing cerebral ischemia.
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PMID:Monitoring of cerebral perfusion during anesthesia by time-compressed Fourier analysis of the electroencephalogram. 32 37

A randomized study was carried out to determine if the administration of reserpine and kanamycin to lower the concentration of vasoactive biogenic monoamines would reduce the incidence of cerebral vascular ischemic complications and death following the rupture of intracranial aneurysms. Twenty-six treated and twenty-eight control (untreated) patients were studied. In the preoperative period, eight control (untreated) patients developed symptomatic cerebral ischemia as opposed to one treated patient. There was no correlation between the preoperative clinical findings of ischemia and angiographic evidence of vasospasm. In the post-operative period four control and one treated patient developed symptomatic cerebral ischemia; vasospasm, as demonstrated by cerebral angiography, paralleled these findings.
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PMID:Reduced incidence of cerebral ischemia following rupture of intracranial aneurysms. 37 49

Selective embolization of the internal carotid artery bifurcation (ICA bifurcation) was performed in monkeys (Macaca mulatta) to study acute regional cerebral ischemia in the middle cerebral artery (MCA) territory with minimum surgical intervention in the neck under sedated conditions. The anthropomorphic similarity in angio-anatomy of the carotid system of monkeys and the use of silastic spheres, as artificial emboli, of the critical diameter of 1.2 to 1.4 mm resulted in the overall success rate of 87% in localizing the site of embolization to the ICA bifurcation, producing ischemia in the whole middle cerebral artery territory. All the animals with ICA-bifurcation embolization had contralateral deep motor weakness and conjugate eye deviation with nystagmus toward the site of embolization. Simultaneous EEG recording showed flattening of the basic background activities over the affected MCA area and cerebral arteriograms showed definite retrograde filling of the proximally occluded MCA. Clinical recovery was observed in a few animals within two to five hours of embolization. Gross ischemic swelling in the affected MCA territory, particularly in the gray matter, became obvious in six of eight animals which were exposed to four to five hours of ischemia. The angio-anatomical study of the carotid system of this experimental animal as a background for this MCA stroke model confirmed the previous observations of other investigators that the extremely abundant leptomeningeal anastomoses would be one of the major factors leading to the variability in the clinicopathological pictures seen in the models of proximal MCA occlusion. In addition, the pre-parenchymal anastomoses in the base of brain between the medial striate arteries from the proximal anterior cerebral (ACA) and lateral lenticulostriate arteries from the MCA were observed and described as a possible functional collateral to the basal ganglia in case of proximal MCA occlusion.
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PMID:Experimental regional cerebral ischemia in the middle cerebral artery territory in primates. Part 1: Angio-anatomy and description of an experimental model with selective embolization of the internal carotid artery bifurcation. 40 41

The feline right cerebral hemisphere was subjected to regional (incomplete) ischemia after clipping the middle cerebral artery for 5, 10, 15, 30 or 60 min, respectively. After each ischemic episode, a 10-min recirculation period was allowed, following which the brain was fixed and processed for electron microscopy. The earliest alterations, detected in the cerebral cortex after 15 min, increased in severity with longer ischemic episodes and were distributed multifocally. There was: (a) marked neuronal mitochondrial matrical swelling and progressive condensation of cytoplasm and nucleoplasm; (b) cytoplasmic swelling of astrocytes with preservation of glial mitochondrial volume; (c) capillaries, oligodendrocytes, myelin sheaths and axis cylinders did not change significantly, even after the longest interval studied: 60 min. This type of tissue reaction appears to be common for those forms of cerebral ischemia, in which circulation is either sustained partially (via collateral arteries) or restored after a period of absolute ischemia. Under these conditions, as yet undefined permeability changes in cell membranes lead to pronounced volumetric alterations of cellular compartments. Although no softening is detectable by digital examination, we suggest that such a set of structural abnormalities constitutes encephalomalacia, or the earliest stage of a lesion which is designated infarction, once it reaches irreversibility.
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PMID:Cellular events during partial cerebral ischemia. I. Electron microscopy of feline cerebral cortex after middle-cerebral-artery occlusion. 41 52

Permanent, complete global cerebral ischemia was induced in cats by filling the cardiovascular system with a plasma substitute (37 degrees C). At variable intervals and up to 120 min thereafter, these feline brains were perfused with aldehydes and processed for electron microscopy. The resulting cellular alterations were homogeneous and uniform throughout the entire brain; they included early chromatin clumping, gradually increasing electron lucency of the cell sap, distention of endoplasmic reticulum and Golgi cisternae, transient mitochondrial condensation followed by swelling and appearance of flocculent densities, and dispersion of ribosomal rosettes. The marked contrast between the structural alterations in permanent, complete ischemia and incomplete cerebral ischemia, suggest differences in their pathogenesis. A basic determinant factor of the structural changes appears to be the volume of flow (serum, plasma, other) which is available at the time of the injury. This analysis of global cerebral ischemia provides some insight on the nature of cellular changes occurring shortly after somatic death.
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PMID:The ultrastructure of "brain death". II. Electron microscopy of feline cortex after complete ischemia. 41 53

The pathophysiology of post-cardiac arrest brain damage is not well understood. Many of the model systems presently used to study global ischemia have serious limitations. A new model system for total cerebral ischemia (TCI), using aortic and inferior vena caval occlusion balloons, is described. This model system produces verifiable TCI and avoids surgical invasion of the thorax or the use of vasoactive drugs. It does not impede cerebral venous return and protects the cardiopulmonary system from damage. This model system can be used to study the efficacy of various therapeutic interventions following a standardized CNS global ischemic insult.
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PMID:Total cerebral ischemia: a new model system for the study of post-cardiac arrest brain damage. 43 99

Cerebral infarction was produced in rats by a combination of transient unilateral common carotid artery occlusion and systemic hypoxia. Horseradish peroxidase (HRP) and Evans blue were given 5 minutes prior to sacrifice to assess the integrity of the blood-brain barrier (BBB) at 1 minute, 30 minutes, and 2 hours following the ischemic insult. There was immediate permeability to HRP in the early (1 minute and 30 minutes) post-ischemic period, whereas, Evans blue was not seen until the late (1.5 to 2 hours) post-ischemic period. Ultrastructural examination showed two routes of barrier permeability to HRP. In the early post-ischemic period, HRP was transported by pinocytosis through endothelial cells in areas of brain containing ischemic neurons. In the late post-ischemic period, HRP diffusely leaked into the brain through the necrotic walls of vessels in areas of infarction. In contrast to previous reports, these results show that the BBB becomes permeable immediately following hypoxia-ischemia. In addition, this study shows that BBB permeability to HRP during cerebral ischemia occurs through two mechanisms: an active, energy-requiring permeability through enhanced pinocytosis within endothelial cells and a passive leakage of protein tracers through necrotic vessel walls.
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PMID:Early and late mechanisms of increased vascular permeability following experimental cerebral infarction. 43 63

The neuropathological consequences of sever diffuse cerebral ischemia were investigated in an animal model in which postischemic alterations of regional brain blood flow and energy metabolism had been previously characterized. Pentobarbital-anesthetized cats received either 15 or 30 minutes of ischemia produced by basilar artery and bilateral carotid artery occlusions plus mild hypotension; this was followed by 60 to 90 minutes of normotensive recirculation. The brains were perfusion-fixed for light microscopy. Both insult durations resulted in unequivocal ischemic cell change affecting neurons of the cerebral neocortex, striatum, thalamus, and hippocampus and portions of the rostral brainstem. Animals with 30 minutes of prior ischemia differed from those with 15 minutes of ischemia in showing a more apparent regional accentuation of ischemic change in the parasagittal cortical gyri--the sites of previously documented focal postischemic heterogeneities of blood flow and metabolism. In other respects, however, the overall distribution and spectrum of severity of the ischemic alterations were similar for the two insult durations. These data support the view that significant permanent neuronal injury may result from a period of cerebral ischemia as brief as 15 minutes.
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PMID:Diffuse cerebral ischemia in the cat: III. Neuropathological sequelae of severe ischemia. 44 69


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