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Query: UMLS:C0917798 (cerebral ischemia)
 17,036 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

The authors have assessed the effects of subacute traumatic brain edema (BE) on cerebral circulation and metabolism, and on clinical outcome. Fifty-five severely injured, comatose, young patients who survived for more than 24 hours were studied on 78 occasions within 30 days of injury. After hematomas had been surgically evacuated, BE was diagnosed by radiological evidence of brain swelling, demonstrated by cerebral angiograms and ventriculograms. At identical levels of carbon dioxide pressure, intracranial pressure was significantly elevated in the Edema Group to twice the value in the No Edema Group (27.1 vs 14.1 torr). There were, however, no significant differences in cerebral perfusion pressure cerebral blood flow, resistance to blood flow, cerebral metabolic oxygen rate, ventricular cerebrospinal fluid acid-base, lactate, K+ or Na+ concentrations, or in clinical outcome. It is concluded that this type of subacute traumatic BE, which is significantly associated with surgical lesions, is not of major hemodynamic or clinical significance in intensively treated patients, and does not cause cerebral ischemia. Patient outcome is determined more by the severity of the initial diffuse cortical and subcortical injury than by the presence or absence of subacute BE.
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PMID:Cerebral circulation after head injury. Part 2: The effects of traumatic brain edema. 94 15

Controlled cerebral ischemia was produced in rabbits by bilateral occlusion of the common carotid arteries and restriction of collateral blood flow by a decrease of the systemic arterial pressure to a desirable level (by hemorrhage into a pressurized reservior system). The following circulatory parameters were simultaneously monitored: systemic arterial pressure (SAP), pressure in the circle of Willis (Pcw), systemic venous pressure (SVP), and pressure in the sagittal venous sinus of brain (Pvs). The cerebral blood flow (CBF) was measured by means of the H2-clearance method, and the brain volume (BrV) changes were evaluated with a mechanical system of the sterotaxic device. It has been concluded that the pre-edematous changes in the brain tissue arise during deep ischemis but an important factor in the brain edema development is the recovery of the CBF with and increase of the intravascular pressure closely related to the brain blood volume augmentation. The latter may be pronouced because of diminution of the blood outflow from the brain when the SVP is increased. The compensation for the BrV increase (caused either by brain blood volume augmentation or by brain edema) is obtained by Pcw decrease probably due to resistance rise in the internal carotid and vertebral arteries. The brain edema may be additionally compensated by an active decrease of the systemic arterial pressure.
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PMID:Mechanisms of postischemic brain edema: contribution of circulatory factors. 96 Jan 63

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

In the cerebral ischemic pathophysiologic mechanism, lactic acidosis is a important factor to exacerbate cerebral damage. Our research showed that the lactic level of cerebral cortex in rats increased rapidly after the focal cerebral ischemia or during blood reperfusion after cerebral ischemia, 26.99 +/- 5.89 and 28.63 +/- 5.08 mumol/g brain wight respectively, it exacerbated significantly brain edema and pathological damage. The lactic level decreased rapidly to treat with dichloroacetate (50 mg/kg body weight) after cerebral ischemia or during blood reperfusion, 14.11 +/- 2.06 and 13.23 +/- 1.71 mumol/g brain wight respectively, brain edema and pathology improved significantly. It suggested that dichloroacetate might across blood-brain barrier into the cerebral ischemic region and lowered lactic level, improved brain internal environment, relieved cerebral damage after focal cerebral ischemia or during blood reperfusion. It may improve the prognosis of patient with ischemic cerebral vascular disease to be treated with dichloroacetate early.
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PMID:[Treatment of experimental ischemic cerebral lactic acidosis in rats with dichloroacetate]. 130

Copper-zinc-superoxide dismutase (CuZn-SOD), a cytosolic antioxidant enzyme that is specific for scavenging superoxide radicals, is involved in neuroprotective mechanisms in brain injury following trauma and cerebral ischemia. Liposome-entrapped CuZn-SOD exhibit beneficial effects in vivo on cold-induced vasogenic edema and on blood-brain barrier disruption. The increased levels of edema and infarction following a focal cerebral ischemia also are decreased by the pretreatment of liposome-entrapped CuZn-SOD. The protective role of SOD on brain injury was further extended and confirmed in studies using transgenic mice overexpressing human CuZn-SOD. Our studies so far suggest that increased cerebral levels of SOD, either by means of external pharmacological application or by genetic manipulations, ameliorate brain edema and infarction induced by trauma and focal cerebral ischemia.
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PMID:Antioxidant-dependent amelioration of brain injury: role of CuZn-superoxide dismutase. 131 99

In addition to the important role of leukotrienes as mediators in allergy and inflammation, these compounds are also linked to pathophysiological events in the brain including cerebral ischemia, brain edema, and increased permeability of the blood-brain barrier in brain tumors. Although brain tumors have been shown to secrete leukotrienes, no studies to date have provided evidence for the tumor expression of genes encoding enzymes involved in leukotriene production. Therefore, the present study determined the abundance of the mRNA for arachidonate 5-lipoxygenase (5-LO; arachidonate:oxygen 5-oxidoreductase, EC 1.13.11.34), which is the rate-limiting enzyme in leukotriene synthesis, in a series of human brain tumors. Macrophage/monocyte infiltration of the tumor was estimated by measuring the abundance of the transcript for the 91-kDa glycoprotein phagocyte-specific oxidase (gp91-phox), which is the phagocyte-specific cytochrome b heavy chain. The present study shows that (i) the 5-LO transcript is expressed in normal bovine brain and in human brain tumors; (ii) the 5-LO gene in human brain tumors and in the dimethyl sulfoxide-induced promyelocytic human leukemic HL-60 cells is expressed as a multitranscript family (2.7, 3.1, 4.8, 6.4, 8.6 kilobases); and (iii) the abundance of 5-LO transcripts, the expression of the larger transcripts, and the 5-LO/gp91-phox ratio correlate with the tumor malignancy. Overall, the present study supports the hypothesis that the 5-LO gene product may play a role in human tumor-induced brain edemas and provides evidence for tumor-associated expression of high molecular weight 5-LO transcripts in human brain tumors.
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PMID:Differential expression of arachidonate 5-lipoxygenase transcripts in human brain tumors: evidence for the expression of a multitranscript family. 135 59

The effect of adrenalectomy has been investigated in a model of global cerebral ischemia. After bilateral carotid ligation the mortality rate was increased in adrenalectomized rats, and this effect was prevented by glucocorticoid pre-treatment. Adrenalectomy accelerated the appearance of the symptoms of cerebral ischemia, resulting in a moderate aggravation of brain edema and in a significant decrease in the concentration of high-energy phosphate esters. Our findings support the view that endogenous glucocorticoids may play a role in the amelioration of ischemic brain injuries in rats.
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PMID:Adrenalectomy aggravates ischemic brain edema in female Sprague-Dawley rats with carotid arteries ligated. 141 Apr 8

It is impossible to predict what compounds of pharmacological interest may be present in an unexamined species. The extinction of such species may result, therefore, in the loss of therapeutically significant compounds. The fact that science will never know what has been lost does not lessen the significance of the loss. A number of species are discussed to exemplify the potential loss. Ginkgo biloba is an ancient plant, apparently saved from a natural extinction by human intervention. From this tree, the ginkgolides have been isolated. These are potent inhibitors of platelet activating factor and hold promise in the treatment of cerebral ischemia and brain edema. Two species, the tree Taxus brevifolia and the leech Hirudo medicinalis, are threatened as a result of human activity. Both have recently yielded complex compounds of therapeutic importance. The antitumor agent, taxol, is obtained from T. brevifolia and the thrombin inhibitor, hirudin, is found in H. medicinalis. Catharanthus roseus, source of the anticancer agents vincristine and vinblastine, although not threatened, derives from a largely unexamined but severely stressed ecosystem of some 5000 plant species. In other examples, ethnobotanical knowledge of certain plants may be lost while the species survive, as exemplified by the suppression of the Aztec ethnobotany of Mesoamerica by the invading Spanish. Finally, the fallacy of the 'snail darter syndrome', where species may be viewed as too insignificant to worry about, is exposed by consideration of the pharmacological activities of a sea hare (a shell-less marine mollusc) and various leeches.
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PMID:The pharmacology of extinction. 145 1


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