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

The effect of ischemia-reperfusion on endothelium-dependent relaxations and reactivity of vascular smooth-muscle cells was studied in rings of basilar arteries obtained from six dogs exposed to 12 min of complete global cerebral ischemia followed by 100 min of reperfusion. Three sham-operated control dogs served as controls. Ischemia was induced either by an increase in intracranial pressure or by aortic occlusion. The rings were suspended for isometric tension recording in physiological salt solution. Ischemia-reperfusion did not affect endothelium-dependent relaxations to vasopressin and bradykinin. In rings without endothelium relaxations to sodium nitroprusside, molsidomine (SIN-1), and papaverine as well as contractions to 5-hydroxytryptamine and KCl were preserved. These results demonstrate that in large canine cerebral arteries, ischemia-reperfusion of these durations does not affect relaxations mediated by activation of endothelium or direct relaxations and contractions of vascular smooth-muscle cells.
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PMID:Ischemia-reperfusion does not affect reactivity of isolated canine basilar artery. 187 14

We tested the hypothesis that cerebral blood flow (CBF) reactivity to CO2 after global ischemia takes longer to recover in 1- to 2-wk-old piglets than in 6- to 10-mo-old pigs. All animals were sedated with ketamine and anesthetized with pentobarbital sodium. Cerebral ischemia was produced by sequentially tightening ligatures around the inferior vena cava and ascending aorta for 10 min. The microsphere-determined CBF response to hypercapnia (arterial PCO2 approximately 65 mmHg) was depressed at 60 min of reperfusion (9 +/- 6% of preischemia; means +/- SE) and remained depressed at 120 min (33 +/- 23% of preischemia, means +/- SE) in young pigs. In older pigs, the response was also depressed at 60 min of reperfusion (21 +/- 9% of preischemia) but was not depressed at 120 min. The pattern for recovery of hypercapnic reactivity was present in most brain regions except cerebellum, where CO2 reactivity returned to control in young animals by 120 min of reperfusion. The response to hypocapnia (arterial PCO2 approximately 25 mmHg) was also better preserved in older pigs. In older pigs recovery of CO2 reactivity during reperfusion paralleled recovery of cerebral O2 consumption over time. We conclude that older pigs have quicker return of CBF CO2 reactivity following transient global ischemia, which may be due to age-related differences in mechanisms of vascular reactivity.
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PMID:Age-related cerebrovascular reactivity to CO2 after cerebral ischemia in swine. 190 1

We tested the hypotheses that with the onset of cerebral ischemia, massive cellular sodium influx does not occur until adenosine triphosphate is fully depleted and that on reperfusion, neuronal sodium efflux does not occur until adenosine triphosphate is fully restored. We examined the temporal relationships among transcellular sodium, energy metabolism, and intracellular pH with sodium and phosphorus magnetic resonance spectroscopy in a new, hemodynamically stable, brain stem-sparing model of reversible, complete cerebral ischemia in eight anesthetized dogs. Inflation of a neck tourniquet after placement of glue at the tip of the basilar artery resulted in decreased blood flow to the cerebrum from 29 +/- 5 to 0.3 +/- 0.5 ml/min/100 g. Medullary blood flow was not significantly affected, and arterial blood pressure was unchanged. Sodium signal intensity decreased and did not lag behind the fall in adenosine triphosphate. After 12 minutes of ischemia, reperfusion resulted in a more rapid recovery of sodium intensity (12.4 +/- 4.8 minutes) than either adenosine triphosphate (16.5 +/- 3.7 minutes) or intracellular pH (38.9 +/- 1.8 minutes). Because intracellular sodium has a weaker signal than extracellular sodium, the decreased sodium intensity is interpreted as sodium influx and indicates that sodium influx does not require full depletion of adenosine triphosphate. Rapid recovery of sodium intensity during early reperfusion may represent sodium efflux, although increased plasma volume and sodium uptake from plasma may also contribute. If our interpretation of the sodium signal is correct, delayed recovery of adenosine triphosphate may be due to the utilization of adenosine triphosphate for the restoration of transcellular sodium gradient.
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PMID:Sodium, ATP, and intracellular pH transients during reversible complete ischemia of dog cerebrum. 200 87

Impairment of cerebral autoregulation and development of hyponatraemia are both implicated in the pathogenesis of delayed cerebral ischaemia and infarction following subarachnoid haemorrhage (SAH) but the pathophysiology and interactions involved are not fully understood. We have studied the effects of hyponatraemia and SAH on the cerebral vasomotor responses of the rabbit. Cerebrovascular reactivity to hypercapnia and cerebral autoregulation to trimetaphan-induced hypotension were determined in normal and hyponatraemic rabbits before and 6 days after experimental SAH produced by two intracisternal injections of autologous blood. Hyponatraemia (mean plasma sodium of 119 mM) was induced gradually over 48 h by administration of Desmopressin and intraperitoneal 5% dextrose. Sham animals received normal saline. The cerebrovascular reactivity (% change +/- SD in cortical CBF/mm Hg PaCO2, measured by hydrogen clearance) of hyponatraemic (4.8 +/- 3.0%) and SAH (1.3 +/- 2.0%) animals was significantly less (p less than 0.05) than control (11.6 +/- 4.0%) and sham (8 +/- 2.0%) animals, whereas the reactivity of hyponatraemic-SAH animals was preserved (9.8 +/- 6.0%). Hyponatraemia and SAH alone each significantly impaired CBF autoregulation but their combined effects were not additive. Systemic hyponatraemia impairs normal cerebral vasomotor responses but does not augment the effects of experimental SAH in the rabbit.
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PMID:The effects of hyponatraemia and subarachnoid haemorrhage on the cerebral vasomotor responses of the rabbit. 205 Jul 54

These experiments examine the transfer of urea, sodium, and sucrose from blood to brain in an animal model of newborn cerebral ischemia-reperfusion injury. Cerebral ischemia (20 min) was produced in anesthetized, ventilated piglets by increasing intracranial pressure above mean arterial blood pressure, thereby reducing cerebral perfusion pressure to zero. The blood to brain transfer of urea, sodium, and sucrose was then measured in sham control piglets and at 30 min and 2 hr of reperfusion following ischemia. At 30 min of reperfusion, urea and sodium transfer were increased while sucrose transfer was unchanged. However, at 2 hr of reperfusion, transfer of all three tracers was elevated. The difference in the time course of increased transport of these substances into the brain following ischemia cannot be explained by size differences, indicating that changes in the blood-brain barrier following ischemia are more complex than merely opening junctions between cells and creating leaky sites. Alterations in blood-brain barrier transport could participate in altered neuronal function after ischemia-reperfusion injury.
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PMID:Blood to brain transport after newborn cerebral ischemia/reperfusion injury. 206 19

Cerebral ischaemia was produced in 2 groups of gerbils by occlusion of the common carotid arteries for 30 minutes, resulting in cerebral oedema. In group 1 cerebral oedema was measured by specific gravity microgravimetry, and in group 2 brain metabolism and blood flow were measured by 31P and 1H NMR spectroscopy and hydrogen clearance respectively. In group 1 the brain water content did not return to control levels by 180 minutes of reperfusion. Energy metabolism, determined by 31P NMR spectroscopy returned to control by 12 minutes, intracellular pH (pHi) by 20 minutes, and lactate, determined by 1H NMR spectroscopy, by 50 minutes. There was a lag of about 10 minutes before lactate began to be cleared from the brain. We suggest that while pHi is low, Na+/H+ exchange will negate the Na+ extrusion driven by the Na+/K+ ATPase. When pHi approaches normal there will be a net extrusion of Na+, taking osmotic water with it, and presumably with passive washout of lactate. This may be the cause of the initial delay in lactate clearance.
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PMID:Restoration of energy metabolism and resolution of oedema following profound ischaemia. 208 88

1. A possible cerebroprotective effect of a chemically stable prostacyclin analogue, beraprost sodium, was investigated in a canine model of cerebral ischaemia. Cerebral ischaemia was produced by the combined occlusions of the left subclavian and the brachiocephalic arteries with preceding ligations of the intercostal arteries. 2. The decrease in baroreceptor reflex sensitivity (BRS), measured by phenylephrine-induced reflex bradycardia, following 5 min ischaemia was used to assess the cerebroprotective effect. 3. Beraprost (1 microgram kg-1 min-1 i.v., infused for 15 min just before ischaemia) completely prevented the decrease in BRS. Although the lower dose of beraprost (0.1 microgram kg-1 min-1 i.v.) failed to show such a protective effect, its inhibitory effect on ADP-induced platelet aggregation was as potent as that of the higher dose. 4. The extent of decrease in BRS was inversely correlated with the extent of the residual blood flow in the medulla oblongata during ischaemia. Since beraprost did not affect the extent of the residual blood flow during ischaemia, its cerebroprotective effect could not be ascribed to the reduction of the degree of ischaemia by increasing collateral blood flow to the brain. 5. Post-ischaemic reduction of the regional blood flow in the medulla and the cerebral cortex was completely prevented by the higher dose of beraprost. 6. The present study suggests that the cerebroprotective effect of beraprost may be independent of its anti-aggregatory and vasodilator effects. It is possible that the protection may be due to a prostacyclin-like cytoprotective effect through membrane stabilization.
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PMID:Protective effect of beraprost sodium, a new chemically stable prostacyclin analogue, against the deterioration of baroreceptor reflex following transient global cerebral ischaemia in dogs. 211 14

The efficacy of free radical scavengers (mannitol and n-2-mercaptopropionyl glycine) and a vasodilator (sodium nitroprusside) on the EEG recovery following cerebral ischemia was studied in the anesthetized rat. Global ischemia of brain was produced by the four-vessel occlusion for 30 min followed by 3 h reperfusion. Blood pressure, heart rate and EEG were monitored. The test agents were infused intravenously 15 min before and immediately after cerebral ischemia. The results indicate that mannitol 20-50 mg/kg, n-2-mercaptopropionyl glycine 10-20 mg/kg and sodium nitroprusside 20-50 micrograms/kg singly or in combination improved EEG recovery during reperfusion.
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PMID:Effect of mannitol, n-2-mercaptopropionyl glycine and sodium nitroprusside on EEG recovery following cerebral ischemia and reperfusion in the rat. 212 81

Transient global forebrain ischaemia was produced in Mongolian gerbils by occluding both common carotid arteries for 10 min followed by 48 h recirculation. Dexamethasone, 5 mg/kg i.p., was given 5 h before the occlusion and every 12 h thereafter. After occlusion an increase in water, sodium and calcium content was found in the parietal cortex and hippocampus, while the concentration of potassium decreased. Exudation of plasma albumin was not found in the brain. The activity of Na+, K(+)-ATPase decreased in the hippocampus. Morphological signs of cerebral oedema were also observed, both in the CA1 region of the hippocampus and in the cortex. Dexamethasone treatment prevented the accumulation of water, sodium and calcium in the ischaemic brain. It also attenuated the oedematous morphological changes of the blood-brain barrier. Thus dexamethasone treatment may also have therapeutic relevance in the acute, high-risk phase of patients suffering from repetitive, transitoric cerebral ischaemia.
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PMID:Dexamethasone treatment attenuates the development of ischaemic brain oedema in gerbils. 215 6

Brain edema is a frequent complication of cerebral ischemia; however, its mechanism of formation is not well understood. Sodium is known to accumulate in brain during the early stages of partial ischemia. Therefore, the present studies were undertaken to determine the relation among BBB sodium transport, integrity of the BBB, and development of brain edema during the first 24 hr after the onset of cerebral ischemia. Partial cerebral ischemia was produced in gerbils by ligation of the left common carotid artery under ether anesthesia. After recovery from the anesthetic, animals were scored for the presence of symptoms, and those with scores greater than 10 of 25 (n = 87) were chosen for this study. Measurements of tissue water, sodium, and potassium contents, and brain uptake of 22Na and 3H-mannitol were made in each group at 1.5, 3, 6, 12, and 24 hr after carotid ligation. Accumulation of sodium and water in the ischemic compared with the nonischemic cerebral cortex was progressive. This edema formation was not of the vasogenic type because the permeability of the BBB to mannitol was unchanged. Blood-to-brain sodium transport was reduced by 30% to 40% at all time points in the ischemic cortex. Nevertheless, the remaining sodium transport activity appeared to play a role in the development of brain edema because Na accumulated in the tissue at a rate that was approximately the same as the rate of 22Na uptake from blood.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Blood-to-brain sodium transport in ischemic brain edema. 216 71


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