bluuebunny/crossref_metadata_2025_split huggingface dataset:
Endothelium-derived nitric oxide synthase inhibition. Effects on cerebral blood flow, pial artery diameter, and vascular morphology in rats.
Authors: Prado R , Watson B D , Kuluz J , Dietrich W D 
Published: June 2011

We determined the effects of inhibiting the production of cerebral endothelium-derived nitric oxide on pial artery diameter, cortical blood flow, and vascular morphology.
An inhibitor of endothelium-derived nitric oxide synthesis, NG-nitro-L-arginine methyl ester hydrochloride (L-NAME), or an equivalent volume of 0.9% saline was infused into rats intra-arterially in a retrograde fashion via the right external carotid artery at a rate of 3 mg/kg/min to a total dose of 190 mg/kg or intravenously at 1 mg/kg/min to a total dose of 15 mg/kg. Large pial arteries were continuously visualized through an operating microscope, and cortical cerebral blood flow was monitored by laser-Doppler flowmetry. To localize areas of morphological interest, the protein tracer horseradish peroxidase was injected 15 minutes before termination of the L-NAME infusion and the rats were perfusion-fixed 15 minutes later for light and electron microscopic analysis.
Infusion of L-NAME significantly raised arterial blood pressure at both doses (for 190 mg/kg, from 103.2 +/- 3.4 to 135 +/- 3.4 mm Hg; for 15 mg/kg, from 125 +/- 2.8 to 144.4 +/- 4.0 mm Hg). Pial arteries constricted within 10 minutes after the start of the intracarotid infusion to 40% of the preinfusion diameter, while cortical cerebral blood flow decreased to an average of 72.5% of that at baseline. Morphological abnormalities in the experimental rats included microvascular stasis and focal areas of blood-brain barrier disruption to protein. Ultrastructural examination of cortical leaky sites revealed constricted arterioles with many endothelial pinocytotic vesicles and microvilli.
These observations suggest that inhibition of endothelium-derived nitric oxide synthesis affects the relation between cerebral arterial diameter and cerebral blood flow and can lead to subtle cerebral vascular pathological changes consistent with focal brain ischemia.
Early changes in rabbit cerebral artery reactivity after subarachnoid hemorrhage.
Authors: Debdi M , Seylaz J , Sercombe R 
Published: June 2011

Subarachnoid hemorrhage frequently leads to long-term cerebral artery narrowing called vasospasm. Very early changes in cerebral arteries have not been studied extensively and may be critical for the later pathological developments. We therefore determined what changes in the reactivity of cerebral arteries could be observed after 10 minutes' or 24 hours' contact with subarachnoid blood.
Ten minutes or 24 hours after the injection of blood or physiological solution (sham hemorrhage) into the cisterna magna of anesthetized rabbits or no injection (control rabbits), segments of the middle cerebral, basilar, and vertebral arteries were removed for conventional in vitro tension measurements. Concentration-response curves to four endogenous constrictors likely to be released after hemorrhage were obtained, and the maximum relaxation to acetylcholine was determined.
There were no significant differences between the sham hemorrhage and control groups. Compared with control rabbits, treated animals showed increased reactivity to uridine triphosphate in the basilar and vertebral arteries at 10 minutes but not at 24 hours, whereas reactivity was increased in the middle cerebral artery only at 24 hours. Reactivity to serotonin was greatly increased in all arteries at both latencies (up to 2.7 times). Reactivity to noradrenaline was unchanged in the basilar and vertebral arteries at 10 minutes; reactivity in both the basilar and middle cerebral arteries was increased at 24 hours, which is compatible with denervation supersensitivity. There were only minor changes in the reactivity to histamine, and only at 10 minutes. Relaxation to acetylcholine was increased for the middle cerebral artery at 10 minutes but otherwise was not significantly changed.
Reactivity to uridine triphosphate, serotonin, and noradrenaline greatly increases by 10 minutes to 24 hours after subarachnoid hemorrhage, and this increase is not owing to the mechanical effects of intracranial hypertension, nor is it related to impaired endothelium-dependent relaxation. It is suggested that these and other spasmogens cause excessive muscular calcium loading with a very rapid onset after subarachnoid hemorrhage.
Fatal basilar vasculopathy complicating bacterial meningitis.
Authors: Perry J R , Bilbao J M , Gray T 
Published: June 2011

Bacterial meningitis complicated by thrombosis, vasculitis, and aneurysm formation affecting both small and distal branches of cerebral vessels has been well described. Involvement of major cerebral vessels is rare and has only been documented late in the course of disease.
We describe the clinical and pathological findings in a young man who presented with pontine infarction as an early manifestation of bacterial meningitis. Streptococcus milleri, an unusual organism in this setting, was cultured. Despite improvement with antibiotic therapy, the patient experienced fatal subarachnoid hemorrhage. A ruptured inflammatory aneurysm of the basilar artery, evidence of residual meningitis and vasculitis, and basilar thrombosis associated with pontine infarction were found.
Bacterial meningitis, which may be associated with severe vasculopathy of the basilar artery and lead to cerebral infarction, aneurysm formation, and subarachnoid hemorrhage, should be considered in the differential diagnosis of these conditions. The role of S. milleri in meningitis and its vascular complications merits further study.
Dementia associated with lacunar infarction.
Authors: Loeb C , Gandolfo C , Croce R , Conti M 
Published: June 2011

The purpose of this study was to assess the number of patients with lacunar lesions who develop dementia and to evaluate in patients with and without dementia the relevance of risk factors for cerebrovascular disease, the occurrence of leukoaraiosis, the volume and location of vascular lesions, the size of ventricular and subarachnoid spaces, and stroke recurrence.
One hundred eight patients in whom computed tomograms revealed lacunar lesions that could account for their clinical neurological pictures were followed up for an average of 4 years after their first lacunar stroke.
Twenty-five patients (23.1%) developed dementia. The prognosis regarding occurrence of dementia during the follow-up period, evaluated by the Kaplan-Meier method, was significantly worse in subjects with the greatest evidence of cerebral atrophy (p less than 0.009) and in subjects who underwent new focal cerebrovascular episodes (p less than 0.000001). No differences were seen in the frequency of vascular risk factors or the site or volume of lesions between the demented and nondemented groups.
Patients with lacunar infarcts suffer from dementia 4-12 times more frequently than the normal population. Cerebral atrophy and recurrent stroke, as well as other as-yet unclarified factors, are involved in producing dementia.
Cigarette smoking, alcohol use, and subarachnoid hemorrhage.
Authors: Longstreth W T , Nelson L M , Koepsell T D , van Belle G 
Published: June 2011

Subarachnoid hemorrhage remains a devastating disease. Identification of etiologic risk factors would allow the possibility of prevention.
We conducted a population-based case-control study in King County, Washington. Patients whose bleeds originated from a source other than an aneurysm were excluded. Two age- and gender-matched control subjects were identified for each case through random digit telephone dialing. A standardized in-person interview was conducted with the patient whenever possible, a proxy respondent for the case in all instances, the two control subjects, and their proxies. Analyses involved conditional logistic regression taking into account matching on age, gender and respondent type.
Over 2 years, 169 cases were identified, and 149 participated in the case-control study. Compared with those who never smoked, the odds ratio for current heavy smokers (greater than 20 cigarettes/day) was 11.1 (95% confidence interval [CI], 5.0-24.9); for current light smokers (less than or equal to 20 cigarettes/day), 4.1 (95% CI, 2.3-7.3); and for former smokers, 1.8 (95% CI, 1.0-3.2). The risk associated with smoking was greatest in the 3 hours after a cigarette (odds ratio [OR] = 7.0; 95% CI, 3.7-13.1) and then fell, not reaching the risk in those who had never smoked until more than 10 years had passed since the last cigarette. Heavy alcohol use (greater than 2 drinks/day) was also associated with bleeds (OR = 2.2; 95% CI, 0.9-5.1, after adjusting for smoking status). These associations were not substantially altered after adjusting for several possible confounding factors, including a history of hypertension.
Cigarette smoking and heavy alcohol use are associated with the occurrence of subarachnoid hemorrhage.
Laser doppler flowmetry in CA1 sector of hippocampus and cortex after transient forebrain ischemia in gerbils.
Authors: Kuroiwa T , Bonnekoh P , Hossmann K A 
Published: June 2011

Local differences in the hemodynamic response to transient ischemia could be involved in the development of selective vulnerability. These differences were studied in vulnerable and nonvulnerable regions of the brain.
Five gerbils were subjected to 10 minutes of bilateral forebrain ischemia, and cerebral blood flow was measured continuously in the frontal cortex and CA1 sector of the hippocampus using laser Doppler flowmetry. Carotid artery pressure was recorded simultaneously with a pressure transducer.
After induction of ischemia, blood flow in the cortex and CA1 sector decreased to 11.8% and 18.0% of the baseline value, respectively. After release of the vascular occlusion, blood flow in the cortex returned to the preischemic level at 7.5 minutes (recovery time), reached the hyperemic peak (123.8%) at 12.4 minutes (peak latency), and again decreased to the preischemic level at 27.2 minutes. In the CA1 sector, blood flow returned to the preischemic level at 2.1 minutes, reached the hyperemic peak (122.2%) at 5.7 minutes, and decreased again to the preischemic level at 21.3 minutes. In both the cortex and CA1 sector, recovery time and peak latency correlated inversely with the amount of residual blood flow during ischemia. Histologically, cortical neurons were not injured but only 14.6% of CA1 neurons survived 1 week after ischemia.
CA1 neurons were selectively injured despite the milder percentage decrease of blood flow during ischemia and the more prompt recovery of flow after ischemia. These findings stress the importance of intrinsic rather than hemodynamic factors in the pathogenesis of selective vulnerability of CA1 neurons after transient bilateral forebrain ischemia.
Ipsilateral hypohidrosis in brain stem infarction.
Authors: Korpelainen J T , Sotaniemi K A , Myllylä V V 
Published: June 2011

The brain stem is the most important autonomic processing center, but very little attention has been given to clinical manifestations of autonomic failure in brain stem stroke. Our purpose was to evaluate the prevalence, characteristics, and prognostic significance of sweating dysfunction in brain stem infarctions.
We carried out a prospective study using quantitative evaporimetry to investigate spontaneous and heat-stimulated sweating in 18 healthy control subjects and 18 patients with ischemic brain stem stroke in the acute phase and at 1 and 6 months after infarction.
The sweating response induced by a heating stimulus was significantly lower on the ipsilateral side to the infarction than on the contralateral side. Constant ipsilateral hypohidrosis was established in 83% of the patients in the acute phase, in 100% at 1 month, and in 76% at 6 months after infarction. No differences of sweating response were found between medullary and pontine infarcts.
Hypohidrosis throughout the whole ipsilateral side of the body, a long-lasting phenomenon that has not previously been described, is an essential feature of autonomic failure in brain stem infarction.
Effect of brain edema on infarct volume in a focal cerebral ischemia model in rats.
Authors: Lin T N , He Y Y , Wu G , Khan M , Hsu C Y 
Published: June 2011

Infarct volume is one of the common indexes for assessing the extent of ischemic brain injury following focal cerebral ischemia. Accuracy in the measurement of infarct volume is compounded by postischemic brain edema that may increase brain volume in the infarcted region. We evaluated the effect of brain edema on infarct volume determined by triphenyltetrazolium chloride and hematoxylin and eosin stains in a focal cerebral ischemia model in rats.
In a middle cerebral artery occlusion model in rats, infarction is confined to the cerebral cortex. The infarct was delineated by triphenyltetrazolium chloride stain and, in selected samples, by hematoxylin and eosin stain. We determined infarct size at different times after the ischemic insult (6 hours to 7 days) in relation to the evolution of brain edema by the direct measurement of infarct volume. Indirect measurement to reduce the effect of edema on infarct volume was also conducted in the same brain samples.
Direct measurement showed that infarct volume fluctuated with the evolution of brain edema (one-way analysis of variance, p < 0.0001). Infarct volume determined by indirect measurement was independent of the extent of brain edema and remained stable from 6 hours to 3 days after ischemia. There was a good correlation between triphenyltetrazolium chloride and hematoxylin and eosin stains in delineating infarct volume with both direct and indirect measurement.
Traditional direct measurement of infarct volume is associated with an overestimation of infarct volume during the development of brain edema in the first 3 days after ischemia. This artifact can be reduced with indirect measurement, which is based on noninfarcted cortex volume.
Platelet-activating factor acetylhydrolase in red cell membranes. Does decreased activity impair erythrocyte deformability in ischemic stroke patients?
Authors: Yoshida H , Satoh K , Takamatsu S 
Published: June 2011

Platelet-activating factor acetylhydrolase hydrolyzes platelet-activating factor (1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine). It also hydrolyzes oxidized derivatives of phosphatidylcholine that have a short-chain acyl residue at the sn-2 position. This enzyme may act mainly in the degradation of oxidized phospholipids and may play a role in maintaining erythrocyte deformability. Therefore, we assessed the activity of red cell membrane platelet-activating factor acetylhydrolase in patients with ischemic stroke and studied the relation of the enzyme activity to red cell deformability.
Enzyme activity was measured in the detergent extract of red cell membranes from 38 patients with cerebral thrombosis and 38 age-matched healthy volunteers. Red cell filterability, an index of red cell deformability, was also measured.
The enzyme activity in patients and control subjects was 100 +/- 74 and 148 +/- 128 nmol/g protein per minute (2.68 +/- 2.11 and 3.79 +/- 2.46 pmol/10(9) cells per minute) (mean +/- SD), respectively, and the difference was significant (p < 0.05 by the Mann-Whitney U test, two-sided test). Enzyme activity was correlated positively with red cell filterability in the patients (n = 20, r = 0.565, p < 0.01).
Red blood cells from stroke patients have lower levels of platelet-activating factor acetylhydrolase activity when compared with those from healthy subjects. This may result in the accumulation of oxidized lipids in the cell membrane and lead to impaired red cell deformability in patients with cerebral thrombosis.
Atrial fibrillation after acute stroke.
Authors: Vingerhoets F , Bogousslavsky J , Regli F , Van Melle G 
Published: June 2011

Atrial fibrillation (AF) is a risk factor for stroke, although it may not always be directly responsible for the stroke. On the other hand, cardiac arrhythmias and electrocardiographic changes have been reported after ischemic stroke and numerous other intracranial pathologies. We tested the hypothesis that some patients with acute stroke may develop transient AF as a consequence of the stroke.
This study was based on 1,661 patients with first-ever stroke consecutively hospitalized and prospectively included into the Lausanne Stroke Registry. "Recent AF" was defined as AF discovered at or after ("after-admission" AF) admission in patients without any previous history of AF. Populations with recent AF and after-admission AF were compared for AF evolution, risk factors, and lesion type and distribution with patients with previous history of AF (known AF) and with patients with another recognized cardiac source of embolism (cardioembolic).
Twenty-four patients had recent AF on admission, and 17 developed it a few hours to 3 days after stroke. AF disappeared after a few days in 26 (63%; 94% of after-admission AF) patients. Stroke was a primary hematoma in 9.8% of patients with recent AF, 2.8% of patients with known AF, and 0.9% (p < 0.001) of patients with cardiac source of embolism. Parietoinsular (32%) and brain stem (11%) involvement were more common in recent AF than in cardioembolic stroke in general (16.7% and 6.7%, respectively; p < 0.05).
AF discovered after an acute stroke lasted no more than a few days, suggesting that it may have occurred as a consequence of the stroke. This possibility is emphasized by the significant predominance in patients with recent AF of primary hematoma, which cannot be caused by AF, and of parietoinsular and brain stem involvement, which are experimentally known as arrhythmogenic. This hypothesis should be considered in patients with acute stroke and previously unknown AF before therapeutic decisions are made.
Callosal atrophy with reduced cortical oxygen metabolism in carotid artery disease.
Authors: Yamauchi H , Fukuyama H , Nabatame H , Harada K , Kimura J 
Published: June 2011

In cerebrovascular disease, brain atrophy may be a reflection of ischemic changes. Minor changes that are not detectable as infarction on computed tomography may result in atrophy with metabolic depression. We evaluated the relation between size of the corpus callosum and cerebral cortical oxygen metabolism in carotid artery disease.
We used magnetic resonance imaging and positron emission tomography to evaluate 13 right-handed male patients with transient ischemic attacks or minor strokes and unilateral internal carotid artery occlusive disease, two with stenosis and 11 with occlusion. Computed tomography showed only minor subcortical abnormalities in the affected hemisphere. Midsagittal corpus callosum areas on T1-weighted magnetic resonance images, white matter lesions on T2-weighted images, and the cerebral metabolic rate of oxygen measured by the oxygen-15 steady-state technique were analyzed.
Compared with 13 age- and sex-matched control subjects showing the same degree of white matter areas of high intensity, the patients had significantly decreased callosal areas. The degree of corpus callosum atrophy was significantly correlated with the mean cortical oxygen metabolic rate. The same tendency was also found in five patients without infarcts on computed tomography. However, neither the callosal area nor the hemispheric metabolic rate was correlated with the extent of white matter lesions.
These findings indicate that atrophy of the corpus callosum occurs in association with a decrease in cortical oxygen metabolism. Corpus callosum atrophy may be a useful morphological index that reflects the cerebral cortical metabolic state in carotid artery occlusive disease.
Improved neurological recovery of cerebral infarctions after plasmapheretic reduction of lipids and fibrinogen.
Authors: Walzl M , Lechner H , Walzl B , Schied G 
Published: June 2011

High fibrinogen levels have been assessed in cerebrovascular disease with a direct relation to both plasma and whole-blood viscosity, as well as cerebral blood flow. Heparin-induced extracorporeal low density lipoprotein precipitation (HELP) is a new method that safely and effectively reduces fibrinogen and plasma lipoproteins and improves blood flow properties.
We studied 26 patients with acute embolic stroke and 22 with multi-infarct dementia. Each received two treatments with HELP within 8 days. Each patient had measurement of the important blood constituents and evaluation of changes in clinical signs and symptoms related to their cerebrovascular disease.
Each HELP treatment safely produced an immediate and significant reduction in rheological measures, including fibrinogen (P < .001), whole-blood viscosity at high and low shear rates, plasma viscosity, and red cell transit time (P < .01 each). Total cholesterol, low density lipoprotein (P < .0001 each), lipoprotein(a) (P < .003), and triglycerides (P < .0001) were also reduced. The treated group in both the acute stroke group and the multi-infarct group showed improvement relative to the untreated control subjects in Mathew scale, Mini-Mental State Examination, and activities of daily living test scores. These uniform improvements persisted at least 3 days past the second HELP treatment.
These results support the hypothesis that the improved hemorheologic property of blood is an important factor in clinical recovery as well as basic neurological function.
Improving stroke rehabilitation. A controlled study.
Authors: Kalra L , Dale P , Crome P 
Published: June 2011

Assessment of stroke rehabilitation is complicated by the heterogeneity of patients and settings and by difficulties in disentangling effects of organization from effects of types and amounts of treatment input.
A prospective controlled study was undertaken in 245 stroke patients stratified into three groups according to prognosis and managed on a stroke rehabilitation unit (n = 124) or general medical wards (n = 121). Patients were randomly allocated to either setting 2 weeks after stroke and were comparable for baseline characteristics.
Patients on general medical wards received more physiotherapy on average (16.2 +/- 7.2 versus 14.3 +/- 3.2 hours; P < .05) but similar amounts of occupational therapy (9.3 +/- 2.8 versus 9.5 +/- 3.2 hours) compared with stroke unit patients. More time was spent on individual rehabilitation on the stroke unit compared with general wards (P < .001). Functional abilities at discharge, destination of discharge, and length of hospital stay in patients with good prognosis were comparable in both settings. Patients with poor prognosis managed on general wards showed higher mortality (P < .05) and longer hospital stay (123.2 +/- 48.2 versus 52.3 +/- 19.8 days; P < .001), but functional abilities at discharge in survivors were comparable with those of stroke unit patients. Patients with intermediate prognosis had significantly better outcome on the stroke unit, with more patients being discharged home (75% versus 52%; P < .001), shorter average length of hospital stay (48.7 +/- 17.2 versus 104.6 +/- 28.6 days; P < .001), and better functional abilities at discharge (P < .05).
Stroke units improve outcome and reduce hospital stay without increasing therapy time. Their effectiveness may be enhanced by patient selection.