bluuebunny/crossref_metadata_2025_split huggingface dataset:
Superoxide production in experimental seizures in cats.
Authors: Bauknight G C , Wei E P , Kontos H A 
Published: June 2011

Seizures cause cerebrovascular responses similar to those seen in conditions such as acute hypertension, ischemia/reperfusion, or fluid-percussion brain injury, which are associated with the generation of superoxide. Accordingly, we studied production of superoxide in experimental seizures.
Superoxide production was measured in anesthetized cats equipped with double cranial windows using the superoxide dismutase-inhibitable reduction of nitro blue tetrazolium as a measure of superoxide production. Seizures were induced by intravenous bicuculline. The contribution of hypertension associated with seizures was studied by maintaining arterial blood pressure constant by bleeding.
Significant superoxide dismutase-inhibitable reduction of nitro blue tetrazolium indicative of superoxide production was found during seizures with or without control of arterial blood pressure (1.10 +/- 0.27 and 1.29 +/- 0.16 nmol/l/min, respectively).
The results show that experimental seizures are associated with superoxide generation that is independent of the rise in arterial blood pressure. It is likely that superoxide generation is due to the metabolic changes that occur during seizures.
Endothelium-derived relaxing factor modulates noradrenergic constriction of cerebral arterioles in rabbits.
Authors: Bauknight G C , Faraci F M , Heistad D D 
Published: June 2011

Cerebral arterioles are relatively unresponsive to norepinephrine. We tested the hypothesis that release of endothelium-derived relaxing factor is stimulated by norepinephrine and attenuates adrenergic constriction of pial arterioles.
In seven anesthetized New Zealand White rabbits, diameter of pial arterioles was measured through a cranial window. Responses to topical application of norepinephrine and arginine vasopressin were examined before and during application of NG-nitro-L-arginine, which inhibits synthesis of endothelium-derived relaxing factor.
Norepinephrine (10(-6) M) had no effect (0 +/- 3%, mean +/- SE) on arteriolar diameter under basal conditions. Norepinephrine decreased arteriolar diameter by 15 +/- 4% during application of nitro-L-arginine (10(-4) M) (p less than 0.05 versus basal response). L-arginine inhibited the effect of nitro-L-arginine on responses of pial arterioles to norepinephrine. In contrast to norepinephrine, constrictor responses of pial arterioles to vasopressin were not potentiated by nitro-L-arginine.
Norepinephrine, but not arginine vasopressin, releases endothelium-derived relaxing factor, which inhibits constrictor responses of cerebral arterioles in rabbits. This mechanism contributes to the finding that cerebral vessels in rabbits are relatively unresponsive to noradrenergic stimuli.
Abnormalities at different levels of the hypothalamic-pituitary-adrenocortical axis early after stroke.
Authors: Olsson T , Marklund N , Gustafson Y , Näsman B 
Published: June 2011

Hypercortisolism is common in stroke patients. The aim of this study was to investigate possible disturbances at different sites within the hypothalamic-pituitary-adrenal axis. We also studied possible associations between hypercortisolism and clinical manifestations of brain dysfunction.
Patients with an acute ischemic stroke (n = 16; mean +/- SD age, 71 +/- 11 years) were compared with healthy elderly subjects (n = 9). We performed a short adrenocorticotropic hormone (ACTH) test with 0.25 mg 1-24 ACTH injected intravenously and an overnight dexamethasone suppression test with 1 mg dexamethasone given orally at 11 PM.
Serum cortisol levels after dexamethasone at 8 AM were significantly higher in stroke patients (p = 0.003). The area under the curve for the cortisol response to ACTH was elevated in seven (47%) of stroke patients, and the centered cumulative cortisol response was elevated in three (20%) patients. The area under the curve response correlated significantly to the presence of an acute confusional state and male sex in stroke patients (rs = 0.63 and rs = 0.62, respectively; p < 0.05), whereas the centered cumulative cortisol response diminished with increasing age (rs = -0.62; p < 0.05). Postdexamethasone cortisol levels were significantly correlated to the presence of an acute confusional state and to extensive limb paresis (rs = 0.66 and rs = 0.62, respectively; p < 0.05).
There are abnormalities in the cortisol axis both at the central level and at the adrenal level early after stroke. Hypercortisolism is closely associated with cognitive disturbances and extensive motor impairment.
Cerebral vasoconstriction in response to hypocapnia is maintained after ischemia/reperfusion injury in newborn pigs.
Authors: Mirro R , Lowery-Smith L , Armstead W M , Shibata M , Zuckerman S L , Leffler C W 
Published: June 2011

Hypocapnic cerebral vasoconstriction is used therapeutically to reduce elevated intracranial pressure caused by cerebral edema. Because cerebral ischemia/reperfusion injury causes a selective loss of prostanoid-dependent responses, including vasodilation to hypercapnia, we designed these experiments to examine the effect of ischemia/reperfusion on hypocapnic cerebral vasoconstriction.
Microvascular responses were studied in 10 newborn pigs (closed cranial window) in response to hyperventilation-induced hypocapnia (PaCO2, 22 +/- 2 mm Hg) both before and 45 minutes after 20 minutes of global cerebral ischemia. Responses to hypercapnia (PaCO2, 63 +/- 3 mm Hg), topical isoproterenol (10(-7) M), and norepinephrine (10(-4) M) were also studied before and after ischemia in the same animals for comparison.
Before ischemia/reperfusion, pial arterioles vasoconstricted to hypocapnia (-17 +/- 2%) and norepinephrine (-35 +/- 4%) and vasodilated to CO2 (37 +/- 7%) and isoproterenol (25 +/- 2%). After ischemia/reperfusion, the constriction of pial arterioles to hypocapnia (-19 +/- 2%) was similar to that before ischemia. This is in contrast to the loss of dilation to hypercapnia. Dilation to isoproterenol and constriction to norepinephrine were not affected by ischemia.
Hypocapnic cerebral vasoconstriction is maintained after ischemia/reperfusion. Since prostanoid-dependent responses, such as hypercapnic dilation, are lost following cerebral ischemia, these data suggest that hypocapnic constriction is not dependent on an intact prostanoid system and that cerebral vascular responses to CO2 involve multiple mechanisms, depending on whether CO2 is increasing or decreasing from baseline.
Fructose-1,6-bisphosphate stabilizes brain intracellular calcium during hypoxia in rats.
Authors: Bickler P E , Kelleher J A 
Published: June 2011

Exogenously administered fructose-1,6-bisphosphate reduces neuronal injury from hypoxic or ischemic brain insults. To test the hypothesis that fructose-1,6-bisphosphate prevents changes in intracellular calcium ([Ca2+]i) and high-energy phosphate levels, we measured [Ca2+]i, intracellular pH (pHi), and adenosine triphosphate in cultured rat cortical astrocytes and cortical brain slices during hypoxia.
The fluorescent indicators fura-2 and bis-carboxyethyl-carboxyfluorescein were used to simultaneously measure [Ca2+]i and pHi with a fluorometer.
Exposure to hypoxia (95% N2, 5% CO2) or 100 microM sodium cyanide produced transient increases in [Ca2+]i in astrocytes and sustained increases in [Ca2+]i in brain slices. Adenosine triphosphate levels fell in slices exposed to hypoxia or cyanide. Fructose-1,6-bisphosphate (3.5 mM) blocked increases in [Ca2+]i and prevented depletion of adenosine triphosphate. Fructose-1,6-bisphosphate also partially prevented adenosine triphosphate depletion in brain slices incubated in glucose-free medium. Iodoacetate (a specific inhibitor of glycolysis) elevated [Ca2+]i and partially prevented these actions of fructose-1,6-bisphosphate. Changes in pHi during hypoxia were not affected by fructose-1,6-bisphosphate.
Fructose-1,6-bisphosphate supports adenosine triphosphate production via stimulation of glycolysis and results in the maintenance of normal [Ca2+]i during hypoxia or hypoglycemia.
Effects in cats of inhibition of nitric oxide synthesis on cerebral vasodilation and endothelium-derived relaxing factor from acetylcholine.
Authors: Wei E P , Kukreja R , Kontos H A 
Published: June 2011

We investigated the chemical identity of the endothelium-derived relaxing factor generated by acetylcholine in cerebral microvessels by studying the effects and mechanism of action of inhibitors of nitric oxide synthesis from arginine on the vasodilation and endothelium-derived relaxing factor production induced by topical application of acetylcholine in cerebral arterioles.
We determined cerebral arteriolar dilation and endothelium-derived relaxing factor production by bioassay in anesthetized cats equipped with cranial windows during superfusion of 10(-7) M acetylcholine before and after administration of either NG-monomethyl L-arginine or NG-nitro-L-arginine, two inhibitors of nitric oxide synthesis.
NG-Nitro-L-arginine abolished the vasodilation from acetylcholine and eliminated the production of endothelium-derived relaxing factor in the bioassay experiments. NG-Monomethyl L-arginine had no effect on the response to acetylcholine in the absence of pretreatment. However, after pretreatment with the detergent sodium dodecyl sulfate to increase cell membrane permeability, the inhibitor had effects identical to those of NG-nitro-L-arginine. L-Arginine reversed the effects of the inhibitors of nitric oxide synthesis. Neither inhibitor affected baseline vascular caliber, nor did they generate a vasoconstrictor agent in the bioassay experiments. The two inhibitors of nitric oxide synthesis did not affect the response to nitroprusside or adenosine, showing that the effect on responses to acetylcholine was specific. Also, the blockade of the response to acetylcholine induced by the inhibitors of nitric oxide synthesis was unaffected by treatment with superoxide dismutase and catalase, showing that the effect was not mediated by oxygen radicals.
The endothelium-derived relaxing factor generated by acetylcholine in cerebral arterioles of cats is either nitric oxide or a nitric oxide-containing substance. The effect of these inhibitors on the response to acetylcholine is mediated by inhibition of the synthesis of nitric oxide. There is no involvement of radicals, and no vasoconstrictor agent is generated.
Detection of intracranial emboli in patients with symptomatic extracranial carotid artery disease.
Authors: Siebler M , Sitzer M , Steinmetz H 
Published: June 2011

Cerebral embolism from extracranial sources is an important cause of ischemic stroke. The purpose of this limited study using long-term transcranial Doppler ultrasonographic monitoring was to estimate the frequency of clinically silent intracranial embolisms in patients with symptomatic extracranial carotid artery disease.
By means of a 2-MHz pulsed-wave transcranial Doppler instrumentation, three consecutive patients with extracranial internal carotid artery stenosis (n = 2) or occlusion (n = 1) and recurrent ipsilateral ischemic events were monitored (19 hours total recording time). In addition, 10 control subjects without cerebrovascular disease were studied (25 hours total recording time). Formed-element emboli were defined as distinct signals within the fast Fourier-transform Doppler spectrum that were < 70 msec in duration and > 9dB greater in intensity than the background signal. Clinically silent formed-element embolism of ophthalmic or cerebral arteries was demonstrated in all three patients. Embolic events occurred only in the territory of the symptomatic internal carotid artery. The average rate of cerebral embolization at transcranial Doppler ultrasonography was 4.1/hr, with a mean signal duration of 47 msec. No emboli were found in control subjects.
The observed high frequency of silent embolism of the intracranial arteries detected by transcranial Doppler monitoring in patients with recurrently symptomatic extracranial carotid artery disease should encourage studies of the prognostic and therapeutic implications of this method.
Irish brogue after stroke.
Authors: Seliger G M , Abrams G M , Horton A 
Published: June 2011

We describe a patient who presented a unique variation of the previously described acquired foreign accent syndrome.
A 65-year-old women developed an Irish brogue immediately after a deep left hemisphere stroke. The newly accented speech possibly represented a previously learned speech pattern.
Suppressed prosodic speech patterns may reemerge in the setting of brain injury.
The role of transesophageal echocardiography in the acute onset of paraplegia.
Authors: Walsh D V , Uppal J A , Karalis D G , Chandrasekaran K 
Published: June 2011

Acute paraplegia must be investigated promptly to exclude reversible causes. In this report we illustrate the usefulness of transesophageal echocardiography in identifying the vascular etiologies of acute paraplegia.
Two patients presented with acute paraplegia, one spontaneously and the other after removal of an intra-aortic balloon pump catheter. Through the use of transesophageal echocardiography, we excluded aortic dissection and identified protruding atherosclerotic plaques in the descending thoracic aorta of each patient. Embolization of atheromatous material from the thoracic aorta was considered the most likely etiology of paraplegia in both cases.
Embolization from atherosclerotic plaques in the thoracic aorta may be an underestimated cause of acute paraplegia. Transesophageal echocardiography provides a safe, rapid, and reliable tool for investigating a vascular etiology of acute paraplegia.
Thrombotic occlusion of the middle cerebral artery.
Authors: Ueda S , Fujitsu K , Inomori S , Kuwabara T 
Published: June 2011

Epidemiological study of middle cerebral artery occlusion is important because the indication for extracranial-intracranial arterial bypass remains in dispute. To help clarify this issue, we investigated the prognosis of thrombotic middle cerebral artery occlusion in Japanese patients.
We studied 40 patients with thrombotic middle cerebral artery occlusion who were selected on the basis of clinical features, computed tomographic findings, and angiographic findings. Patients with causes of embolism (i.e., cardiomyopathy, valvular heart disease, cardiac arrhythmia, and carotid ulceration) were excluded. The 40 patients were classified into three groups according to the site of middle cerebral artery occlusion: there were 13 patients with occlusion of the proximal portion of the M1 segment, 13 with distal M1 segment occlusion, and 14 with occlusion of the M2 segment.
Good collateral circulation was associated with improved outcomes both clinically and by computed tomography in patients with occlusion of the proximal and distal portions of the M1 segment but not in those with M2 occlusion.
It is reasonable to assume that not only collateral circulation but also the site of occlusion plays an important role in the outcome of middle cerebral artery occlusion. Our finding that good collateral circulation improves the outcome for thrombotic occlusion of the proximal and distal M1 segments supports the possible benefits of such surgery.
Hydroxyethyl starch 200/0.5 reduces infarct volume after embolic stroke in rats.
Authors: Perez-Trepichio A D , Furlan A J , Little J R , Jones S C 
Published: June 2011

We evaluated isovolumic hemodilution with hydroxyethyl starch 200/0.5 in a rat model of focal cerebral ischemia. This compound avoids the unfavorable viscosity and erythrocyte aggregation abnormalities of low molecular weight dextran during administration over a period of several days.
Sprague-Dawley rats, anesthetized with 0.5-1% halothane and 70% N2O, were subjected to silicon cylinder (treated and control groups) or sham (sham group) embolization of the cerebral circulation. Thirty minutes after embolization, the treated group (n = 5) was infused with 11 ml/kg of 10% hydroxyethyl starch 200/0.5, and the control (n = 5) and sham (n = 4) groups were infused with saline for 1 hour. In the treated group, 7.1 ml/kg of blood was withdrawn. After 24 hours, the animals were reanesthetized, and cerebral blood flow was determined with [14C]iodoantipyrine. Alternative brain slices were either incubated with 2,3,5-triphenyltetrazolium chloride for infarct volume determination or frozen for ischemic volume and cerebral blood flow determination using autoradiography.
The hematocrit in the treated group was reduced from (mean +/- SEM) 46 +/- 1% to 35 +/- 2% at 1.5 hours (p < 0.01). Cortical blood flow was within the normal range of 115-185 ml/min/100 g, except for the ischemic cortex in the embolized groups, treated and control. The ischemic and infarct volume of the treated group was reduced by 74% (p < 0.05) and 89% (p < 0.05), respectively, from the control group. The treated and sham ischemic and infarct volumes were not statistically different.
These data suggest that hydroxyethyl starch 200/0.5 could be an effective treatment for ischemic stroke when administered early, because it reduces infarct and ischemic volumes from control values to levels indistinguishable from those of the sham group.
Clinical presentation as a guide to early prognosis in vertebrobasilar stroke.
Authors: Nadeau S , Jordan J , Mishra S 
Published: June 2011

This study attempts to assess the feasibility and heuristic value of a classification scheme for vertebrobasilar stroke.
Fifty-seven consecutive patients with vertebrobasilar stroke were classified on the basis of clinical features and computed tomographic abnormalities into single-sector (n = 19), multisector (n = 11), and top-of-the-basilar (n = 27) groups; a sector was defined as that portion of the brain stem supplied by a single penetrating (median) or branch (paramedian or lateral) artery.
Thirty-day and 3-year survival rates were 100% and 71%, respectively, in the single-sector group, and 96% and 73%, respectively, in the top-of-the-basilar group. Thirty-day and 3-year stroke recurrence free survival rates were 89% and 76%, respectively, in the single-sector group, and 96% and 88%, respectively, in the top-of-the-basilar group. Seven of the 11 patients in the multisector group died within 2 months of ictus, three having experienced recurrence.
These data, in part supported by prior studies, demonstrate the feasibility and heuristic value of the classification scheme and suggest that single-sector and top-of-the-basilar stroke patients have a relatively benign early prognosis and modest long-term stroke rates.
The International Cooperative Study on the Timing of Aneurysm Surgery. The North American experience.
Authors: Haley E C , Kassell N F , Torner J C 
Published: June 2011

The timing of aneurysm surgery after subarachnoid hemorrhage is a major neurosurgical controversy addressed by the International Cooperative Study on the Timing of Aneurysm Surgery (1980-1983). The present report examines the results of this trial in the subgroup of patients admitted to North American centers.
The method of study was a large, multicenter, prospective, epidemiological survey. Neurosurgeons were required to indicate prospectively the interval to planned aneurysm surgery at the time of patient admission. Outcome at 6 months was determined by a blinded evaluator, and overall management results were analyzed by the planned surgical interval.
Seven hundred seventy-two (21.9% of the total study population) patients admitted from days 0 to 3 after subarachnoid hemorrhage were accrued in North American centers. Overall outcome in patients planned for surgery in days 0-3 was equivalent in terms of mortality (after adjustment for prognostic variables) to patients planned for days 11-32, but the early patients had significantly improved rates of good recovery (70.9% versus 61.7%, p less than 0.01). Patients planned for surgery during the days 7-10 interval had nearly twice the mortality of patients in the other intervals.
In contrast to the results from the overall trial, which found no difference between early and delayed surgery, results were best in North American centers when surgery was planned between days 0 and 3 after subarachnoid hemorrhage. These findings argue strongly for early diagnosis and referral for surgical intervention of North American patients suspected of having a ruptured cerebral aneurysm.
Cerebral cysticercosis and stroke.
Authors: Alarcón F , Hidalgo F , Moncayo J , Viñán I , Dueñas G 
Published: June 2011

In 1985 we initiated a protocol for examining the relationship between cerebral cysticercosis and stroke.
In 420 stroke patients admitted to our department, our standard protocol of tests included blood tests, cardiac investigations, angiography, and immunologic cerebrospinal fluid measures. We assessed the following possible risk factors: arterial hypertension, diabetes, cardiopathy, high levels of cholesterol and triglycerides, smoking, alcohol abuse, and cerebral cysticercosis.
Of the 420 patients with stroke, we found cerebral cysticercosis in 31, five of whom were greater than 65 years of age and 26 of whom were less than or equal to 65 years. We determined that cerebral cysticercosis was the only possible risk factor for stroke in one of the five older patients and 15 of the 26 younger and middle-aged patients. Cortical infarctions were found in five of the 31 patients, with cerebral cysticercosis and lacunar infarctions in nine of these patients. One patient had intracystic hemorrhage. In 16 cases, neurological deficit was related to single or multiple cysts, colloids, granulomas, diffuse lesions, or pericystic edema. All patients with cerebral cysticercosis quickly recovered from their neurological deficit, except one who had a hemorrhagic cyst and died and another who remained disabled.
We established that, in patients with neurocysticercosis, occlusion of the small cortical or penetrating vessels at the base of the brain caused by arteriopathy was the most common mechanism of the stroke. Moreover, there is a probable association between cerebral cysticercosis and the susceptibility to stroke, particularly among young and middle-aged patients.
Siagoside selectively attenuates morphological and functional striatal impairments induced by transient forebrain ischemia in rats.
Authors: Merlo Pich E , Grimaldi R , Zoli M , Biagini G , Solfrini V , Toffano G , Fuxe K , Agnati L F 
Published: June 2011

Transient forebrain ischemia induced in rats by the four-vessel occlusion method is known to produce severe neural damage in the hippocampus and striatum and a behavioral syndrome the major symptom of which is a working memory deficit. Recent evidence suggests that monosialogangliosides can ameliorate postischemic symptoms. Our purpose was to study the effect of siagoside, the inner ester of GM1 ganglioside, on some behavioral and morphological impairments induced by four-vessel occlusion in rats.
Rats were injected daily with 5 mg/kg i.p. siagoside starting 4 hours after the cerebral ischemia. After 14 days the rats were tested for working memory in a water T maze or scored for apomorphine-induced stereotypy. The rats were killed 21 days after the cerebral ischemia. Histological and computer-assisted morphometric analyses were performed on cresyl violet-stained brain sections, which were graded according to a neuropathologic score, and on sections stained with a monoclonal antiserum against dopamine and cyclic adenosine-3',5'-monophosphate-regulated phosphoprotein, a marker for striatal dopaminoceptive neurons.
Siagoside treatment reduced the stereotypy score induced by low doses of apomorphine and the extent of striatal lesions but did not affect the working memory deficit or the extent of hippocampal lesions.
Daily siagoside treatment after acute cerebral ischemia attenuates some morphological and functional deficits related to striatal damage. These effects can be interpreted as a selective protective action on striatal neural populations or as a modulatory action on neural systems involved in striatal control. These data are consistent with preliminary clinical reports showing that monosialogangliosides enhance motor recovery after acute ischemic stroke.