bluuebunny/crossref_metadata_2025_split huggingface dataset:
Age-related vulnerability to cerebral ischemia in spontaneously hypertensive rats.
Authors: Yao H , Sadoshima S , Ooboshi H , Sato Y , Uchimura H , Fujishima M 
Published: June 2011

We sought to determine the effects of aging on regional cerebral blood flow and ischemic brain damage in transient cerebral ischemia in rats.
Five adult (5-6 months) and five aged (18-22 months) female spontaneously hypertensive rats were subjected to 20 minutes of bilateral carotid occlusion and 60 minutes of recirculation under amobarbital anesthesia (100 mg/kg i.p.). Regional cerebral blood flow in the hippocampus and striatum was measured using the hydrogen clearance method. Nine adult and 14 aged rats were subjected to 20 minutes of bilateral carotid occlusion or were sham-operated under ether anesthesia. Seven days after 20 minutes of cerebral ischemia, the rats' brains were perfusion fixed. Ischemic damage in the hippocampus and striatum was graded (0 [normal] to 3 [majority of neurons damaged]).
After 20 minutes of bilateral carotid occlusion, striatal cerebral blood flow decreased to 9.1 +/- 1.5 and 3.9 +/- 2.0 ml/100 g/min in aged and adult rats, respectively, and hippocampal cerebral blood flow decreased to 8.6 +/- 2.4 and 5.7 +/- 2.4 in aged and adult rats, respectively. Although these ischemic cerebral blood flow values were not significantly different between the two age groups, scores for ischemic damage in the hippocampus CA-1 subfield and striatum were significantly higher in aged than in adult rats (p less than 0.05, Kruskal-Wallis' h test with Bonferroni correction).
We conclude that aging may be a primary factor in the development of greater ischemic neuronal damage observed in aged hypertensive rats.
Does vasospasm occur in small pial arteries and arterioles of rabbits?
Authors: Nihei H , Kassell N F , Dougherty D A , Sasaki T 
Published: June 2011

Vasospasm is a serious complication associated with subarachnoid hemorrhage. Successful management of vasospasm will ultimately depend on a clear understanding of the scope of this phenomenon, including whether arterial elements of different calibers are equally affected. We therefore examined the responses to subarachnoid hemorrhage in rabbit basilar arteries, small pial arteries, and arterioles.
We compared the brain stem pial arteries of 10 perfusion-fixed male New Zealand White rabbits after experimental subarachnoid hemorrhage to those of five control rabbits using morphological analysis of cross-sections of plastic-embedded vessels. After subarachnoid hemorrhage, the internal elastic lamina was highly corrugated in all basilar arteries (mean diameter 319 +/- 51 microns). These arteries were severely constricted in comparison with the control group, in which the mean diameter was 691 +/- 17 microns, and corrugation of the internal elastic lamina was not present. In contrast, small pial arteries and arterioles very rarely demonstrated a vasoconstrictive configuration after subarachnoid hemorrhage. The contractility of the smaller vessels was confirmed by injecting 2 mg/kg BaCl2 intracisternally. Following BaCl2 injection, corrugation of the internal elastic lamina was detected in the small arteries and arterioles as well as the basilar arteries.
We conclude that experimental chronic vasospasm after subarachnoid hemorrhage in rabbits tends to occur in large conducting arteries rather than in smaller pial arteries and arterioles.
Increase in cerebrospinal fluid and plasma levels of 3-methoxy-4-hydroxyphenylglycol in acute stroke.
Authors: Kanda T , Azuma K , Sakai F , Tazaki Y 
Published: June 2011

3-Methoxy-4-hydroxyphenylglycol is known to be a principal metabolite of brain norepinephrine and to be released into the blood and cerebrospinal fluid in association with activation of the central noradrenergic system. We examined changes in plasma and cerebrospinal fluid levels of 3-methoxy-4-hydroxyphenylglycol during acute stroke to see if there might be a correlation between these and the patient's clinical state.
We measured plasma levels of 3-methoxy-4-hydroxyphenylglycol in 32 control subjects and in 50 patients with brain hemorrhage and 57 patients with brain infarction who were admitted to the hospital within 72 hours after onset. In addition, we estimated 3-methoxy-4-hydroxyphenylglycol concentrations in the cerebrospinal fluid of 37 patients with brain infarction and eight control patients.
Mean +/- SEM values for plasma 3-methoxy-4-hydroxyphenylglycol in the patients with brain hemorrhage and those with brain infarction were 7.3 +/- 0.5 and 6.6 +/- 0.5 ng/ml, respectively. Both values were significantly higher than that obtained in the 32 control subjects (4.6 +/- 0.3 ng/ml, p less than 0.01). Plasma levels of 3-methoxy-4-hydroxyphenylglycol correlated well with state of consciousness and prognosis. The mean +/- SEM level of 3-methoxy-4-hydroxyphenylglycol in the cerebrospinal fluid of the 37 patients with brain infarction (10.9 +/- 0.6 ng/ml) was also significantly higher than that in the eight control patients (7.9 +/- 0.6 ng/ml, p less than 0.01).
The observed increase in plasma and cerebrospinal fluid levels of 3-methoxy-4-hydroxyphenylglycol implies that the activity of the central noradrenergic neurons may be enhanced at the onset of stroke, and these levels may be related to some extent to the clinical state and prognosis of stroke patients.
Effect of hemorrhagic hypotension on cerebrovascular reactivity and ultrastructure in the cat.
Authors: Kovách A G , Szabó C , Faragó M , Lohinai Z , Fehér E 
Published: June 2011

The goal of this study was to determine the alterations in contractile and dilatory responses and ultrastructure of the feline middle cerebral artery after hemorrhagic hypotension.
In the sodium pentobarbital anesthetized cats, a steady 50 mm Hg level of hypotension was reached by bleeding into a reservoir and maintained at this level by further bleeding or autotransfusion for 2 hours. Rings of the arteries, from control animals and from animals after hypotension, were suspended for isometric tension recording in organ chambers filled with modified Krebs-Henseleit solution, aerated with 95% O2-5% CO2 at 37 degrees C, and their reactions to contractile and relaxant agents were tested. Vascular ultrastructure was studied by electron microscope.
Endothelium-dependent relaxations induced by 10(-8) M acetylcholine were enhanced, whereas there was a marked inhibition of the relaxation at 10(-6) M. Relaxations induced by adenosine triphosphate and adenosine showed an impairment. Contractions induced by norepinephrine and prostaglandin F2 alpha remained unchanged, whereas 5-hydroxytryptamine caused a more pronounced contraction after hypotension. No alterations in the morphology of endothelium or smooth muscle were found after hemorrhage. There was, however, a marked decrease in the number of transmitter vesicles in the perivascular nerve terminals.
The present results show marked alterations in cerebrovascular reactivity and ultrastructure of the adventitia after hypotension. These alterations might play an important role in the development of cerebral vasoconstriction during and after this hemorrhagic state.
Global cerebral ischemia in piglets under conditions of mild and deep hypothermia.
Authors: Sutton L N , Clark B J , Norwood C R , Woodford E J , Welsh F A 
Published: June 2011

To investigate the effects of hypothermia on the rate of change and degree of recovery of brain adenosine triphosphate and phosphocreatine concentrations and intracellular pH, we have developed a model that allows phosphorus nuclear magnetic resonance spectroscopy of the intact piglet brain during circulatory arrest.
Three groups of piglets were studied. Three control animals underwent cardiopulmonary bypass at normothermia for 1 hour; five group 1 animals underwent bypass at a brain temperature of 15 degrees C, followed by a period of circulatory arrest such that adenosine triphosphate was absent for 21 minutes, followed by 1 hour of reperfusion; and five group 2 animals underwent bypass at a brain temperature of 37 degrees C, followed by a period of circulatory arrest such that adenosine triphosphate was absent for 21 minutes, followed by reperfusion for 1 hour.
Control animals showed no significant metabolic effects of bypass. Group 1 animals showed a slower decay of the adenosine triphosphate and phosphocreatine concentrations than group 2 animals, consistent with a lower metabolic rate, and had a higher pH at the onset of ischemia. Recovery of the adenosine triphosphate concentration was significantly better in group 1 animals (95%) than in group 2 animals (30%) (p less than 0.02), and recovery of the phosphocreatine concentration was also better in group 1 animals (93%) than in group 2 animals (32%) (p less than 0.02). Intracellular pH recovered in group 1 animals, but not in group 2 animals. Regional biochemical assays of metabolites performed in the group 2 piglets and in five pilot piglets exposed to deep hypothermia generally confirmed the spectroscopic findings but demonstrated considerable regional variation, specially in the group 2 piglets' brains.
We conclude that hypothermia exerts a protective effect on the piglet brain during global ischemia even after the adenosine triphosphate pool has been completely depleted.
Myoendothelial junctions in human brain arterioles.
Authors: Aydin F , Rosenblum W I , Povlishock J T 
Published: June 2011

The purpose of this work was to determine whether myoendothelial junctions were present in human brains.
We examined vessels of approximately 30-70 microns i.d. from the brains of five autopsied adult patients. Myoendothelial junctions were found in vessels throughout this range, in both surface arterioles and penetrating arterioles, and were classified into three types. The number of myoendothelial junctions, expressed per unit length of vessels, was five times greater in the smallest than in the largest vessels. Thus, we found 1.62 junctions per millimeter length in arterioles less than 60 microns diameter and 0.31 junctions per millimeter length in arterioles greater than 220 microns diameter.
These findings provide an anatomic basis for communication between endothelial cells and smooth muscle of brain microvessels in humans. The function of this intercellular communication is not yet known; however, findings in animals suggest that endothelium may be required for propagated constriction in brain vessels. The existence of myoendothelial junctions in human brain provides a basis for the hypothesis that propagated constriction depends on transmission of some message or messenger between endothelial cells and muscle.
Stroke in a young adult with familial plasminogen disorder.
Authors: Furlan A J , Lucas F V , Craciun R , Wohl R C 
Published: June 2011

We report a new plasminogen disorder detected in a 29-year-old man with a cerebellar infarct. To our knowledge, plasminogen disorders have not been previously linked with stroke.
Tests for well-recognized causes of stroke were negative. However, a screening hypercoagulation profile indicated low functional levels of plasminogen activity. Immunologic plasminogen (Laurell technique) was 64% of normal (normal level, 80-130%). The rate of plasmin generation induced by adding urokinase to plasma was also low. Plasminogen activator, free protease, and alpha 2-plasmin inhibitor levels were normal. Family studies detected a similar plasminogen abnormality in the patient's mother and 9-year-old son, both of whom are asymptomatic.
Our patient shows a congenital, heterozygous, functionally abnormal plasminogen. Although the exact relationship to stroke is unclear, we suggest screening young patients with unexplained stroke for plasminogen defects using commercially available assay systems.
Hypothermia reduces 72-kDa heat-shock protein induction in rat brain after transient forebrain ischemia.
Authors: Chopp M , Li Y , Dereski M O , Levine S R , Yoshida Y , Garcia J H 
Published: June 2011

We examined the influence of concurrent moderate hypothermia (30 degrees C) and transient forebrain ischemia on the induction of 72-kDa heat-shock protein and neuronal damage in male Wistar rats.
Experimental groups included: normothermic with 8 minutes of transient forebrain ischemia (group 1, n = 7), hypothermic without ischemia (group 2, n = 9), and hypothermic (30 degrees C) with 8 minutes of transient forebrain ischemia (group 3, n = 5). Intense 72-kDa heat-shock protein immunoreactivity was demonstrated in rat forebrain 48 hours after induction of normothermic forebrain ischemia (group 1); it was not detected in the brain of animals subjected to hypothermia without ischemia (group 2), and hypothermia during ischemia (group 3) significantly inhibited its expression compared with that in normothermic ischemia animals (group 1).
These observations suggest that 72-kDa heat-shock protein induction is not the mechanism by which moderate hypothermia protects against ischemic cell damage.
Cerebral infarction associated with protein C deficiency.
Authors: Matsushita K , Kuriyama Y , Sawada T , Uchida K 
Published: June 2011

A deficiency of plasma protein C, both the hereditary and acquired types, is one cause of thromboembolic disease. Several antineoplastic agents have been reported to decrease the production of protein C in the liver by impairing either the absorption or metabolism of vitamin K, leading to acquired protein C deficiency.
We treated a young woman with protein C deficiency, who had developed a cerebral infarction of the right parietal cortex of sudden onset. On admission, the antigenic level of plasma protein C was 38%. Serial cerebral angiography revealed occlusion of the right middle cerebral artery, which subsequently recanalized completely. This patient had taken fluorouracil derivatives orally for as long as 3 years following a left mastectomy for stage II breast cancer. Tests revealed that the patient's mother had only one-half the normal activity of plasma protein C despite a normal antigenic level.
We speculate that the etiology of the cerebral infarction in this patient might involve an embolic mechanism associated with protein C deficiency induced by an interaction between inherited and acquired factors.
Granulocyte adhesion, deformability, and superoxide formation in acute stroke.
Authors: Grau A J , Berger E , Sung K L , Schmid-Schönbein G W 
Published: June 2011

Impaired rheological properties of as well as cytotoxic substances produced by granulocytes may contribute to tissue damage in acute ischemic stroke. To assess changes in the properties of circulating granulocytes, we measured their adhesion, deformability, and superoxide generation in the first 3 days after ischemic stroke.
Granulocytes from 18 male patients and 20 age- and risk-matched controls were investigated. Adhesion to murine laminin-, human fibronectin-, and bovine serum albumin-coated surfaces was measured with and without the stimulus phorbol myristate acetate and the antiadhesion antibody IB4. Superoxide anion formation was assessed by the reduction of ferricytochrome C. In a subgroup of 10 patients and 11 controls, granulocyte deformability was determined using the micropipette aspiration technique.
The patients had significantly greater granulocyte adhesion to laminin (p less than 0.005) and fibronectin (p less than 0.05) but not bovine serum albumin. Cell stimulation enhanced the differences between the groups, whereas the antiadhesion antibody inhibited adhesion in both patients and controls. There were no significant differences in granulocyte deformability. Superoxide production by granulocytes was significantly lower in the patients without the stimulus (p less than 0.05) and with 10 nM phorbol myristate acetate (p less than 0.005).
These findings suggest that circulating granulocytes in ischemic stroke exhibit increased adhesive properties, a feature that represents one of the risk factors for granulocyte entrapment, impairment of microvascular flow, and tissue injury.
Sustained damage to energy metabolism of brain regions after microsphere embolism in rats.
Authors: Takeo S , Taguchi T , Tanonaka K , Miyake K , Horiguchi T , Takagi N , Fujimori K 
Published: June 2011

Information on sustained damage to cerebral function and metabolism after cerebral ischemia is useful for prophylaxis and therapeutics of cerebral infarction. The purpose of the present study was to induce sustained damage to brain regions after cerebral ischemia in experimental animals. For this purpose, we examined animal behavior and cerebral energy metabolism following microsphere embolism in rats.
We injected 900 microspheres (48 microns in diameter) into the right internal carotid artery of 110 rats and determined the time course of changes in the rats' behavior and the energy metabolism of the cortex, striatum, and hippocampus of both hemispheres. We injected the same volume of vehicle, without microspheres, into 28 sham-operated rats; there were 14 nonoperated control rats.
Peak increase in lactate content and decrease in adenosine triphosphate and creatine phosphate of these brain regions of the right hemisphere were seen on the first day after microsphere embolism, whereas peak increases in glucose and glycogen contents of these regions were observed on the third day. Most of the metabolic alterations in all these regions continued for up to 28 days after operation, although they recovered toward control levels with time after the operation. The extent and trend of metabolite changes of the right hemisphere after microsphere embolism were similar in the three brain regions. In the left hemisphere, similar metabolic changes were observed, but to a lesser degree. The time course of changes in behavioral scores following microsphere embolism revealed marked stroke-like symptoms on the first day and relatively rapid disappearance of the symptoms with time after embolism.
Microsphere embolism is capable of inducing widespread, sustained damage to energy metabolism of brain regions.
Protective effects of human recombinant superoxide dismutase on transient ischemic injury of CA1 neurons in gerbils.
Authors: Uyama O , Matsuyama T , Michishita H , Nakamura H , Sugita M 
Published: June 2011

It has been postulated that oxygen-derived free radicals are produced in significant quantities upon reperfusion of ischemic brain and that the free radicals play a pivotal role in triggering the ischemic neuronal damage causing delayed neuronal death. This study was undertaken to examine the effects of human recombinant superoxide dismutase on the delayed neuronal death of CA1 neurons and on the change in the expression of messenger ribonucleic acid for endogenous copper-zinc superoxide dismutase after transient ischemia.
Human recombinant superoxide dismutase (8 x 10(5) units/kg) or apo-superoxide dismutase was administered intravenously 1 minute before bilateral carotid artery occlusion in gerbils divided among four experimental groups. Endogenous copper-zinc superoxide dismutase messenger ribonucleic acid was analyzed by in situ hybridization histochemistry using a sulfur-35-labeled oligonucleotide probe. Immunohistochemical localizations of administered human recombinant superoxide dismutase were investigated.
All gerbils receiving apo-superoxide dismutase exhibited almost complete destruction of CA1 neurons 7 days after 5 minutes of ischemia. The gerbils treated with human recombinant superoxide dismutase showed mild lesions (p less than 0.01). Discrete localizations were observed for endogenous copper-zinc superoxide dismutase messenger ribonucleic acid. Transient ischemia increased labeling throughout the hippocampus after 30 minutes and 24 hours of reperfusion. This increase was abolished by treatment with human recombinant superoxide dismutase. This phenomenon was confirmed by Northern blot analysis. The interneurons in CA3 and cells in the hilus were mainly stained against administered superoxide dismutase at 5 and 30 minutes, and these reactions had disappeared at 20 hours after the administration.
Our data demonstrate protective effects of human recombinant superoxide dismutase against ischemic neuronal damage and support the hypothesis that the generated free radicals induce a vicious cycle leading to delayed neuronal death.
Stroke incidence rates were unchanged, while fatality rates declined, during 1971-1987 in Göteborg, Sweden.
Authors: Harmsen P , Tsipogianni A , Wilhelmsen L 
Published: June 2011

Stroke risk factors have been shown to change with time in several places; simultaneously, stroke incidence rates have increased in some and decreased in other places. In Göteborg, Sweden, cardiovascular epidemiological research has included stroke registration since 1971. From these data on stroke, incidence and fatality rates from a 17-year period are given.
During the period 1971-1987 all cases of stroke occurring in people aged 15-65 years in the city of Göteborg were uniformly recorded, with an estimated case detection rate of 90% or more.
Age-adjusted incidence rates of first-ever stroke by sex did not change during the period. Age-specific rates and rates for individual types of stroke (subarachnoid hemorrhage, intracerebral hemorrhage, and cerebral infarction-unspecified stroke combined) were also largely unchanged. A slight increase in the incidence rate of intracerebral hemorrhage may be due to better detection after computed tomography came into use in 1976. Stroke fatality rates declined through the whole period in both sexes and all age groups, markedly so for intracerebral hemorrhage and subarachnoid hemorrhage.
This conforms with vital statistics for Göteborg and for Sweden of declining stroke mortality during the period. The decline in stroke fatality rates may be related to decreases in smoking habits and blood pressure together with an increase in the percentage of people on antihypertensive treatment among middle-aged men, and to some extent even middle-aged women, reported from the same population. Why stroke incidence rates did not decline concomitantly is unexplained.
Anosognosia in patients with cerebrovascular lesions. A study of causative factors.
Authors: Starkstein S E , Fedoroff J P , Price T R , Leiguarda R , Robinson R G 
Published: June 2011

Psychological and biological hypotheses have been proposed to explain anosognosia. We correlated the presence of anosognosia with the presence and severity of psychiatric disturbances, neglect, intellectual impairments, and computed tomographic evidence of lesion size, location, and measurements of brain atrophy.
A series of 80 patients with acute stroke were assessed using a battery of psychiatric and neuropsychological tests and computed tomography.
There were five main findings. First, 27 (28%) of the 96 patients originally screened showed anosognosia. Second, patients with anosognosia had significantly higher frequencies of hemispatial neglect and related phenomena, as well as deficits in recognizing facial emotions and in receptive prosody. Third, depression was equally frequent among patients with and without anosognosia. Fourth, patients with anosognosia had a significantly higher frequency of right hemisphere lesions, primarily involving the temporoparietal junction, thalamus, and basal ganglia. Fifth, patients with anosognosia showed significantly more subcortical brain atrophy, primarily involving the frontal white matter and diencephalic areas.
The present study demonstrates that anosognosia does not "protect" stroke patients from depressive feelings; rather, it represents arousal-attentional disorders after lesions in specific areas of the right hemisphere in nonaphasic patients with preexisting subcortical atrophy.