Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To assess the effect of supratentorial cerebral ischemia on infratentorial brain function, changes in regional cerebellar blood flow (rCeBF), after right carotid occlusion for 4 hours, were studied in 30 mongolian gerbils. The regional cerebral blood flow (rCBF) in the occluded cerebral hemisphere and rCeBF in both cerebellar hemispheres were measured simultaneously by hydrogen clearance methods. Before carotid occlusion, rCBF was 0.44 +/- 0.07 ml/g brain/min, and rCeBF in the left and right cerebellar hemispheres was 0.37 +/- 0.09 and 0.40 +/- 0.09 ml/g brain/min, respectively. After carotid occlusion, rCBF decreased in all animals showing levels of above 0.20 ml/g brain/min in 14 (group A), between 0.10 and 0.19 ml/g brain/min in 7 (group B) and below 0.10 ml/g brain/min in 9 (group C). rCeBF exhibited no changes in group A and a mild reduction in group B after carotid occlusion. In group C, rCeBF was significantly reduced 30 min after carotid occlusion in the left cerebellar hemisphere followed subsequently by bilateral reduction. In groups B and C, supratentorial brain edema was observed 4 hours after occlusion, but the degree of edema was moderate. The results of the present study suggest that depression of infratentorial brain function may occur after supratentorial local cerebral ischemia, presumably due to diaschisis.
 ...
PMID:Transtentorial diaschisis: reduction of cerebellar blood flow caused by supratentorial local cerebral ischemia in the gerbil. 683 46

Central nervous system infections may be complicated by development of severe brain edema, which can be a significant factor in mortality and morbidity. Increased intracranial pressure can cause additional damage to the central nervous system by impairment of cerebral blood flow, which is dependent on cerebral perfusion pressure. A reduction of cerebral perfusion pressure, caused by elevation of intracranial pressure, may cause cerebral ischemia. We studied cerebral perfusion pressure in 17 patients, ages 45 days to 11 years, with severe central nervous system infections and who were in deep coma. Meningitis was diagnosed in 64.7%, and encephalitis in 29.4%. The patients who survived (64.7%) did not differ significantly from those who died (36.5%) in severity of disease and maximal intracranial pressure during the course of the illness. A striking difference in minimal cerebral perfusion pressure recorded was found between survivors and nonsurvivors: all patients with minimal cerebral perfusion pressure greater than 30 mm Hg survived, whereas those with lower pressure died. In survivors, cerebral perfusion pressure could be maintained adequately by reduction of intracranial pressure, but nonsurvivors developed noncompliance of brain tissue, and cerebral perfusion pressure could not be maintained at levels that ensure adequate cerebral blood flow, resulting in cerebral ischemia and death. Continuous monitoring of mean arterial blood pressure and intracranial pressure in children with severe central nervous system infections will enable rapid diagnosis and initiation of treatment when cerebral perfusion pressure is reduced to critical levels. Such treatment might improve the prognosis.
 ...
PMID:Cerebral perfusion pressure in central nervous system infections of infancy and childhood. 686 94

The purpose of this study is to clarify the usefulness and the limitations of the dopamine induced hypertension therapy (DIH) in the treatment of symptomatic vasospasm secondary to aneurysmal rupture. Twelve patients suffering from ischemic complications of vasospasm were treated with DIH and large quantities of intravascular fluids. All underwent cerebral angiography and CT scan in order to ascertain if their neurological deteriorations were due to vasospasm. In 9 cases, the levels of consciousness and neurological state were improved within a few hours after DIH started. It suggests that their ischemic symptoms were dependent on their systemic blood pressure. In one case, whose vasospasm was extensive and diffuse, DIH was life-saving, however the patient remained bedridden. In 2 cases, vasospasm was too intense for DIH to prevent continued neurological deteriorations. There seems to be a correlation between the effect of DIH and the angiographic grade of vasospasm (Table 1). The ultimate results of these 12 cases were compared with those of 46 cases which suffered from symptomatic vasospasm but were not treated with DIH (Table 3). There was no significant difference between the two groups. One died of severe brain edema, which may have been aggravated by DIH. In such a case where diffuse brain edema and breakdown of blood-brain barrier are observed on CT scan, DIH can be hazardous. However, in a case where CT scan before or during the therapy shows a localized low density area of infarction, DIH can be beneficial by preventing the progression of cerebral ischemia, in spite of a possible risk of bringing about hemorrhagic infarction. Our conclusions are as follows: 1) DIH is useful in many cases involving significant vasospasm. 2) DIH is less useful in such a case whose angiogram shows extensive vasospasm throughout the internal carotid and vertebro-basilar systems, and should be performed carefully in coordination with measures to reduce intracranial pressure. DIH is expected to protect the brain tissue from ischemia by increasing blood flow through the arteries of vasospasm and collateral circulation, but should not dilate the histologically changed arteries. Further clinical studies including cerebral blood flow measurements are necessary to define precisely the effectiveness, the indication and contraindication, and the mechanism of action of DIH.
 ...
PMID:[Evaluation of the dopamine induced hypertension therapy for vasospasm (author's transl)]. 709 70

In 30 adult cats, anesthetized with nitrous oxide and halothane, the middle cerebral artery was occluded using a transorbital approach. Extracellular volume changes were assessed by recording cortical impedance, and correlated with blood flow, tissue osmolality, and water and electrolyte content of brain tissue. Following middle cerebral artery occlusion, cortical impedance, after a free interval of about 1 min, sharply increased and after 30 to 60 min gradually stabilized between 180 and 200% of control. Calculated extracellular fluid volume decreased from 23.8 +/- 1.2 to 1.3 +/- 1.0% after 1 h and to 12.5 +/- 1.0% after 2 h of ischemia. Shortly after middle cerebral artery occlusion, extracellular volume shifts correlated with blood flow over a range from 3 to 50 ml/100 g/min. Two hours later, a threshold-like dependency existed: below 25 ml/100 g/min extracellular space was reduced to about 50% of control; above 32 ml/100 g/min extracellular space was normal. Non-threshold correlations existed between extracellular space, tissue osmolality, and the electroencephalogram. Final water content of brain tissue correlated with the size of the extracellular space after 15 min, but ont after 2 h of ischemia. This indicates that the narrowing of the extracellular compartment and ischemic brain edema are relatively independent consequences of cerebral ischemia.
 ...
PMID:Cortical impedance and extracellular volume changes following middle cerebral artery occlusion in cats. 714 10

The authors describe an experimental model of transient (15 min). unilateral, cerebral ischemia followed by 60 min of reperfusion in anesthetized rats. Zones of non perfusion are recorded and referred to as the "no-reflow phenomenon". The authors believe that vascular changes which interfere with postischemic reperfusion are due to ischemia-induced swelling of perivascular glia. The effects of the intracarotid injection of dexamethasone, furosemide and escina are evaluated in the attempt to show the importance of brain edema in ischemic cerebral damage.
 ...
PMID:Experimental cerebral "no-reflow phenomenon". 732 37

Brain oedema is an important factor which compromises maintenance of the cerebral blood flow. Conversely, primary blood flow disturbances are leading to brain oedema. The mechanisms underlying blood flow impairment by brain oedema are associated with an increased regional tissue pressure in proportion to the degree of water accumulation in the parenchyma. The release of vasoactive mediator compounds might be considered in addition. Primary disturbances of the cerebral blood flow, such as focal or global cerebral ischaemia are leading to an increased cerebral water content. A decrease of the cerebral blood flow to ca. 40% of normal or below has been found to result in the development of brain oedema. This flow threshold is in the neighbourhood of the ischaemic flow level causing irreversible tissue damage. Whereas in focal ischaemia oedema formation is a function of the severity of the flow decrease, it is a pathophysiological hallmark of early postischaemic recirculation in global cerebral ischaemia. Nevertheless, during complete interruption of cerebral blood flow translocation of interstitial fluid into the intracellular compartment occurs as manifestation of ischaemic cell swelling. Cell swelling under these conditions may, however, not necessarily indicate cell damage, but more likely a compensatory response attributable to the uptake of excitotoxic transmitters such as glutamate, and of K(+)-ions which are excessively released at the onset of ischaemia into the extracellular space. Purpose of the swelling process, thus, is clearance of extracellular fluid from this material to re-establish homeostasis.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Relationship of cerebral blood flow disturbances with brain oedema formation. 750 76

There has been considerable interest in the use of synthetic hydroxyethyl starch macromolecules (e.g., pentastarch, a colloid used for intravascular fluid replacement) to reduce microvascular permeability and reperfusion injury after cerebral ischemia. A recent report found that hemodilution with pentastarch reduced brain injury and cerebral edema after temporary focal ischemia. We compared the effects of pentastarch versus 0.9% saline on brain edema after reperfusion in a model of temporary global ischemia in halothane-anesthetized rabbits. To ensure the validity of our model, we studied an additional group of animals in which we deliberately raised plasma osmolality with hypertonic saline (1.5%) in the expectation of finding a decreased brain water content at the conclusion of the experiment. Animals were hemodiluted to a hematocrit of 20% with normal saline (control group) (n = 9), pentastarch (n = 7), or hypertonic saline (n = 5). After hemodilution, the animals underwent a 25-min period of global cerebral ischemia, followed by 180 min of reperfusion. The animals were then killed and brain water content was assessed by microgravimetry and by the wet-dry weight method. As anticipated, colloid osmotic pressure was maintained in the pentastarch group, and plasma osmolality became significantly increased in the hypertonic saline group. There were no intergroup differences at any time for central venous pressure, mean arterial pressure, intracranial pressure, or PaCO2. Brain water content was significantly decreased in the hypertonic saline group. No difference in brain water content was detected between the control group and the pentastarch group.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Global cerebral ischemia: effects of pentastarch after reperfusion. 754 34

Ischemic brain edema promotes focal cerebral ischemia by increasing intracranial pressure and thereby reducing perfusion pressure, obstructing capillaries and prolonging transport routes within ischemic tissue. There is clinical and experimental evidence that osmotic agents counteract these mechanisms. Moreover, glycerol may act as a free radical scavenger, antioxidant, and activator of plasma prostaglandin (PGI2), resulting in vasodilation. Improvements in ischemic brain energy metabolism after glycerol administration has also been postulated. Results of clinical trials on glycerol treatment of acute ischemic stroke were not conclusive: some demonstrated improved survival in the acute stage, in others survivors benefited in terms of neurological status and/or daily living activities. Other trials did not reveal any superiority of glycerol treatment over placebo. Glycerol is given intravenously as a 10% solution or orally. By the oral route higher intravascular glycerol concentration can be achieved with smaller quantities of fluid. Possible side effects include elevation of blood glucose level with subsequent lactate acidosis in the ischemic brain, serum hyperosmolarity after long-term glycerol administration and--when given intravenously--volume overload in patients with congestive heart failure and hemolysis that may cause renal failure.
 ...
PMID:[Treatment of ischemic cerebral infarct with glycerine]. 756 70

Clinical and neuroradiological studies involving cerebral angiography were conducted in four patients with eclampsia. In three cases (case 1, 2 and 4), neurological focal signs, abnormal low density areas on cranial CT and T2 high intensity areas on cranial MRI disappeared within a month. But in one case (case 3), cerebral infarction occurred and right hemiparesis and aphasia persisted. Cerebral angiography in the acute phase demonstrated vasospasm in all cases and arterial occlusion in the middle cerebral artery due to vasospasm in case 3. Angiography demonstrated several types of spasms, including diffuse, peripheral and multi local. Furthermore, in some cases, diffuse vasospasms were recognized at the siphon and extracranial portions of the internal carotid artery. In one case (Case 4), segmental vasospasms were detected in the bilateral vertebral arteries. Three to four weeks later, follow-up cerebral angiography was performed in three cases. Cerebral vasospasms had partially or completely recovered. Subarachnoid hemorrhage (SAH) was excluded by lumbar puncture and neuroradiological findings in all cases. We concluded that eclampsia itself causes cerebral vasospasm and that the mechanism of vasospasm is different from that of SAH, since cerebral vasospasm occurred in the extracranial cerebral arteries. We suspected that cerebral vasospasm in eclampsia causes cerebral ischemia, which leads to cytotoxic edema and dysfunction of the blood-brain barrier (BBB) and cerebral autoregulation. With this background, brain edema, especially vasogenic edema, may easily occur and clinical symptoms of eclampsia may appear when the blood pressure rapidly increases.
 ...
PMID:[Clinical and neuroradiological studies of eclampsia--cerebral vasospasm and relation to the brain edema]. 761 60

Na(+)K(+)-ATPase activity, water content, and Na+/K+ concentrations in the parietal cortex were measured in untreated and phenytoin-treated rats following global cerebral ischemia. Inhibitory effects of phenytoin treatment on brain edema and changes in Na(+)-K+ concentration with ischemia or ischemia followed by recirculation of varying intervals were assessed. The cortical Na(+)-K(+)-ATPase activity increased in the phenytoin-treated group during and after ischemia. Based on these results, we conclude that phenytoin provides ischemic brain protection by activating cortical Na(+)-K(+)-ATPase activity and by reducing intracellular Na+ and water content.
 ...
PMID:Effect of phenytoin on cortical Na(+)-K(+)-ATPase activity in global ischemic rat brain. 762 69


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>