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

The left cerebral hemisphere of Mongolian gerbils was used to elucidate the mechanisms of brain edema which develop during cerebral ischemia and after restoration of cerebral blood flow following temporary ischemia. Water content was measured by the tissue-drying method. Sodium and potssium ion concentration was measured by flame photometry. Passage of 131I-albumin (RISA) from blood to the cerebral parenchyma was measured on a gamma scintillation counter. Our findings indicate that pure cytotoxic edema develops during ischemia and during a short period after restoration of cerebral blood flow. Vasogenic edema, which is accelerated by the leakage of plasma constitutents from blood due to blood-brain barrier damage, developed after restoration of the cerebral blood flow. After less than 1 hr of ischemia, restoration of the cerebral blood flow drastically reduced the degree of brain edema. However, restoration of the cerebral blood flow greatly worsened the brain edema following more than 3 hr of ischemia.
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PMID:Brain edema during ischemia and after restoration of blood flow. Measurement of water, sodium, potassium content and plasma protein permeability. 50 96

Ischemic brain damage can be partially ameliorated by barbiturate therapy applied postinsult. Catabolism-induced brain hyperosmolality during ischemia may contribute to the development of brain edema after restoration of circulation. To determine changes in brain osmolality during ischemia and the effect of barbiturate anesthetics in altering its course, we measured whole and regional (cerebral cortex, diencephalon-midbrain, and cerebellum) brain osmolality for up to 2 hours after decapitation ischemia in unanesthetized and pentobarbital anesthetized rats. Normal (nonischemic) brain osmolality in pentobarbital anesthetized rats was 319 +/- 2 mOsm/1 (mean +/- SEM) and higher than in unanesthetized rats (307 +/- 6 mOsm/1). The rate of increase in whole brain osmolality was 60% slower in pentobarbital anesthetized rats in the first 60 minutes of ischemia and regional brain osmolality increased by a maximum of 32 mOsm/1 compared to 45 mOsm/1 in unanesthetized rats. The potential for edema based on percent change in brain osmolality as well as the rapidity of the change was greater in unanesthetized rats. The significance of the increase in brain osmolality with barbiturate anesthesia and its attenuation of the rate and magnitude of increase during ischemia is discussed.
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PMID:Rat brain osmolality during barbiturate anesthesia and global brain ischemia. 64 23

The pathological findings in four patients with courses characterized by acute coma and respiratory insufficiency occurring in obscure circumstances are presented. Carbon monoxide intoxication was excluded. After an early partial recovery from coma, the patients remained in a persistent vegetative state, with a tetrapyramidal syndrome. Pathologic changes consisted of infarction and demyelination of periventricular white matter, with associated necrotic foci in the basal ganglia in some cases. We propose that the prolonged hypoxia and ischemia produce a "no reflow" phenomenon causing brain edema (more pronounced in the white matter); this resulted in infarctions of white matter in the periventricular arterial end and border zones.
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PMID:Periventricular leukomalacia in adults. Clinicopathological study of four cases. 66 10

Analysing the data of electronomicroscopical studies on the dominant hemispheres of the cerebral cortex in 9 patients who died due to strokes, the authors consider the main types of pathological changes in the ultrastructure of capillaries that are of a diffuse generalizing character. They are the following: 1) dystrophy of the capillary wall with the accumulation in it of lysosomal inclusions, lipofuscin granules, with the disintegration of mitochondrias and disturbances of oxidation-reduction processes in the vessel tissues connected with it; 2) the growth and hyperplasia of the endothelium. These changes lead to dystrophic damages of neurons, the maintainance and loading of the course of the main pathological process. Hypoxia, as a result of local ischemia, has an important pathogenetical significance in the disturbances of brain circulation and leads to plasmorrhagia, brain edema and even greater affection of neurons.
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PMID:[Ultrastructure of cerebral cortex capillaries in stroke]. 89 17

Unilateral embolization of the brain was performed in cats by intracarotid injection of 10.5 million carbonized microspheres (15 +/- 5 mu). Intracranial pressure increased from 6.1 +/- 1.5 to 14 +/- 2.3 mm Hg within two minutes and continued to rise more slowly to 24 +/- 18.3 mm Hg within four hours. Embolization caused a nonhomogenous distribution of microflow, but initially had no effect on global cerebral blood flow, nor on cortical oxygen tension. Yet, a functional suppression of cortical electrical and metabolic activity occurred. The ipsilateral EEG flattened irreversibly after 15 seconds; the contralateral EEG was transiently suppressed shortly thereafter. Arteriovenous difference of oxygen fell from 10.5 +/- 0.7 to 5.3 +/- 0.6 vol%, and the arteriovenous difference of glucose fell from 11.7 +/- 3.9 to 2.6 +/- 2.1 mg/100 ml as a consequence of reduced oxygen and glucose extraction. Subsequently, severe vasogenic brain edema, secondary ischemia, and severe functional suppression developed between two and four hours.
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PMID:Cerebral microembolization. I. Pathophysiological studies. 91 Dec 25

The behavior of the BBB in cerebral ischemia was studied in symptom-positive Mongolian gerbils subjected to left common carotid artery occlusion using Evans Blue dye as indicator of BBB injury. The BBB damage was demonstrable grossly by the presence of areas of blue discoloration, and microscopically by the presence of a bright red fluorescent tracer, localized mostly in the neurons. The survey of various groups of animals revealed a direct relationship between the incidence and time of appearance of the BBB lesions and the duration of the ischemic occlusion. This relationship can be interpreted as another example of the previously described "maturation" phenomenon. A relatively late occurrence of the BBB injury in cerebral ischemia, at the time when the affected brain tissue shows severe, edematous histopathologic changes indicates that the brain edema, as the main complication of ischemia, could be regarded as being primarily of the cytotoxic type.
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PMID:Experimental cerebral ischemia in Mongolian gerbils III. Behaviour of the blood-brain barrier. 125 83

With the animal model of cerebral ischemia and reperfusion, we conducted experiments on such model to study the effects of Ligustrazine(LZ) and Salvia Miltirrhizae(SM). The results obtained are as follows: (1) The ischemic brain showed hyperperfusion (congestion period) after 10 min reperfusion following 50 min of ischemia, and then entered a delayed hypoperfusion period after 60 minutes reperfusion and afterward the hypoperfusion was remained till the end of 120 min reperfusion. (2) Following 50 min of ischemic insult, ATP and glucose contents in brain tissue were almost depleted and much of lactate accumulated. Although rapid recovery of energy metabolism occurred within 60 min of reperfusion, a secondary deterioration emerged at 120 min of reperfusion. (3) Apparent brain edema occurred after cerebral ischemia and its further development was observed at the early stage of reperfusion owing to congestive response. Despite the degree of brain edema alleviated obviously after 60 min of reperfusion, the condition become worse at 120 min of reperfusion, which was accompanied by secondary metabolic deterioration. (4) Experimental results showed that LZ and SM could significantly elevate rCBF during the delayed hypoperfusion period, and limit the development of secondary deterioration in energy metabolism and brain edema after 120 min of reperfusion. (5) Notably, LZ and SM had no significant effect on MABP when these two Chinese drugs manifested their therapeutic actions in the animal model of cerebral ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Changes in gerbil brain tissue following cerebral ischemia and postischemic reperfusion and studies of the effects of the Chinese drugs]. 130 98

Hypertension causes vascular changes of essentially three types: structurally adaptative changes, degenerative alterations unrelated to atherosclerosis, and atherosclerosis. Structural changes result in an increased peripheral resistance, even in the relaxed vascular bed, and a reduced collateral capacity, thus predisposing to ischemia distal to an arterial stenosis/occlusion and to "watershed" infarcts in connection with a drop in blood pressure. Degenerative changes in the small intracerebral arteries can lead to plasma extravasation and focal brain edema, lacunar infarcts, and intracerebral hemorrhages. Hypertension also predisposes to saccular aneurysms and subarachnoid hemorrhages. Finally, atherosclerotic changes including stenoses or occlusions of predominantly extracranial and pial arteries give rise to transitory ischemic attacks and brain infarcts by artery-to-artery embolism or distal hemodynamic perfusion insufficiency.
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PMID:Vascular mechanisms in hypertensive cerebrovascular disease. 137 27

To determine the contribution of interleukin 1 (IL-1) on ischemic brain edema formation, the effect of recombinant human interleukin 1 beta (rhIL-1 beta), or zinc protoporphyrin (ZnPP) as an IL-1 blocker, on brain edema was studied in rats. The animals were subjected to 60 min of ischemia in a middle cerebral artery occlusion model. Immediately after reperfusion, rhIL-1 beta at a dose of 10 ng/2 microliters, or ZnPP at doses of 1 and 10 micrograms/2 microliters were topically applied into lateral cerebroventricle. In rhIL-1 beta-treated rats, ischemic brain edema formation was significantly increased in the dorsal and ventral areas of the caudate putamen 24 h after reperfusion, compared to that of vehicle-treated control rats. Furthermore, in ZnPP-treated rats, brain edema was decreased in both caudate-putamen areas. This suggests that IL-1 plays an important role in pathogenesis for post-ischemic brain edema.
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PMID:Possible involvement of interleukin-1 in ischemic brain edema formation. 140 16

Eyes with macular edema caused by retinal branch vein occlusion underwent masked evaluation of fluorescein angiography to determine complete macular perfusion vs incomplete macular perfusion (capillary dropout, ischemia). Cases evaluated as incomplete macular perfusion showed a greater frequency of improvement (91%) in visual acuity than did perfused cases (29%) (P = .003) after a mean follow-up of 39 months. Ischemic edema is often transient, and is associated with a good outcome in visual acuity (median final visual acuity was 20/30). Perfused macular edema has a poorer prognosis for visual acuity (median final visual acuity was 20/80). Macular ischemia is usually associated with a broken foveal capillary ring. Previous animal research on ischemic brain edema has shown that following brain ischemia, an intracellular and an extracellular hypertonic environment lead to intracellular and extracellular edema (cytotoxic edema), which is often followed by vascular protein leakage (vasogenic edema). A similar occurrence in ischemic retina could explain the transient edema reported herein, with good outcome in visual acuity following the spontaneous resolution of edema.
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PMID:Ischemic macular edema. Recognition and favorable natural history in branch vein occlusion. 141 44


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