bluuebunny/crossref_metadata_2025_split huggingface dataset:
Inhibition of Inducible Nitric Oxide Synthase Restores Endothelium-Dependent Relaxations in Proinflammatory Mediator-Induced Blood Vessels
Authors: Kessler Paul , Bauersachs Johann , Busse Rudi , Schini-Kerth Valerié B. 
Published: June 2011

AbstractEndothelium-dependent relaxations mediated by nitric oxide (NO) are attenuated in arteries exposed to proinflammatory mediators. Because proinflammatory mediators stimulate the expression of the inducible NO synthase (iNOS) in vascular cells, the role of iNOS-derived NO in the impaired endothelium-dependent relaxation was examined in arterial ring preparations. Exposure of rabbit carotid arteries to interleukin-1 β (IL-1 β; 100 U/mL for 7 hours) and porcine coronary arteries to a combination of tumor necrosis factor-α (1000 U/mL), interferon-γ (500 U/mL), and lipopolysaccharide (10 μg/mL) for 15 hours (conditions that are associated with iNOS expression) markedly attenuated relaxations to receptor-dependent agonists, whereas those to the calcium ionophore A23187 and sodium nitroprusside were virtually unchanged. The impaired relaxation was not associated with a reduced level of the constitutive endothelial NOS (cNOS) but was accompanied by a reduced formation of biologically active NO as assessed in a bioassay system. The attenuated relaxation of carotid arteries to acetylcholine was not affected by superoxide dismutase and was neither found in arteries exposed to IL-1 β for only 15 minutes nor in IL-1 β-treated arteries for 7 hours followed by a 17-hour incubation period without the cytokine. Furthermore, no impaired relaxation was found in rings exposed to IL-1 β in combination with either cycloheximide orN-α-tosyl-l-lysine chloromethyl ketone or pyrrolidine dithiocarbamate, treatments that prevent iNOS expression. In addition, selective inhibition of iNOS withS-methylisothiourea (10 μmol/L) completely restored acetylcholine-induced relaxations.These findings indicate that the continuous generation of NO induced by proinflammatory mediators plays a major role in the inhibition of endothelium-dependent relaxation, most likely by impairing a step in the signal transduction cascade that links activation of endothelial receptors to the calcium-calmodulin-dependent activation of NOS.
Metabolic Changes in Response to Acute Cerebral Ischemia Following Unilateral Carotid Artery Ligation in Arteriosclerotic Versus Nonarteriosclerotic Rats
Authors: WEXLER BERNARD C. , SAROFF JACK 
Published: June 2011

The left carotid artery of arteriosclerotic and nonarteriosclerotic male and female rats was surgically ligated to induce a state of cerebral ischemia. The animals promptly developed signs of cerebral impairment and were sacrificed 2, 4, 6, 8, 10, 12, 24, and 48 hours later to determine what dynamic pathophysiological changes attend acute cerebral ischemia.
Several of the arteriosclerotic animals developed myocardial infarcts concomitant with the cerebral edema, hemorrhage, necrosis, and leptomeningitis observed in general. All of the experimental animals manifested necrosis and fatty infiltration of the liver, and their adrenal glands were hypertrophied, hemorrhagic, and depleted of lipid.
Serum creatine phosphokinase and glutamic oxalacetic transaminase rose abruptly after 24 hours of cerebral ischemia. Triglycerides, free fatty acids, and cholesterol alterations were in keeping with intense lipid mobilization, dissolution of peripheral adipose tissue sites, and fatty metamorphosis of the liver. The animals also showed marked hyperglycemia and increased secretion of corticosterone. These investigations indicate that acute cerebral ischemia is a severe stress and will elicit dynamic alterations in serum parameters such as enzymes, lipids, glucose, and the adrenocortical stress hormones. Animals with pre-existing arteriosclerosis manifest more untoward effects and greater excursion in serum metabolic parameters than nonarteriosclerotic subjects.
Nationwide Cerebrovascular Disease Morbidity Study
Authors: KULLER LEWIS , ANDERSON HERBERT , PETERSON DONALD , CASSEL JOHN , SPIERS PHILLIP , CURRY HIRAM , PAEGEL BERTHA , SASLAW MILTON , SISK CHARLES , WILBER JOSEPH , MILLWARD DAVID , WINKELSTEIN WARREN , LILIENFELD ABRAHAM , SELSTER RAYMOND 
Published: June 2011

Previous studies have noted that the geographic differences in stroke mortality among areas of the United States were not due to artifacts of certification practices or accuracy of the diagnosis. A study of hospitalized stroke patients was completed in order to determine whether the mortality differences were due to a higher incidence or case fatality following a stroke in areas with high stroke death rates. Eight of the nine areas that participated in the Nationwide Mortality Study were included in this study. A total of 2,619 stroke cases were ascertained including 1,631 (62.3%) who were alive at the time of hospital discharge, 937 (35.8%) dead at discharge, 46 (1.7%) who were discharged alive but died outside of the hospital, and five (0.2%) who were dead at discharge and certified by the medical examiner.
The incidence of stroke was higher in the high stroke death rate areas especially for men. The ratio of the incidence of stroke in men as compared to women was higher in the younger age groups (45–54, 55–64) and in the high-incidence as compared to low-incidence areas.
The case-fatality percentage was lowest in Denver and highest in South Carolina. Presence of coma on admission was the principal determinant of subsequent mortality in all areas.
Finally, there was no consistent difference in the distribution of symptoms of stroke among the areas, and diagnostic procedures were performed more often in urban than rural areas. Approximately 80% of the stroke cases could be substantiated by either an autopsy verifying diagnosis, arteriography, hemorrhagic spinal fluid, hemiplegia or coma on admission. Several hypotheses to explain the differences have been suggested as well as the need for new information.
Abnormal Hemispheric Blood Flow and Metabolism Despite Normal Angiograms in Patients with Stroke
Authors: MEYER JOHN STIRLING , SHINOHARA YUKITO , KANDA TADASHI , FUKUUCHI YASUO , KOK NORMA K. , ERICSSON ARTHUR DALE 
Published: June 2011

Hemispheric blood flow (HBF) and metabolism were measured using the intracarotid injection of hydrogen-saturated saline in a group of patients with unilateral hemispheric infarction, some of whom had normal angiograms.
Blood flow was calculated from the formula derived from the Stewart-Hamilton principle using the clearance curve of hydrogen in the cerebral transverse sinus. Hemispheric metabolic index was estimated using a newly developed formula by assuming that the distribution of hydrogen into each transverse sinus following intracarotid injection indicates the distribution of blood from each hemisphere into each transverse sinus.
HBF and oxygen metabolism on the affected side were reduced in all groups, but the reduction was greater in patients with angiographical evidence of vascular occlusion.
In many patients, HBF and metabolism on the nonaffected side which angiograms showed to be normal were reduced in the acute phase.
It is apparent that by using the hydrogen bolus technique of measuring HBF and metabolism, small disturbances in cerebral circulation can be detected which are not discernible in angiograms.
Reflections on "The Subclavian Steal"
Authors: FIELDS WILLIAM S. 
Published: June 2011

Reversal of blood flow in the vertebral artery, demonstrated by angiography, was reported ten years ago and immediately given the colorful name of "The Subclavian Steal." Since then, numerous articles have appeared, in English and other languages, reporting both clinical and arteriographical descriptions of the phenomenon.
A search of the literature has turned up a most interesting early report in which cerebrovascular symptoms were ascribed to the hemodynamic alterations. This case report appeared almost 100 years prior to the aforementioned article in the modern medical literature.
It was further suggested by the physician describing this case that ligature of the vertebral artery would be the treatment of choice in the relief of symptoms.
Noradrenergic Mediation of Experimental Cerebrovascular Spasm
Authors: FRASER R. A. R. , STEIN B. M. , BARRETT R. E. , POOL J. L. 
Published: June 2011

Catecholamine fluorescent techniques demonstrate an abundant noradrenergic periarterial nerve plexus in the adventitia of the major intracranial vessels. After repeated spasm of these vessels, a marked reduction to complete absence of catecholamine fluorescence is noted. Seemingly, an exhaustion of noradrenalin stores from the nerve terminals has taken place. This has suggested the possibility of noradrenergic mediation of cerebrovascular spasm. Pharmacological depletion of the noradrenalin stores of this plexus produces a dilated vessel, but blood-induced vasospasm is not prevented. Alpha adrenergic blockade at the receptor prevents the induction of vasospasm and dilates both normal and spastic vessels above normal caliber.
These data suggest that cerebral vasospasm is produced by substances acting at the alpha adrenergic receptor of the vessel wall, and that blood contains a vasoconstrictor substance capable of acting at the receptor site.
Quantitative Comparison of Passive Motion and Tendon Reflex Responses in Biceps and Triceps Brachii Muscles in Hemiplegic or Hemiparetic Man
Authors: SIMONS DAVID G. , BINGEL A.G. A. 
Published: June 2011

The clinical impression that severe hyperreflexia is not consistently associated with severe spasticity in hemiplegia or hemiparesis due to vascular pathology was tested by objective measurement in 11 patients. The intensity of tendon reflex responses of the triceps and biceps brachii muscles was measured as the reflex sensitivity ratio (evoked twitch tension/stimulating hammer force). The degree of spasticity was measured as the threshold rate of elbow flexion or extension above which a myotatic response was elicited, determined by both a sudden increase in passive resistance and a burst of antagonist electromyographical activity.
Rate thresholds were rank ordered for flexion data and for extension data with their corresponding reflex sensitivity ratios. Numerous individual discrepancies stood out. Correlation coefficients between rate thresholds and reflex sensitivities determined at two elbow angles were -0.52 and -0.35 during extension, and -0.47 and 0.03 during flexion.
Differences in rate of stretch, differences in the sensory structures stimulated, and differences in the distortion of the organization of motor control may account for the difference in responses to the two tests.
Fatal Foam Cell Arteritis of the Brain After Irradiation for Hodgkin's Disease: Angiography and Pathology
Authors: KAGAN A. ROBERT , BRUCE DANIEL W. , DI CHIRO GIOVANNI 
Published: June 2011

A case of foam cell arteritis of the brain following irradiation of the neighboring structures for Hodgkin's disease is described. A differential diagnosis of the unique angiographical findings is presented.
The etiology of foam cell arteritis restricted to the brain is considered. It is hoped that the experience of this case encourages a careful neuroradiological and neuropathological examination of the brain in all patients with Hodgkin's disease who present with the stroke syndrome.
Cerebral Atherosclerosis in Japanese. I. Age Related to Atherosclerosis
Authors: NAKAMURA M. , YAMAMOTO H. , KIKUCHI Y. , ISHIHARA Y. , SATA T. , YOSHIMURA S. 
Published: June 2011

During a period of approximately two years (1965 through 1966), 717 intracranial cerebral arteries (males and females) were obtained from the medicolegal autopsy cases. Systematic grading of the macroscopic severity of cerebral atherosclerosis was performed and the results were reported. In general, cerebral atherosclerosis appeared as early as the second decade and increased in severity with age, particularly at the fifth decade in males and the sixth decade in females. The prevalence of localization of early and/or severe cerebral atherosclerosis was studied. The results in the present study were not the same as in the previous investigations on Caucasians. The common sites of the severe cerebral atherosclerosis causing marked lumen narrowing were the proximal portion of posterior cerebral arteries, peripheral portion of the middle cerebral arteries, and the vertebral arteries and their fusing site at the basilar artery; the internal carotid artery was the least commonly involved.
In the present study, the influence of sex in the production of cerebral atherosclerosis was suggested, and the simple senescence theory of cerebral atherosclerosis was not supported. The macroscopic severity of cerebral atherosclerosis of Japanese in the present study appeared to be equal to or slightly greater than that in Americans and Norwegians reported by Baker et al.
Intimal Fibroplasia of the Internal Carotid Arteries
Authors: SUKOFF M. H. , DORSEY T. J. , JOHNSON D. A. , HEPPS S. A. , BERGGREN R. L. 
Published: June 2011

Intimal fibroplasia of the extracranial internal carotid arteries can cause symptoms of transient neurological deficit in young patients which are similar to the transient ischemic attacks of arteriosclerotic origin.
The clinical, angiographical and histological features of such a case are presented and discussed.
Cerebral Embolization: Prospective Clinical Analysis of 42 Cases
Authors: MEYER JOHN STIRLING , CHARNEY JONATHAN Z. , RIVERA VICTOR M. , MATHEW NINAN T. 
Published: June 2011

The sites, sources, and incidence of cerebral embolization were established in an unselected series of hospitalized patients using recommended epidemiological criteria. Criteria for diagnosis of cerebral embolization as a cause of stroke are defined.
Forty-two (15%) from a total of 280 patients with various forms of cerebrovascular disease were diagnosed as having cerebral embolization. The epidemiology has been altered by antibiotics and cardiac surgery, particularly the use of prosthetic heart valves. In this series, the mortality rate was 9.5%, which is lower than in previously reported series probably due to emergency medical treatment. The heart was the most common source. Prosthetic heart valves emerged as the most common source of emboli in this series. Ulcerated plaques of the carotid arteries in the neck ranked second. Seizures occurred in 42.8% of cases. The left cerebral hemisphere was involved approximately twice as frequently as the right one.
Possible explanations based on the anatomy of the great vessels are described which predispose to embolization of the left carotid artery. Recommendations are suggested for preventing further embolization and for treatment of acute embolic cerebral infarction by the use of anticonvulsant drugs and hyperosmolar agents designed to reduce cerebral edema.
Effect of indomethacin on edema following single and repetitive cerebral ischemia in the gerbil.
Authors: Deluga K S , Plötz F B , Betz A L 
Published: June 2011

Repetitive periods of cerebral ischemia result in more severe injury than a single period of ischemia of similar total duration. We investigated the possibility of prostaglandin mediation of this increased injury by attempting to modify brain edema formation with indomethacin pretreatment.
Under halothane/N2O anesthesia, groups of gerbils underwent bilateral carotid occlusion to induce forebrain ischemia. Group I underwent a single 15-minute period of carotid occlusion. Group II underwent three 5-minute periods of occlusion at hourly intervals. Groups III and IV were similar to groups I and II, respectively, but received 0.2 mg/kg indomethacin before carotid occlusion. Cortical and cerebellar water and sodium contents were determined in control animals (n = 6) at time zero and in experimental animals 24, 48, and 72 hours after ischemia (n = 6-10 gerbils/group at each time point).
Cortical water and sodium contents in group II peaked 48 hours after insult (82.15 +/- 0.31% and 420 +/- 14 meq/kg dry wt, respectively) and were significantly higher than control and group I values at both 24 and 48 hours. Cortical water did not change from control in group I animals. Indomethacin pretreatment significantly attenuated increases in water and sodium content seen at 48 hours in gerbils undergoing repetitive ischemia (peak 80.02 +/- 0.45% and 300 +/- 39 meq/kg dry wt), but did not affect mortality.
Indomethacin lessens edema after repetitive cerebral ischemia, suggesting that elevations of cyclooxygenase products are responsible, at least in part, for severe brain edema following repetitive ischemia.
Protective effect of flunarizine on blood-brain barrier permeability alterations in acutely hypertensive rats.
Authors: Nag S 
Published: June 2011

Increased cerebrovascular permeability to protein is a well-documented finding in acute and chronic hypertension. In this study, we examined the effect of pretreatment with a calcium entry blocker, flunarizine, on the increased cerebrovascular permeability to protein that develops in norepinephrine-induced acute hypertension.
Protein transfer was assessed qualitatively with Evans blue dye and quantitatively with iodine-125-labeled serum albumin.
Brains of hypertensive rats showed increased permeability to both tracers. The number and size of the areas of Evans blue extravasation were smaller in the hypertensive groups pretreated with flunarizine intravenously. This was supported by the quantitative studies, which demonstrated a significant decrease in protein transfer in total brain of hypertensive rats pretreated with intravenous flunarizine, 1 mg/kg (p less than 0.005) and 2.5 mg/kg (p less than 0.001). Data from individual brain regions showed that pretreatment with flunarizine resulted in significant reduction of protein transfer in most brain regions.
These data support the hypothesis that calcium plays a role in increased cerebral endothelial permeability in hypertension.
Cholinergic deafferentation after focal cerebral infarct in rats.
Authors: Kataoka K , Hayakawa T , Kuroda R , Yuguchi T , Yamada K 
Published: June 2011

For a better understanding of neuronal network disturbances after stroke, we investigated the changes in the cholinergic system after experimental focal infarct.
We quantitatively evaluated the highly sensitive acetylcholinesterase histochemistry and local glucose utilization 7 days after left middle cerebral artery occlusion in Wistar rats.
In all rats with occlusion, the ipsilateral frontal cortex and the nucleus basalis Meynert developed no infarct, whereas the subcortical striatum did. In the frontal cortex on the occlusion side, the acetylcholinesterase-positive fiber density was significantly (p less than 0.05) reduced; a computer-assisted image-analyzing system quantified approximately 1.0 m/mm3 brain cortex acetylcholinesterase-positive fibers in the ipsilateral frontal cortex layers II-IV and approximately 9.7 m/mm3 brain cortex acetylcholinesterase-positive fibers in the contralateral frontal cortex layers II-IV. Local glucose utilization was also significantly (p less than 0.05) decreased in the ipsilateral frontal cortex compared to the contralateral side and sham-operated animals.
These results suggest that functional disturbances and disruption of the cholinergic pathway between the frontal cortex and the nucleus basalis Meynert occur after middle cerebral artery occlusion in rats.
Cerebellar glutamine synthetase in children after hypoxia or ischemia.
Authors: Dao D N , Ahdab-Barmada M , Schor N F 
Published: June 2011

Glutamate has been implicated in the pathophysiology of acute hypoxic-ischemic encephalopathy. Glutamine synthetase is an enzyme found in astrocytes that converts glutamate to its nontoxic analogue, glutamine. The present study tests the hypothesis that brain glutamine synthetase activity increases in response to acute hypoxic-ischemic insults and not in response to chronic hypoxia-ischemia or non-hypoxic-ischemic neurological disease.
Frozen sections of cerebellum from children who died with acute or chronic hypoxic-ischemic insults or chronic non-hypoxic-ischemic neurological disease were spectrophotometrically assayed for glutamine synthetase activity by an observer who was blinded to the clinical group assignment of each specimen. Enzyme activity was elevated in specimens from children with acute hypoxic-ischemic insults (mean 6.5; range 5.4-7.2 units/g wet tissue wt) as compared with those from patients with chronic hypoxia-ischemia (mean 2.8; range 0.7-10.2 units/g wet tissue wt) or with non-hypoxic-ischemic neurological disease (mean 2.6; range 1.3-3.9 units/g wet tissue wt). This difference was not due to differences in the degree of histological astrocytosis or edema among the specimens. Statistical analysis by the Kruskal-Wallis one-way analysis of variance by ranks test indicates that the three data groups do not come from one population (p less than 0.05).
These results support the notion that glutamine synthetase activity increases in response to acute hypoxic-ischemic nervous system injury in children and that other compensatory mechanisms prevail in the case of chronic hypoxic-ischemic insults.
Cerebrovascular effects of angiotensin converting enzyme inhibition involve large artery dilatation in rats.
Authors: Postiglione A , Bobkiewicz T , Vinholdt-Pedersen E , Lassen N A , Paulson O B , Barry D I 
Published: June 2011

The aim of the study was to selectively examine the effects of converting enzyme inhibition on the large brain arteries by using concomitant inhibition of carbonic anhydrase to cause severe dilatation of mainly parenchymal resistance vessels.
Cerebral blood flow was measured using the xenon-133 injection technique in three groups of Wistar rats either during carbonic anhydrase inhibition with acetazolamide (treatment A, n = 8), during carbonic anhydrase inhibition followed by converting enzyme inhibition with captopril 40 minutes later (treatment B, n = 10), or during carbonic anhydrase inhibition preceded by converting enzyme inhibition 20 minutes earlier (treatment C, n = 7).
After treatment A, cerebral blood flow rose rapidly and stabilized within 20 minutes at an average of 220 ml/100 g.min; flow remained stable until at least 60 minutes. After treatment B, cerebral blood flow increased by a further 17.4%, from an average of 219 ml/100 g.min to an average of 257 ml/100 g.min (p less than 0.01). After treatment C, cerebral blood flow stabilized at an average of 238 ml/100 g.min, with flow from 20 to 60 minutes always being higher (from 5% to 17%) than during carbonic anhydrase inhibition alone (p less than 0.02). Thus the additional inhibition of converting enzyme resulted in higher cerebral blood flow than during inhibition of carbonic anhydrase alone.
These results suggest that converting enzyme inhibition reduced resistance of large brain arteries and support the hypothesis that there is some angiotensin II-induced tone in large cerebral arteries.