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

Global forebrain ischemia was induced in unanesthetized rats by electrocauterization of the vertebral arteries and transient occlusion of the common carotid arteries for 30 minutes. Local cerebral blood flow (l-CBF), cortical tissular pO2 (tpO2), electrocorticogram (ECoG), mean arterial pressure, pH and blood gas determinations and neurologic deficit were evaluated during and after ischemia. Cerebral ischemia induced a substantial decrease in l-CBF and tpO2 and the ECoG was flattened. One hour after ischemia, the neurologic deficit was at its maximum, l-CBF was still decreased and ECoG depressed. Twenty-four hours later, the neurologic deficit was still present but ECoG, l-CBF and tpO2 had returned to their preischemic values. Treatments with naloxone were performed during, after or during and after ischemia. When naloxone was administered during or after ischemia, postischemic neurologic deficit was not influenced by the treatment. A slight but significant improvement of the neurologic score was observed when naloxone was injected during ischemia and infused thereafter. Our results show that this experimental model of cerebral ischemia is suitable for quantification of neurologic alterations during the postischemic period. The slight improvement observed with naloxone suggests that endogenous opioids may have a minor role in the neurologic consequences of ischemia.
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PMID:Model of global forebrain ischemia in the unanesthetized rat. 356 Sep 68

An experimental model for repeated ischemic attacks, which allows easy induction of cerebral ischemia of any desired duration and frequency, has been developed in the gerbil. With this procedure, a pronounced cumulative effect on development of edema and tissue injury was observed using 3 separate, 5-min bilateral occlusions of the common carotid arteries spaced at various time intervals. This effect was most evident when the occlusions were carried out at 1-h intervals, i.e., during the period of marked postischemic hypoperfusion. Such animals, killed after 24 h of recirculation, showed significantly more severe edema and brain tissue injury in the areas exposed to ischemia than was observed in animals killed 24 h after single 5- or 15-min occlusions. The changes of regional CBF, assayed with a [3H]nicotine method, indicated a relatively rapid onset of hypoperfusion of similar degree after each release of arterial occlusion. The hypoperfusion recovered significantly within 6 h of recirculation following either single or multiple occlusions, and no residual hypoperfusion was observed in animals which, when killed at 24 h, showed severe edema and brain tissue injury. This model should prove useful in elucidating the pathophysiological mechanisms operative in repetitive cerebral ischemia.
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PMID:Experimental model for repetitive ischemic attacks in the gerbil: the cumulative effect of repeated ischemic insults. 369 33

The difference in mean hemispheric CBF was compared in two groups of patients suffering from one-sided cerebral ischemia. One group without significant arteriographic abnormalities and a group with a one-sided internal carotid artery occlusion. The Xenon inhalation method (ISI) was used. It seems to be difficult to draw any conclusions from the differences between mean hemispheric ISI values, especially for patients with fairly severe clinical symptoms. In far the most patients without significant arteriographic abnormalities, no significant difference was found. A great difference (high ISI ratio) for patients with no or only slight symptoms may indicate a disturbed blood flow to the hemisphere with the lower ISI. Such high ratios were only found in patients suffering from a one-sided occlusion of the internal carotid artery. This rather simple and harmless method of blood flow measurement may prove to be a valuable contribution toward insight into the pathophysiology of blood flow in patients, especially those suffering from one-sided internal carotid artery occlusion.
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PMID:The possible significance of symmetry and asymmetry of the mean hemispheric CBF in patients with one-sided cerebral ischemia. 370 99

Alterations in the regional CBF after occlusion of the posterior communicating, middle cerebral, or common carotid artery were investigated in the gerbil with a quantitative autoradiographic technique using [14C]iodoantipyrine. Occlusion of the posterior communicating artery produced severe ischemia in the ipsilateral hippocampus, thalamus, and dorsal mesencephalon. Occlusion of the middle cerebral artery produced severe ischemia in the ipsilateral rostral and central cerebral cortex and lateral caudate-putamen. Occlusion of the common carotid artery produced ipsilateral hemispheric ischemia of variable degrees. The distribution and degree of cerebral ischemia produced by occlusion of one of these arteries correlated closely to the arterial territory and the extent of collateral blood supply. Since the areas affected after occlusion of the posterior communicating or middle cerebral artery differ, those models will be useful for the comparative investigation of the ischemia-related cerebral pathophysiology associated with different sites of primary lesion.
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PMID:Regional cerebral ischemia in the gerbil: measurement of regional cerebral blood flow by quantitative autoradiography. 371 Nov 62

Focal cerebral ischemia was induced in rats by occlusion of the middle cerebral artery. By a triple-tracer technique, cerebral glucose utilization, glucose content, and blood flow were simultaneously determined. Computer-assisted autoradiography revealed a core of dense ischemia in the lateral two-thirds of the striatum. A border zone of increased 2-deoxy-D-glucose (DG) uptake surrounded the ischemic insult in the acute stage. The lumped constant was increased only moderately in the border zone. Therefore, the enhanced DG uptake reflected increased glucose consumption. CBF was reduced to 20-30% in the cortical border, while minor depression and in some animals hyperemia were evident in the striate border. Six hours after the insult, the border zones of increased glucose consumption had disappeared in half the animals. In no animals examined after 20 h was glucose consumption enhanced. The study indicated a stable metabolic response to a reproducible focal insult. We conclude that continued enhancement of glucose consumption in marginally perfused areas indicates neuronal damage.
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PMID:Focal ischemia of the rat brain: autoradiographic determination of cerebral glucose utilization, glucose content, and blood flow. 373 1

Volatile anesthetic agents have profound and heterogeneous effects on global and local cerebral blood flow (l-CBF) and metabolism. The relationship between l-CBF and local cerebral glucose uptake (l-CMRg) during isoflurane anesthesia is unknown. Because these relationships might influence neuronal homeostasis during periods of cerebral ischemia of different causes, it becomes important to understand them. Accordingly, the authors evaluated the l-CBF and l-CMRg effects of isoflurane with quantitative autoradiography in normal rats. As the dose of isoflurane increased in a stepwise fashion to 0.5, 1.0 (1.38%), 1.5, and 2.0 MAC levels, the number of structures with a significant (P less than 0.05) l-CBF increase or l-CMRg decrease became greater. At each respective MAC level l-CBF was increased in 0%, 11%, 34%, and 30%, while l-CMRg decreased in 11%, 70%, 74%, and 81% of the structures in which autoradiographic measurements were performed. Between 1.5 MAC and 2.0 MAC the l-CMRg decrease stabilized at about -50% to -70% of cerebral metabolic values obtained in awake control rats in association with attainment of a burst-suppression of isoelectric electroencephalogram. In contrast to these general changes, l-CMRg in two subcortical limbic system structures (dentate gyrus and interpeduncular nucleus) did not decrease, even at the highest doses of isoflurane. L-CBF was significantly (P less than 0.05) increased only at the highest dose ranges (1.5-2.0 MAC) and increased from 34% to 238% in about one-third of the structures evaluated. Isoflurane anesthesia causes heterogeneous changes in l-CBF and metabolism, which are most apparent at doses at or above 1.0 MAC.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Local cerebral blood flow and glucose utilization during isoflurane anesthesia in the rat. 374 May 3

We have recently reported that middle cerebral artery (MCA) occlusion in the rat produces a uniform pattern of cerebral ischemia in an acute phase. This study was done to determine if this model is also useful for quantitative evaluation of infarction size in a chronic phase. [Methods] Sprague-Dawley rats were anesthetized with halothane and left MCA was occluded via transretro-orbital approach. The following studies were done. Neuropathological study was done one week after MCA occlusion. After perfusion fixation, the brain was cut into 6 coronal slices and stained sections were examined. Local cerebral blood flow patterns were observed by 14C-iodoantipyrine autoradiographic technique 1, 2, and 5 days after the occlusion. [Results] Neuropathological studies invariably showed infarct in the cortex and the lateral part of the basal ganlia. The ratio of the infarct to the total areas of both hemispheres in 6 coronal sections was 14.05 +/- 2.66% (Mean +/- SD) in MCA occluded animals (N = 14) and 0.59 +/- 0.46% in sham operated animals (N = 12). Relative to the contralateral hemisphere, marked reduction in CBF was seen in the territory of the MCA and moderate reductions were also seen in the surrounding areas. The same pattern of increased CBF as previously reported was also seen in the ipsilateral substantia nigra and globus pallidus 1, 2, and 5 days after the occlusion. These results indicate the usefulness of this chronic focal cerebral infarction model in the evaluation of infarction.
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PMID:[Focal cerebral infarction in the rat: II. Neuropathological study and local cerebral blood flow pattern]. 379 Mar 66

The effect of gamma-hydroxybutyrate (GHB) on the reactivity of pial arteries to local metabolic factors was tested in chloralose-anesthetized cats before or after a period of transient ischemia induced by air embolism. The vascular reactions were determined during the perivascular microapplication of artificial CSFs with increasing concentrations of adenosine (10(-11)-10(-3) M), H+ (pH 5.1-7.6), or K+ (0-10 mM). During nonischemic conditions the pial arterial reactivity to adenosine and H+, but not to K+, was significantly increased by GHB (250 mg/kg i.v.) when compared with the control reactivity. After cerebral ischemia the reactivity to adenosine was abolished with and without the administration of GHB prior to air embolism. The reactivity to K+ was partly preserved but not increased by GHB when compared with previous results without GHB. In contrast GHB improved the postischemic reactivity to perivascular H+ that had been found to be abolished in previous experiments without GHB. The perivascular microapplication of GHB showed no influence of GHB on the vascular diameter. An important finding of the present study is the demonstration of an increase in cerebrovascular reactivity, which may give scope for therapeutic improvement of the regulation of CBF in pathophysiological conditions.
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PMID:Effect of gamma-hydroxybutyrate on the reactivity of pial arteries before and after ischemia. 379 1

The effects of prostacyclin, nimodipine, and verapamil on local cerebral pH (LCpH) and CBF (LCBF) in middle cerebral artery (MCA)-occluded rats were compared with those in controls and others receiving nimodipine carrier. LCpH and LCBF were determined simultaneously by a double-label autoradiographic technique. The infusions were intravenous, started 15 min following the occlusion, and ended at decapitation 4 h postocclusion. The dosages were 0.5 micrograms/kg/min for nimodipine, 40 micrograms/kg/min for verapamil, and 5 ng/kg/min for prostacyclin. Cortical LCpH in the MCA territory of control and carrier-infused rats varied between 6.72 +/- 0.05 and 6.76 +/- 0.05 (means +/- SEM). These values were significantly lower than the LCpH in the same structures in the contralateral hemisphere (7.09 +/- 0.06; p less than 0.05). LCBF on the side of occlusion varied between 54 +/- 5 ml/100 g/min for the parietal and 57 +/- 7 ml/100 g/min for the sensorimotor cortex, while on the contralateral side, LCBF in these same structures was 190 +/- 18 and 191 +/- 4 ml/100 g/min, respectively. LCpH was not modified by prostacyclin treatment following MCA occlusion, but the pH in the structures that were acidotic in the controls became indistinguishable from contralateral values in nimodipine- and verapamil-treated animals. In contrast, LCBF was statistically higher than controls in many structures only in rats treated with prostacyclin. This suggested that the correction of LCpH produced by calcium blockers was not related to an effect they had on blood flow. Animals receiving calcium blockers tended to have smaller areas of infarction. These results may have therapeutic implications in cerebral ischemia.
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PMID:Cerebral acidosis in focal ischemia: II. Nimodipine and verapamil normalize cerebral pH following middle cerebral artery occlusion in the rat. 379 3

The effects of the calcium entry blocker nicardipine on CBF, CMRO2, and neurologic outcome following 10 min of complete cerebral ischemia were examined in dogs. In CBF and CMRO2 studies, the CBF in the untreated group (seven dogs) and the nicardipine group (seven dogs; 20 micrograms kg-1 at 30 min postischemia and a subsequent infusion of 2 micrograms kg-1 min-1 for 90 min) initially increased to 300-400% and then returned to preischemic values at 30 min postischemia. Thereafter the CBF in the untreated group significantly decreased to 50% of preischemic values for the following 90-min period (hypoperfusion), while the CBF in the nicardipine group did not differ from preischemic values. The CMRO2 in both groups decreased to approximately 50-80% of preischemic values after 15 min postischemia and did not differ between the groups throughout the study. In neurologic outcome studies, 18 dogs were divided into three groups (of six dogs each): untreated; saline infusion only, posttreated; nicardipine as in CBF and CMRO2 studies, pretreated; nicardipine 20 micrograms kg-1 at 2 min preischemia and a subsequent infusion of 2 micrograms kg-1 min-1 from immediately postischemia to 120 min postischemia. Nicardipine treatment initiated either before or after ischemia failed to improve neurologic outcome at 48 h postischemia. Thus, the increase of postischemic global CBF by nicardipine is not accompanied by neurologic recovery in a canine model of complete cerebral ischemia.
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PMID:Nicardipine increases cerebral blood flow but does not improve neurologic recovery in a canine model of complete cerebral ischemia. 379 4


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