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

Marked hyperemia accompanies reperfusion after ischemia in the brain, and may account for the propensity of cerebral hemorrhage to follow embolic stroke or carotid endarterectomy, and for the morbidity that follows head injury or the ligation of large arteriovenous malformations. To evaluate the contribution of trigeminal sensory fibers to the hyperemic response, CBF was determined in 12 symmetrical brain regions, using microspheres with up to five different isotopic labels, in four groups of cats. Measurements were made at 15-min intervals for up to 2 h of reperfusion after global cerebral ischemia induced by four-vessel occlusion combined with systemic hypotension of either 10- or 20-min duration. In normal animals, hyperemia in cortical gray matter 30 min after reperfusion was significantly greater after 20 min (n = 10) than after 10 min (n = 7) of ischemia (312 ml/100 g/min versus 245 ml/100 g/min; p less than 0.01). CBF returned to preischemic levels approximately 45 min after reperfusion and was reduced to approximately 65% of basal CBF for the remaining 75 min. In cats subjected to chronic trigeminal ganglionectomy (n = 15), postocclusive hyperemia in cortical gray matter was attenuated by up to 48% on the denervated side (249 versus 150 ml/100 g/min; p less than 0.01) after 10 min of ischemia. This effect was maximal in the middle cerebral artery (MCA) territory, and was confined to regions known to receive a trigeminal innervation. In these animals, substance P (SP) levels in the MCA were reduced by 64% (p less than 0.01), and the density of nerve fibers containing calcitonin gene-related peptide (but not vasoactive intestinal polypeptide or neuropeptide Y) was decreased markedly on the lesioned side. Topical application of capsaicin (100 nM; 50 microliters) to the middle or posterior temporal branch of the MCA 10-14 days before ischemia decreased SP levels by 36%. Postocclusive hyperemia in cortical gray matter was attenuated throughout the ipsilateral hemisphere by up to 58%, but the cerebral vascular response to hypercapnia (PaCO2 = 60 mm Hg) was unimpaired. The duration of hyperemia and the severity of the delayed hypoperfusion were not influenced by trigeminalectomy, capsaicin application, or the intravenous administration of ATP. These data demonstrate the importance of neurogenic mechanisms in the development of postischemic hyperperfusion, and suggest the potential utility of strategies aimed at blocking axon reflex-like mechanisms to reduce severe cortical hyperemia.
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PMID:Chronic trigeminal ganglionectomy or topical capsaicin application to pial vessels attenuates postocclusive cortical hyperemia but does not influence postischemic hypoperfusion. 170 54

In a model of focal cerebral ischaemia in the cat (transorbital occlusion of the middle cerebral artery for 60 minutes, thereafter 6 hours reperfusion by clip removal), hydroxyethyl-starch (HAES) (ELOHES; Leopold Pharma GmbH, Graz, Austria) was administered intravenously before and during the ischaemic episode as a 6% or as a 10% solution in a randomised manner (6 animals each group). The size of the developing cerebral infarct was not significantly different when comparing the 6% and the 10% group with the controls (SALINE). Collateral circulation to the infarct border (pial arteries on the suprasylvian gyrus) was also not significantly different between the two groups, except for the first hour of reperfusion, where vessels of the 6% group were wider than vessels of the 10% group. At the infarct border (ectosylvian gyrus) small resistance vessels were significantly more dilated in the 6% than in the 10% group both during the occlusion period and during the reperfusion episode after removal of the clip. Pial arteries dilated less in both HAES-groups than in the controls. It can be assumed, that HAES-incuded decrease of plasma viscosity led to an elevation of blood flow velocity and blood flow quantity (CBF). But the latter might be counteracted by autoregulation of CBF, i.e. vasoconstriction. Thus, a possible positive effect of HAES might in part be counteracted by autoregulation, which explains that no significant therapeutic effect could be achieved.
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PMID:Hydroxyethyl-starch in transient experimental focal cerebral ischemia. 170 55

A new experimental trial to investigate the usefulness of early therapeutic measures in case of acute I.V.D. has been performed, on the basis of a previous already reported experience. A combined treatment consisting of hemodilution and revascularization starting 16 hours after the onset of cerebral ischemia was tested. The study was performed in a population of 20 New Zealand male rabbits in which an acute cerebral ischemia was achieved by means of extracranial ligation of both common carotid artery and of one vertebral artery. The animals were divided into two groups. 1st group: no treatment; 2nd group: revascularization + hemodilution. Better results were observed in treated group considering either CBF rates or histological changes.
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PMID:Hemodilution and revascularization for early treatment of stroke: an experimental trial. 175 18

We examined the effects of a new hyperosmotic agent (NIK-242inj.) on brain edema, energy metabolites and regional cerebral blood flow (r-CBF) during acute cerebral ischemia. Cerebral ischemia was induced by bilateral common carotid artery ligation (BLCL) using spontaneously hypertensive rats (SHR). The experimental animals were divided into 4 groups, A:20% NIK-242inj., B:20% mannitol, C:10% glycerol in 5% fructose, D:normal saline. All the animals were administered the agent or saline intravenously beginning at 1h after BLCL and continuing for 2h for a total dose of 6.8 ml/kg body weight. Brain water content and metabolites (ATP, lactate, pyruvate) were determined 3h after BLCL. Regional cerebral blood flow (r-CBF) in thalamus was also measured by the hydrogen clearance technique. The brain water content in the NIK-242inj. group was significantly lower than that of saline group. The concentration of brain ATP in the NIK-242inj. group remained higher than those of saline group. Accumulation of lactate in the NIK-242inj. group was less than in the mannitol and saline groups. The lactate/pyruvate ratio of the NIK-242 inj. group was significantly lower than that of the saline and mannitol groups. At 3h after BLCL, the reduction of r-CBF in the NIK-242inj. group was smaller than that of saline group. The present study suggests that NIK-242inj. as well as glycerol could ameliorate brain edema, disruption of brain energy metabolism and reduction of r-CBF in acutely induced cerebral ischemia.
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PMID:Effect of a new hyperosmotic agent, NIK-242 injection, on brain water content, metabolites and cerebral blood flow in cerebral ischemia in the spontaneously hypertensive rat. 176 86

Somatosensory evoked potentials (SEPs) were studied during graded incomplete cerebral ischaemia in eight goats and for the following 2 h. Anaesthesia was maintained with etomidate 1-1.5 mg kg-1 h-1 and 50% nitrous oxide in oxygen. Global cerebral blood flow (gCBF) was measured by a magnetic flow transducer at one internal maxillary artery after surgical occlusion of all other major extracranial cerebral arteries. CBF was reduced every 30 min by 25% with a lower limit of 15-20 ml 100 g-1 min-1. Regional cerebral blood flow (rCBF) in the brainstem and cortex was measured by the microsphere technique. The main findings were: (a) a graded decline in cortical SEP and a concurrent prolongation of the central conduction time (CCT) at gCBF values below 35 ml 100 g-1 min-1 and (b) an incomplete recovery of cortical SEP components during recirculation. Reduction of gCBF affected cortical rCBF more severely than brainstem rCBF. As a result, only cortical SEPs were changed. Our data suggest that reduced cerebral perfusion may result in altered cortical brain electrical activity that may be monitored by SEP recordings.
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PMID:Somatosensory evoked responses during and after graded brain ischaemia in goats. 187 23

A new model of temporary complete cerebral ischemia was developed and tested in 64 rats. With use of microsurgical techniques, both pterygopalatine and external carotid arteries were occluded and the basilar artery was coagulated to reduce potential collateral CBF during ischemia. After this preliminary five-vessel occlusion, temporary global ischemia was induced by occluding the common carotid arteries (CCAs) with microclips. To validate the method, CBF was measured autoradiographically in 24 anatomical regions at death after 5 min of ischemia or after 15 min of ischemia followed by 5 min of reperfusion. Mean arterial blood pressure and arterial blood gases remained stable under controlled endotracheal ventilation and anesthesia (halothane, 70% N2O, and 30% O2) throughout the CBF experiments, except for a 10-15% increase in mean arterial blood pressure for 1-5 min after bilateral CCA occlusion. After the initial five-vessel occlusion, the EEG did not change, and local CBF levels were comparable to those in anesthetized non-surgical controls. When the CCAs were occluded, the EEG flattened rapidly; after 5 min of ischemia, autoradiography showed no detectable blood flow in the forebrain and cerebellum. The local CBF levels measured after 15 min of temporary global ischemia and 5 min of reperfusion demonstrated relatively homogeneous postischemic hyperperfusion; only two of eight rats had several 1- to 3-mm areas of no-reflow. Survival studies showed increasing motor impairment after 10, 15, 30, and 60 min of temporary CCA occlusion. Ischemic neuronal damage was observed histologically in the hippocampus and basal ganglia 24 h after 10 min of temporary ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A new method for producing temporary complete cerebral ischemia in rats. 193 88

Cerebral high-energy metabolites and metabolic end products were measured during and following total cerebral ischemia in the rat. During cerebral ischemia, lactate accumulation was greatest in the hippocampus, followed by the cerebral cortex and striatum. Following reperfusion, the rate of lactate clearance was slower in the hippocampus than in the other two regions. Regional CBF, cerebral plasma volume (CPV), and calculated mean transit time (MTT) were determined following reflow of ischemic tissue. During hyperemia, CPV, used as an indicator of capillary volume, increased concomitantly with CBF while the MTT remained near the control value, suggesting that the linear flow rate through the vasculature was unchanged. During hypoperfusion, CPV returned to control values, but there was a significant increase in MTT that would result from a decreased linear velocity. The finding of normal tissue energy charge, pHi, and concentration of other metabolites during hypoperfusion shows that hypoperfusion does not result in CBF-metabolic mismatch.
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PMID:Regional cerebral metabolites, blood flow, plasma volume, and mean transit time in total cerebral ischemia in the rat. 199 98

Using the technology of his day, limited to direct observation and histological techniques, Fisher conclusively established the importance of the atherosclerotic carotid plaque in stroke. Recognizing the limits of his observations, he raised a number of questions as regards the degree of carotid disease necessary to adversely affect the brain and the effects of silent carotid occlusion. He also suggested the possible beneficial effects of revascularization. These questions have been addressed and in large part answered by PET. Thresholds of electrical activity and of cellular viability have been established both for cerebral blood flow and for oxygen metabolism. The effects of severe carotid stenosis have been found to be limited to the anterior border zone, where a decreased CBF and CBF to CBV ratio is seen in association with a trend towards rising OEF and declining CMRO2. The acute effects of a stroke and the passage of ischemia to infarction have been documented as they affect CBF, OEF, and CMRO2 in densely ischemic areas and in the penumbra region. An early pattern of elevated OEF in the face of diminished CBF is recognized and evolves into a later pattern of low OEF and CMRO2 characteristic of cell death. Silent carotid occlusion has been shown to produce widespread hypoperfusion and metabolic depression, the former improved by bypass, the latter not. Finally, the CBF to CBV ratio does not appear to be adequate in identifying patients who would benefit from EC-IC bypass, while an elevated preoperative OEF, an unusual event, does not clearly guarantee improved postoperative oxygen metabolism or the prevention of an ipsilateral stroke. Because the anterior border zone is selectively vulnerable to cerebral ischemia in patients with carotid stenosis, and since irreversible oxygen hypometabolism ensues once occlusion occurs, PET may be useful in identifying patients who may be at risk of further ischemic events should stenosis progress to occlusion. PET may also prove to be helpful in understanding the pathophysiology of ischemic complications associated with cerebral aneurysms and AVMs and may be a useful tool for deciding the timing of therapeutic intervention in these conditions.
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PMID:Physiologic studies of cerebral ischemia. 200 95

Following complete global cerebral ischemia and reperfusion, a brief period of reactive hyperemia is followed by a prolonged period of low flow commonly referred to as the delayed postischemic hypoperfusion state. It is generally assumed that this low-flow state may be injurious because of inadequate substrate delivery, thus implying that flow is no longer coupled to metabolic needs. This relationship of CBF to CMRO2 was examined in six anesthetized dogs that were subjected to 12 min of complete ischemia induced either by CSF compression or aortic occlusion. Following reperfusion and onset of the low-flow state, which stabilized at 45 min postischemia, control normothermic (37 degrees C) measurements of CBF and CMRO2 were determined. Thereafter, femoral arterial blood was circulated through a heat exchanger (42.5 degrees C), and brain temperature was increased to 40 degrees C and measurements were repeated. The brain was then cooled back to 37 degrees C for a final set of normothermic measurements. Thereafter, brain biopsies were taken to determine the energy state of the brain. CMRO2 changed approximately 6%/degrees C. CBF paralleled the change in CMRO2. Accordingly, the ratio of CBF to CMRO2 remained constant throughout at a value of 8 to 9, demonstrating maintained coupling. The brain energy state was normal at the end of the study. The authors conclude that postischemic CBF is modulated by the brain's metabolic needs.
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PMID:Postischemic canine cerebral blood flow is coupled to cerebral metabolic rate. 205 Jul 48

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


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