bluuebunny/crossref_metadata_2025_split huggingface dataset:
Incidence of silent lacunar lesion in normal adults and its relation to cerebral blood flow and risk factors.
Authors: Kobayashi S , Okada K , Yamashita K 
Published: June 2011

There are few reports comparing incidence of silent lacunar lesions detected by magnetic resonance imaging and cerebral blood flow in neurologically normal adults.
We studied the incidence of such lesions and its relation to cerebral blood flow and risk factors in 246 neurologically normal adults (145 men, mean age 62 years; 101 women, mean age 60 years) who received health screening examinations of the brain.
Thirty-two subjects (13%) had possible silent lacunar lesions (66% of these were recognized by both T1- and T2-weighted image). The regional cerebral blood flow measured by the xenon-133 inhalation method was significantly lower in subjects with silent lacunes than in those without (p less than 0.02). Cerebral blood flow was mildly but significantly decreased in those with silent lacunes (p less than 0.05). Periventricular hyperintensity was closely related to silent lacune (p less than 0.01). However, there was no significant difference in cerebral blood flow between subjects with and without apparent periventricular hyperintensity.
Silent lacunar lesion was closely related to decrease of cerebral circulation and may be an important risk factor for symptomatic cerebrovascular disease.
Evaluation of 2,3,5-triphenyltetrazolium chloride staining to delineate rat brain infarcts.
Authors: Isayama K , Pitts L H , Nishimura M C 
Published: June 2011

Accurate and reproducible determination of the size and location of cerebral infarcts is critical for the evaluation of experimental focal cerebral ischemia. The purpose of this study was to compare intracardiac perfusion of 2,3,5-triphenyltetrazolium chloride with immersion of brain tissue in 2,3,5-triphenyltetrazolium chloride to delineate brain infarcts in rats.
After 6, 24, or 48 hours of ischemia induced by permanent middle cerebral artery occlusion, some rats were perfused with 2,3,5-triphenyltetrazolium chloride; other rats were given an overdose of barbiturates, after which brain sections were immersed in 2,3,5-triphenyltetrazolium chloride. Coronal sections were taken 4, 6, and 8 mm from the frontal pole, and infarct areas in perfused and immersed sections were compared; subsequently, the same sections were stained with hematoxylin and eosin.
In rats subjected to 24 or 48 hours of occlusion, areas of infarction were clearly defined with both 2,3,5-triphenyltetrazolium chloride staining techniques, and the infarct sizes correlated well with the results of hematoxylin and eosin staining (r = 0.85-0.94).
These results demonstrate that intracardiac perfusion of 2,3,5-triphenyltetrazolium chloride is an accurate, inexpensive, and efficient staining method to detect infarcted tissue 24 and 48 hours after the onset of ischemia in rats.
Clentiazem protects against chronic cerebral vasospasm in rabbit basilar artery.
Authors: Vorkapic P , Bevan J A , Bevan R D 
Published: June 2011

Experiments were carried out in rabbits to determine whether clentiazem (8-chlorodiltiazem), a cerebrovascular-selective calcium channel blocker, administered 24 hours before subarachnoid hemorrhage influenced the subsequent cerebral vasospasm.
Subarachnoid hemorrhage was induced by multiple injections of blood into the prepontine cisterns of 35 male New Zealand White rabbits, and clentiazem (5 mg/kg) was administered 4 times daily until sacrifice. Cerebral artery diameter was assessed in vivo by angiography. Functional features of basilar arteries were measured using conventional in vitro methodology.
Clentiazem reduced the angiographic narrowing seen on days 2 and 5 from 35% and 34%, respectively (sham control, 1.42 +/- 0.31 mm [n = 22]), to 8% and 11%, respectively, and prevented the narrowing (32%) that occurred on day 9. Narrowing in the untreated rabbits was only partly reversed by papaverine; all narrowing in clentiazem-treated animals was papaverine sensitive. Clentiazem prevented or reduced many of the changes in the basilar artery caused by the subarachnoid hemorrhage. Of particular relevance to arterial narrowing were the increased wall stiffness, the transient spontaneous changes in wall force, and the reduction in relaxation to acetylcholine. Reduction of the changes in wall force induced by agonists and by stimulation of intramural sympathetic nerves was observed.
The vascular damage associated with chronic cerebral vasospasm is related to calcium entry into the smooth muscle and endothelial cells, and possibly sympathetic nerve terminals, through calcium channels sensitive to clentiazem, which suggests that clentiazem may be of value in the management of chronic cerebral vasospasm.
Racial variations in ischemic stroke-related physical and functional impairments.
Authors: Horner R D , Matchar D B , Divine G W , Feussner J R 
Published: June 2011

We sought to determine whether there are racial differences in physical and functional impairments resulting from an initial ischemic stroke.
We conducted a prospective, county-wide, multisite cohort study including a university hospital, a community hospital, and a Veterans Affairs hospital. The study population was an inception cohort of 145 patients hospitalized for ischemic stroke. Physical and functional impairments were measured using a modified form of the Fugl-Meyer test and the Barthel Index, respectively. Nurses trained to use these tests made assessments at admission and 5, 30, 90, and 180 days after admission. Patient and disease-specific data along with treatment data and vital status were collected.
Forty-one patients (28%) were black. Compared with whites, black stroke patients were more likely to be widowed (51% versus 26%) and hypertensive (83% versus 63%) but less likely to be male (42% versus 69%) and alert on admission (66% versus 76%). There were no racial differences in mortality. Physical impairment was significantly more severe in black than in white patients at admission, and although physical impairment improved, it remained significantly worse in blacks. Functional impairment was also greater in black patients initially but was similar to that in white patients 90 days after the event. Multivariable analyses confirmed these findings.
These results indicate that blacks may have greater residual physical deficits from stroke than whites.
Efficacy of retrograde perfusion of the cerebral vein with verapamil after focal ischemia in rat brain.
Authors: Hosaka T , Yamamoto Y L , Diksic M 
Published: June 2011

For treatment of acute stroke, drug therapy administered systemically has been unreliable due to inadequate delivery of drug into ischemic tissue. We have developed a new method to deliver drugs into the ischemic tissue by retrograde perfusion of the cerebral vein.
We examined in rats the effectiveness of administering verapamil into ischemic tissue by retrograde perfusion through the cerebral vein, starting 3 hours after occlusion of the middle cerebral artery. Twenty-four Fischer-344 rats with occlusion of the middle cerebral artery were divided into four groups of six rats each. Group A rats had no treatment, group B rats received verapamil intravenously, and groups C and D rats received verapamil by transvenous perfusion of the brain with blood and with saline, respectively. We studied local cerebral blood flow using the autoradiographic method with carbon-14-labeled iodoantipyrine and examined cerebral infarct volume with cresyl violet and Luxol fast blue staining.
As compared with group A rats, in groups C and D rats we found a significant and extensive increase of cerebral blood flow in the ischemic cortical and subcortical areas (55-119%, p less than 0.05) and a significant reduction of cerebral infarct volume (31-39%, p less than 0.05). We found no significant changes in group B rats.
This study shows that transvenous perfusion of the brain with verapamil starting 3 hours after occlusion of the middle cerebral artery produces a significantly beneficial effect in rats.
Mild hypothermia ameliorates ubiquitin synthesis and prevents delayed neuronal death in the gerbil hippocampus.
Authors: Yamashita K , Eguchi Y , Kajiwara K , Ito H 
Published: June 2011

The purpose of the present study is to determine the effect of mild hypothermia on the synthesis of ubiquitin, an important protein for maintenance of cell viability, in the hippocampal neurons following transient cerebral ischemia.
Transient ischemia was induced by occluding both common carotid arteries for 5 minutes. In experiment 1, the animals were divided into four groups according to the rectal and scalp temperatures during ischemia: the normothermia group and the graded hypothermia A, B, and C groups (n = 9 per group). CA1 neuronal density was assessed at 7 days after ischemia. In experiment 2, the animals were divided into two groups designated the normothermia and the hypothermia groups (n = 6 per group). The presence of ubiquitin was examined by immunohistochemistry at 6, 24, and 48 hours after transient ischemia in various regions of the hippocampus.
In experiment 1, the mean +/- SEM neuronal density per millimeter was 12 +/- 1 in the normothermia group and 126 +/- 25, 225 +/- 10, and 214 +/- 9 in hypothermia groups A, B, and C, respectively. Mild hypothermia in groups B and C, in which the brain temperature was below 33 degrees C, ameliorated markedly the extent of ischemic neuronal damage in the CA1 sector (p less than 0.01). In experiment 2, ubiquitin immunoreactivity had disappeared in all regions of the hippocampus at 6 hours after ischemia and showed no subsequent recovery in the CA1 pyramidal neurons under normothermic conditions. Under hypothermic conditions, however, it had recovered significantly in the CA1 pyramidal neurons at 24 and 48 hours after ischemia (p less than 0.01).
We conclude that mild hypothermia, in which the brain temperature is below 33 degrees C, markedly improves the ischemic delayed neuronal damage in the CA1 sector, and that increased ubiquitin synthesis and protein ubiquitination could be one essential part of the protective mechanism afforded by mild hypothermia against delayed neuronal death.
Embolic stroke in aged rats.
Authors: Futrell N , Garcia J H , Peterson E , Millikan C 
Published: June 2011

Although stroke is a disorder associated with aging, experimental studies of stroke are conducted in young adult (2-4-month-old) animals (rat life span, 27-29 months). To determine whether histopathologic changes caused by cerebral infarction would be altered in aged animals, we produced embolic cerebral infarction in 17 aged (23-24-month-old) and 16 young (2-4-month-old) rats.
The right common carotid artery was irradiated with a laser (632 nm, 200 mW/cm2, 15-20 minutes) after the intravenous injection of the photosensitizing dye Photofrin II (12.5 mg/kg). This produces a nonocclusive platelet thrombus that spontaneously embolizes to the brain. Animals were killed 4 days later.
Analysis was done on 142 infarcts, 68 in aged rats and 74 in young rats. Hypercellularity, with infiltration of macrophages, was more common within small infarcts (less than 1 mm) in young than in aged rats (p = 0.002), and hypertrophy of astroglial fibers surrounding the infarcts was more prominent in young rats. Larger infarcts (greater than or equal to 1 mm) were often hypocellular, with a trend toward more macrophages in the periphery of the infarcts in young than in old animals (p = 0.170).
The infiltration of macrophages into cerebral infarcts and the hypertrophy of astroglial fibrils surrounding these infarcts are reduced in the aged rat. These age-related differences emphasize the importance of using appropriately aged animals in experimental models of stroke.
Hypoglycemia presenting as basilar artery thrombosis.
Authors: Röther J , Schreiner A , Wentz K U , Hennerici M 
Published: June 2011

Following our treatment of a patient with hypoglycemia-induced brain stem symptoms, we examined the possible mechanisms for hypoglycemia presenting as basilar artery disease.
We describe a patient who had progressive brain stem symptoms due to a diet-induced hypoglycemia initially diagnosed as basilar artery thrombosis. Symptoms ceased immediately after intravenous glucose.
Before invasive diagnostic and thrombolytic strategies are considered, hypoglycemia as a rare but important cause of acute brain stem dysfunction must be considered in patients suspected to suffer from basilar artery thrombosis.
Postpartum dissecting aneurysm of the basilar artery.
Authors: Van de Kelft E , Kunnen J , Truyen L , Heytens L 
Published: June 2011

Dissecting aneurysms arising from the vertebrobasilar complex are rare and difficult to manage. More of their natural history needs to be known before treatment can be optimized.
We report a postpartum dissecting aneurysm of the right vertebrobasilar artery in a 31-year-old woman that was confirmed by angiographic identification of a double lumen. The intracranial segment of the right vertebral artery was thrombosed proximal to the aneurysm. The patient, managed conservatively, recovered well and, when reexamined 2 months later, was found to be neurologically intact. A repeat angiographic study at that time demonstrated that the aneurysm had resolved.
Proximal occlusion may have protected the aneurysm from rupture and further dissection, thereby making surgery unnecessary.
Seasonal variation of cerebral hemorrhage in 236 consecutive cases in Brussels.
Authors: Capon A , Demeurisse G , Zheng L 
Published: June 2011

Seasonal variation in the incidence of cerebral hemorrhage has been previously demonstrated. In this study, we sought to identify the climatological data best correlated with this seasonal variation.
In a retrospectively studied sequential series of 236 patients with nontraumatic cerebral hemorrhage observed in Brussels over a period of 8 years, we cumulatively grouped the dates of stroke occurrence into a single calendar year.
We found marked seasonal variation in incidence, with the highest value (23%) observed in November-December and the lowest (10%) in July-August. Seasonal variations in incidence of cerebral hemorrhage were shown to be correlated not only with the inverse of ambient temperature, but also with the inverse of hours of sunshine and with ambient humidity. We found no difference between hypertensive and normotensive patients.
Our study fails to bear out the hypothesis that the higher incidence of cerebral hemorrhage in late autumn and winter is due to the influence of low ambient temperature on blood pressure.
Combined treatment with MK-801 and nicardipine reduces global ischemic damage in the gerbil.
Authors: Hewitt K , Corbett D 
Published: June 2011

Excessive activation of the N-methyl-D-aspartate receptor by glutamate produces an influx of Ca2+, which in turn is thought to lead to ischemic cell death. In this study we evaluated the combined treatment of the N-methyl-D-aspartate antagonist dizocilpine (MK-801) and the dihydropyridine Ca2+ channel blocker nicardipine for the reduction of hippocampal CA1 neuronal loss.
Global ischemia was induced by bilateral carotid artery occlusion in the gerbil. Body temperature was maintained between 36.5 degrees C and 37.5 degrees C during surgery. MK-801 (5.0 mg/kg) was injected 15 minutes after occlusion whereas nicardipine was given by injection and via a micro-osmotic pump (1.0 mg/kg/day) for 3 days.
Postischemic treatment with MK-801 reduced CA1 cell loss by 27.0%, whereas nicardipine reduced CA1 cell loss by 13.3%. Combined postischemic treatment with these drugs yielded an additive, protective effect (44.5% reduction of CA1 loss) that did not appear to result from postischemic hypothermia as assessed by skull and rectal temperature recordings.
Our results demonstrate that MK-801 plus nicardipine significantly attenuates CA1 cell death after forebrain ischemia in the gerbil. Excitatory amino acid antagonists in combination with Ca2+ channel antagonists may be an effective therapy in patients exposed to global ischemic insult.
Transcranial Doppler assessment of cerebral flow velocity during cognitive tasks.
Authors: Kelley R E , Chang J Y , Scheinman N J , Levin B E , Duncan R C , Lee S C 
Published: June 2011

The purpose of this study was to assess the ability of transcranial Doppler ultrasonography to detect selective circulatory changes during cognitive activity.
We measured cerebral artery flow velocity in 21 normal volunteers by transcranial Doppler ultrasonography during rest followed by cerebral activation. Mean and peak systolic flow velocities of the anterior, middle, and posterior cerebral arteries were measured during the performance of a commercial video game. We also measured flow velocity of the anterior cerebral arteries in 18 subjects during a mental arithmetic task. Serial measurements of the right and left sides were made with a headband with two probes.
We observed a global increase in the flow velocity above baseline measurements during task performance. During the video game, both middle cerebral arteries (t = 2.6, p = 0.02 for the left; t = 3.3, p = 0.004 for the right) and the left posterior cerebral artery (t = 2.2, p = 0.004) had selective increase in mean flow velocity compared with the ipsilateral anterior cerebral artery. This selective activation was most prominent in the right middle cerebral artery, which had a greater degree of activation than the right posterior cerebral artery (t = 2.8, p = 0.013). We did not observe a statistically significant difference between the right and left middle cerebral arteries, but there was a trend toward a greater activation on the right for both the mean velocity (t = 1.7, p = 0.098) and the peak velocity (t = 1.9, p = 0.079).
Our preliminary investigation suggests that this noninvasive technique has the potential to correlate selective cerebral artery flow dynamics with cognitive activity.
Effects of ischemia duration on neurological outcome, CA1 histopathology, and nonmatching to sample learning in monkeys.
Authors: Scheller M S , Grafe M R , Zornow M H , Fleischer J E 
Published: June 2011

Male cynomolgus monkeys (n = 10) were subjected to varying durations of global cerebral ischemia to determine the relation between dose (ischemic duration) and response (outcome).
Each monkey was anesthetized with halothane, and global cerebral ischemia was produced by a neck tourniquet and trimethaphan-induced hypotension. The animal was subjected to 3 (n = 3), 9 (n = 3), or 12 (n = 4) minutes of ischemia. Neurological examinations were performed daily for 30 days or until the monkey was neurologically normal. Approximately 1 month after ischemia, the animal was evaluated for evidence of neurobehavioral abnormalities with the nonmatching to sample test. When testing was complete, the monkey was killed with an overdose of pentobarbital and the brain perfused with formalin and removed for histopathologic analysis, with particular attention devoted to the hippocampal CA1 region.
Monkeys subjected to 3 or 9 minutes of ischemia were neurologically normal (except for a very mild injury in one 9-minute animal) immediately after ischemia and had normal CA1 histology. Monkeys subjected to 12 minutes of ischemia were grossly abnormal neurologically after ischemia, but two of the four animals made a complete recovery (neurological deficit score of 0) by 30 days. Monkeys subjected to 12 minutes of ischemia had mild damage in the CA1 region, with all other brain regions appearing normal. None of the animals had demonstrable decrements in neurobehavioral function as measured by the nonmatching to sample test.
We conclude that neurobehavioral testing after global cerebral ischemia in primates is feasible, but the ischemic time necessary to produce CA1 damage that could potentially be quantified antemortem with the nonmatching to sample test is greater than 12 minutes in cynomolgus monkeys and may produce temporary severe gross neurological abnormalities as well.
Mechanism of cerebral blood flow augmentation by hemodilution in rabbits.
Authors: Korosue K , Heros R C 
Published: June 2011

Hemodilution is known to increase cerebral blood flow, but it is not known whether the increase in flow is a direct result of a decrease in viscosity or whether it may be due to compensatory vasodilatation in response to the decrease in oxygen carrying capacity that results from hemodilution. This study is designed to investigate this question.
Changes in regional cerebral blood flow were studied in normal and ischemic brains of 15 and 18 rabbits, respectively. In one group of rabbits graded hemodilution was used to reduce arterial oxygen content progressively in stages; in the second group the arterial oxygen content was reduced in similar stages by progressively larger reductions in the concentration of inspired oxygen (hypoxic hypoxia). In the ischemic animals focal ischemia was produced by embolic occlusion of the right middle cerebral artery.
In the normal rabbits, hypoxic hypoxia and hemodilution resulted in similar progressive increases in cerebral blood flow as arterial oxygen content fell. In the ischemic animals, there was a significant fall in cerebral blood flow in the ischemic region in all groups after arterial occlusion. Hemodilution resulted in a progressive increase in cerebral blood flow in both ischemic and nonischemic regions. With hypoxic hypoxia, however, cerebral blood flow in the ischemic region showed no increase or a slight decrease.
Even though hypoxic hypoxia results in a marked increase in cerebral blood flow in normal brain, it does not significantly change cerebral blood flow in ischemic brain. In contrast, hemodilution resulting in a comparable degree of hypoxemia is capable of significantly increasing cerebral blood flow in ischemic brain. Therefore, the mechanism of blood flow augmentation by hemodilution in ischemic brain is probably related to a direct hemorheologic effect rather than to the resulting hypoxemia.
Effect of diabetes mellitus on flow-mediated and endothelium-dependent dilatation of the rat basilar artery.
Authors: Fujii K , Heistad D D , Faraci F M 
Published: June 2011

Diabetes mellitus may impair endothelium-dependent responses in cerebral arterioles. The basilar artery dilates in response to increases in blood flow. The goal of this study was to examine effects of diabetes mellitus on "flow-mediated" and endothelium-dependent dilatation of the basilar artery.
Diabetes was induced in rats with 50 mg/kg streptozotocin. Six months later, vessel diameter and velocity of blood flow through the basilar artery were measured using a cranial window in anesthetized rats under baseline conditions and during occlusion of the carotid arteries. Changes in vessel diameter were also measured during topical application of acetylcholine and sodium nitroprusside.
With aortic pressure maintained at baseline levels, blood flow velocity through the basilar artery increased similarly in control and diabetic rats during unilateral common carotid artery occlusion and during bilateral occlusion. In control and diabetic rats, diameter of the basilar artery increased by 10 +/- 2% and 10 +/- 4% during unilateral occlusion and by 27 +/- 5% and 31 +/- 4% during bilateral occlusion, respectively. Thus, diabetes did not impair flow-mediated dilatation of the basilar artery. In contrast, dilatation in response to 10(-5) M topical acetylcholine was less in diabetic rats (13 +/- 2%) than in control rats (45 +/- 8%) (p less than 0.05). Dilator responses to nitroprusside were not impaired by diabetes.
The findings suggest that diabetes produces impairment of endothelium-dependent responses to acetylcholine, but not flow-mediated dilatation, in the basilar artery.