bluuebunny/crossref_metadata_2025_split huggingface dataset:
Low and high density lipoprotein metabolism in atherothrombotic brain infarction.
Authors: Alam R , Yatsu F M , Kasturi R , Bui G 
Published: June 2011

Elevated low density lipoprotein and reduced high density lipoprotein cholesterol may increase the risk of atherothrombotic brain infarction, but the metabolic mechanisms accounting for this relation are poorly understood.
The kinetic parameters of low density and high density lipoprotein were studied in nine subjects with atherothrombotic brain infarction or identifiable (by noninvasive testing) extracranial occlusive disease and in 12 control subjects. Autologous iodine-125-labeled lipoproteins were injected intravenously. Blood samples were drawn 10 minutes after injection and periodically thereafter for 10 days. Kinetic parameters were calculated from the decay curves.
The stroke-risk group showed significantly higher triglyceride (p less than 0.05), total cholesterol (p less than 0.02), and low density lipoprotein cholesterol (p less than 0.01). The fractional catabolic rate of low density lipoprotein was significantly lower (p less than 0.001) and the high density lipoprotein rate higher (p less than 0.02) in the stroke-risk group than in the control group. Regression analysis (using all subjects) of serum lipoproteins and their respective fractional catabolic rates correlated significantly (for low density lipoprotein, r = 0.684, p less than 0.001; for high density lipoprotein, r = 0.595, p less than 0.002). Mean percent stenosis showed a significant relation with triglyceride level (r = 0.678, p less than 0.01) and low density lipoprotein cholesterol (r = 0.535, p less than 0.02) but not with high density lipoprotein cholesterol. Mean percent stenosis also showed correlation with both fractional catabolic rate of low density lipoprotein (r = 0.667, p less than 0.002) and with serum high density lipoprotein levels (r = 0.504, p less than 0.02).
Our study provides insights into the role of altered low and high density lipoprotein metabolism in the pathogenesis of carotid stenosis. The statistically significant association of serum lipoprotein metabolic rates with carotid stenosis, rather than their respective serum concentrations, implies that metabolic parameters may be more important in predicting stroke risk.
Low blood-to-cerebrospinal fluid passage of sorbitol after intravenous infusion.
Authors: Nau R , Dreyhaupt T , Kolenda H , Prange H W 
Published: June 2011

Compared with mannitol, the osmotherapeutic agent sorbitol is less prone to accumulate in the blood and the same quantity may be infused in a smaller volume. Because of these advantageous characteristics, we studied the pharmacokinetics of sorbitol in serum and cerebrospinal fluid.
Six patients (five women and one man; age range, 46-70 years) with an external ventriculostomy and suffering from brain edema due to cerebrovascular disease received sorbitol as part of their therapy. Before and after the first dose of 50 g infused over 20 minutes, sorbitol concentrations in serum and cerebrospinal fluid were determined repeatedly using an enzymatic procedure.
Maximal sorbitol concentrations ranged from 2,705 to 5,821 (median, 3,227) mg/l in serum compared with 6.7-130.7 (median, 19.5) mg/l in cerebrospinal fluid. Cerebrospinal fluid maxima were observed 0.17-3 hours after the end of the infusion. Sorbitol elimination in serum was adequately described by a two-compartment pharmacokinetic model (distribution half-life, 0.05-0.14 hour; elimination half-life, 0.23-0.61 hour). Elimination in cerebrospinal fluid followed a single-exponential decay and was considerably slower than that in serum (half-life, 1.3-7.7 hours).
The maximal cerebrospinal fluid concentration/maximal serum concentration ratio was low for sorbitol, thus suggesting a small potential risk of inducing an increase of intracranial pressure after osmotherapy (rebound effect).
A phenothiazine derivative reduces rat brain damage after global or focal ischemia.
Authors: Yu M J , McCowan J R , Smalstig E B , Bennett D R , Roush M E , Clemens J A 
Published: June 2011

We previously reported that 2-(10H-phenothiazin-2-yloxy)-N,N-dimethylethanamine hydrochloride is a potent inhibitor of iron-dependent lipid peroxidation in vitro and can protect primary cultures of rat hippocampal neurons from hydrogen peroxide-induced toxicity. Because oxidants may play an important role in mediating postischemic tissue injury, we evaluated this agent in two rat models of transient cerebral ischemia.
In a model of global forebrain ischemia, 23 male Wistar rats were subjected to 10 minutes of four-vessel occlusion followed by 72 hours of reperfusion. The rats received three intraperitoneal injections of either vehicle (2% aqueous acacia) or test agent (40 mg/kg). In a model of focal stroke, 19 spontaneously hypertensive rats were subjected to 2 hours of tandem middle cerebral and ipsilateral common carotid artery occlusion followed by 24 hours of reperfusion. The rats received three intraperitoneal injections of either vehicle (2% aqueous acacia) or test agent (40 mg/kg).
In the global model, the phenothiazine significantly protected the CA1 layer of the hippocampus, with a reduction in mean damage score from 2.1 +/- 0.3 for control rats to 1.0 +/- 0.4 for treated rats (p less than 0.05). In the transient focal stroke model, the compound reduced cortical infarct volume from 130.1 +/- 10.3 mm3 for control rats to 95.2 +/- 24.5 mm3 for treated rats (p less than 0.02).
Although the primary mechanism responsible for the protective effect is unclear at the present time, our study is consistent with the hypothesis that oxidant-mediated lipid peroxidation may be involved in the pathophysiology of postischemic brain injury.
Neuroprotective mechanism of (+)SKF 10,047 in vitro and in gerbil global brain ischemia.
Authors: Lysko P G , Yue T L , Gu J L , Feuerstein G 
Published: June 2011

The N-methyl-D-aspartate receptor is believed to mediate part of the ischemic neuronal damage caused by the excitatory amino acid glutamate. (+)SKF 10,047, the prototypic sigma-agonist, interacts with the N-methyl-D-aspartate receptor. Therefore, we studied the neuroprotective effect of (+)SKF 10,047 on cultured rat cerebellar neurons and on CA1 hippocampal neurons of gerbils exposed to brain ischemia.
Mechanisms of neuroprotection were studied in vitro by measuring calcium influx into cultured rat cerebellar granule cells loaded with fura 2-AM. In vivo neuroprotection of gerbil CA1 hippocampal neurons was studied in a posttreatment regimen following 5 minutes of bilateral carotid artery occlusion and 7 days of reperfusion.
In primary cultured rat cerebellar granule cell neurons, (+)SKF 10,047 in a dose-dependent manner diminished intracellular calcium levels of N-methyl-D-aspartate-stimulated neurons by a maximum of 87% (n = 8), with a 50% inhibitory concentration of 0.8 microM. (+)SKF 10,047 did not prevent subsequent calcium influx stimulated by kainic acid or KCl, nor did it interfere with modulation of the kainate response by quisqualic acid. Neuroprotection of 64% (p = 0.006, n = 15) of gerbil CA1 hippocampal neurons was achieved by posttreatment injection followed by minipump infusion.
Neuroprotection by (+)SKF 10,047 most likely involves interaction at the N-methyl-D-aspartate receptor. These results suggest that the benzomorphan class of sigma-agonists may provide neuroprotection in cerebral ischemia and stroke.
Multivariate prediction of the first major cerebrovascular event in an Italian population sample of middle-aged men followed up for 25 years.
Authors: Menotti A , Lanti M , Seccareccia F , Giampaoli S , Dima F 
Published: June 2011

The present investigation was aimed at evaluating the incidence and prediction of a first major cerebrovascular (fatal or nonfatal) event.
The study population included the two Italian rural samples of the Seven Countries Study (namely, Montegiorgio and Crevalcore), accounting for a total of 1,712 men aged 40-59 years at entry and followed up for mortality and morbidity for 25 years. A number of individual variables measured at baseline, at the fifth year, and at the tenth year of follow-up and possibly related to cerebrovascular events were considered. Of the 1,709 subjects free from major cerebrovascular events at entry 171 developed a first major cerebrovascular event, but for the multivariate Cox model analysis only 1,572 subjects and 152 events were employed due to some exclusions for missing data.
Systolic blood pressure, indexes of respiratory function (protective), and physical activity at work (protective) demonstrated significant predictive roles for all ages and all lengths of follow-up considered. Other factors (presence of arrhythmias, presence of arcus senilis, and skinfold thickness [protective]), significantly contributed to the prediction, but in only some models. Time-related changes in systolic blood pressure significantly improved the prediction of cerebrovascular events.
The multivariate prediction performed in this report allowed the validation of three risk factors (systolic blood pressure, respiratory function indexes, and physical activity at work) whose predictive powers remain stable with aging. The need for further studies specifically aimed at discriminating hemorrhagic from thrombotic events is suggested.
Amplitude of the ocular pneumoplethysmography waveform is correlated with cardiac output.
Authors: Bosley T M , Cohen M S , Gee W , Reed J , Sergott R C , Savino P J 
Published: June 2011

Ocular pulse amplitude, the amplitude of the ocular pneumoplethysmographic waveform, is altered in several ophthalmologic diseases that disturb ocular blood flow, implying that ocular pulse amplitude may provide an estimate of ocular blood flow. Because ocular blood flow currently cannot be quantified in humans, two experiments were undertaken to evaluate the association of ocular pulse amplitude with total body blood flow.
In experiment 1, cardiac output was determined by cardiac catheterization in 181 patients who underwent OPG-Gee testing during the same hospitalization. In experiment 2, 110 instances of atrial arrhythmia captured on ocular pneumoplethysmographic tracings were evaluated for transient changes in heart rate (R-R ratio) associated with transient changes in ocular pulse amplitude (ocular pulse amplitude ratio).
In experiment 1, average ocular pulse amplitude in the two eyes (OPAAV) was significantly correlated with cardiac output/heart rate (r = 0.53; p < 0.0001) and cardiac index/heart rate (r = 0.43; p < 0.0001). In experiment 2, R-R ratio was significantly correlated with ocular pulse amplitude ratio (r = 0.85; p < 0.001).
These results show that ocular pulse amplitude, a physiological measurement obtained from the globe, is correlated with cardiac output. They imply that ocular pulse amplitude may provide a clinically useful estimate of at least the pulsatile component of ocular blood flow.
Frequency and prognosis of stroke/TIA among 4808 survivors of acute myocardial infarction. The SPRINT Study Group.
Authors: Tanne D , Goldbourt U , Zion M , Reicher-Reiss H , Kaplinsky E , Behar S 
Published: June 2011

Stroke complicating acute myocardial infarction is associated with substantial morbidity and mortality. The purpose of this study was to assess the incidence, predictors, and impact on mortality of stroke/transient ischemic attacks occurring after hospital discharge in a large unselected population of acute myocardial infarction survivors.
During a secondary prevention study with nifedipine (SPRINT), demographic, anamnestic, and clinical data were collected for 5839 consecutive acute myocardial infarction patients admitted to 13 coronary care units in Israel. Hospital survivors (n = 4808) were followed for a year after their discharge. Mortality was assessed for a mean follow-up of 5.5 years (range, 4.5 to 7 years).
One percent (48/4808) of hospital survivors from acute myocardial infarction experienced a stroke/transient ischemic attack in the year after acute myocardial infarction. Thirty-one percent (15 of 48) of events occurred in the first month after hospital discharge. Incidence was higher among older patients (> 70 years; 1.9%), those with anterior site of myocardial infarction (1.35%), a previous history of myocardial infarction (1.8%), hypertension (1.4%), stroke in the past (4.1%), and chronic atrial fibrillation (9%). Multivariate analysis identified the following as independent predictors of stroke/transient ischemic attacks occurring in the year after hospital discharge: chronic atrial fibrillation, older age, history of previous myocardial infarction, anterior myocardial infarction site, serum glutamic oxaloacetic transaminase levels more than four times above upper normal limits, and stroke in the past. The age-adjusted 1-year and long-term mortality rates (4.5 to 7 years; mean, 5.5 years) were significantly higher in patients with (31% and 62%) than in those without stroke/transient ischemic attacks (9% and 31%, respectively; P < .01).
Stroke/transient ischemic attack is a relatively rare (1%) complication in the year after hospital discharge from acute myocardial infarction, though more frequent in the first month. Chronic atrial fibrillation, older age, anterior myocardial infarction site, serum glutamic oxaloacetic transaminase levels more than four times above upper normal limits, past myocardial infarction, and stroke identify high-risk patients. Patients suffering from subsequent stroke/transient ischemic attacks experienced higher mortality than counterparts who remained free from this complication.
Changes in glucose utilization in the rat brain after transient forebrain ischemia.
Authors: Kozuka M , Kobayashi K , Iwata N 
Published: June 2011

Although several local cerebral glucose utilization (LCGU) studies using rat forebrain ischemia models have been performed to date, none that investigate long-term postischemic changes in LCGU throughout the brain have been reported. We investigated postischemic changes throughout the brain over 14 days using a rat forebrain ischemia model.
Cerebral ischemia was produced using the rat four-vessel occlusion model. After 30 minutes of ischemia cerebral blood flow was restored, and LCGU in 34 structures in the brain was evaluated at 1, 3, 5, 7, and 14 days after ischemia.
LCGU changes were characterized and could be divided into two major patterns, type 1 and type 2. In type 1, LCGU was reduced remarkably at 1 and 3 days, and it returned to near the control level at 5 days. In type 2, LCGU was reduced mildly at 1 day and returned to near the control level at 3 days. Included in type 1 were the severely ischemic structures such as the cerebral cortices and striatum. Included in type 2 were the less severely ischemic structures such as the midbrain, cerebellum, and pons and medulla oblongata. Drastic changes in LCGU took place not only in gray matter but also in white matter, and the patterns of LCGU changes were similar in both regions. Atypical changes in LCGU were observed in the hippocampal CA1 and substantia nigra pars reticulata. In both structures, LCGU was remarkably increased around 7 days after ischemia.
There are two major patterns of LCGU changes after transient forebrain ischemia. LCGU changes in the hippocampal CA1 and substantia nigra pars reticulata are atypical.
Endothelial modulation of contractions caused by oxyhemoglobin and NG-nitro-L-arginine in isolated dog and monkey cerebral arteries.
Authors: Toda N , Ayajiki K , Okamura T 
Published: June 2011

Oxyhemoglobin is a key substance in provoking cerebral vasospasm and a scavenger of nitric oxide. The present study was designed to determine whether suppression of the action of endothelium-derived nitric oxide is involved in oxyhemoglobin-induced cerebroarterial contraction.
Dog and monkey cerebral artery strips with and without endothelium were immersed for isometric tension recording in modified Ringer-Locke solution aerated with 95% oxygen and 5% carbon dioxide.
NG-nitro-L-arginine, a nitric oxide synthase inhibitor, produced concentration-related contraction that was greater in the strips with intact endothelium than in those denuded of endothelium. The D-enantiomer caused no or only a slight contraction. In the presence of NG-nitro-L-arginine, oxyhemoglobin elicited additional contraction that is comparable to or even greater than that obtained in the absence of the inhibitor. The oxyhemoglobin-induced contraction was attenuated by endothelium denudation.
Inhibition of the basal release of nitric oxide from endothelium results in dog and monkey cerebral arterial contraction. However, the inhibition of nitric oxide action is not a major mechanism involved in oxyhemoglobin-induced contraction; other mechanisms, such as the release of prostanoids, appear to be important.
Ischemic and hemorrhagic stroke in patients on oral anticoagulants after reconstruction for chronic lower limb ischemia.
Authors: Dawson I , van Bockel J H , Ferrari M D , van der Meer F J , Brand R , Terpstra J L 
Published: June 2011

Information on the long-term fate of patients with chronic lower limb ischemia is limited. We investigated the long-term risk of the first ischemic and hemorrhagic cerebral stroke in patients on long-term anticoagulant therapy after reconstruction for chronic limb ischemia.
In a retrospective study, 376 consecutive patients were seen at regular intervals according to a standard protocol. Only 3 (0.7%) were lost during follow-up (mean duration, 5.9 years). Anticoagulation was with coumarin derivatives followed by prothrombin times periodically. Primary end points were ischemic and hemorrhagic cerebral stroke events, which were confirmed by CT scan, autopsy, or operation in 85% of the cases. Major vascular events were analyzed as a composite secondary end point. The influence of several clinical variables on these outcome events was evaluated in univariate and multivariate analyses.
Thirty-nine patients (10%) had 41 stroke events (23 ischemic, 18 hemorrhagic); 22 of these patients (56%) died from stroke. The cumulative ischemic stroke risk was 5% at 5 years and 12% at 15 years. Prior myocardial infarction was the only independent predictor (relative risk [RR], 3.1; P < .05). The cumulative hemorrhagic stroke risk was 3% at 5 years and 17% at 15 years. Systolic hypertension (RR, 4.8; P < .01) and insulin-dependent diabetes mellitus (RR, 5.4; P < .01) were significant and independent predictors. The risk for a major vascular event was 29% at 5 years and increased to 56% at 15 years. Independent predictors were advanced age (RR, 1.4; P < .005), insulin-dependent diabetes (RR, 2.2; P < .005), and prior myocardial infarction (RR, 1.8; P < .01).
Patients with chronic lower limb ischemia, notably those with prior myocardial infarction, are at high risk for ischemic stroke. Those with systolic hypertension or insulin-dependent diabetes mellitus are at high risk for hemorrhagic stroke.
Clinical features of recurrent embolization in acute cardioembolic stroke.
Authors: Yasaka M , Yamaguchi T , Oita J , Sawada T , Shichiri M , Omae T 
Published: June 2011

Recurrent embolization is a serious problem in acute cardioembolic stroke. However, the clinical features and predisposing factors of recurrent embolization have not been fully elucidated.
Subjects were 227 consecutive patients (128 men and 99 women, aged 68.6 +/- 13.2 years) with acute cardioembolic stroke who did not receive anticoagulant therapy during the first 14 days after stroke onset. We assigned the subjects to two groups according to the occurrence or nonoccurrence of recurrent attacks within 14 days of the stroke onset. We assessed their clinical features, coagulation study results, and underlying heart disease.
Recurrent brain or systemic embolization during the first 14 days after onset was noted in 46 patients (20.3%, group A) but not in the other 181 (group B). Recurrent embolization was more frequently noted at an early phase than at a late phase during the initial 14 days. Mortality was higher in group A (19.6%) than in group B (8.8%). The mean plasma level of antithrombin III (77.8 +/- 19.5%) at admission in group A patients was significantly lower than that in group B patients (87.9 +/- 15.5%). After admission, hematocrit decreased in group B patients but slightly increased in group A patients, in whom diuretics were more commonly used. Rheumatic heart disease and prosthetic valves, in addition to the presence of intracardiac thrombi, were seen more commonly in group A patients, whereas atrial fibrillation without organic heart disease and myocardial infarction were more frequent in group B patients.
Low plasma levels of antithrombin III, dehydration, the use of diuretics, and the presence of rheumatic heart disease, prosthetic valves, and intracardiac thrombi seem to be predisposing factors for recurrent embolization. Immediate anticoagulation may be considered in acute cardioembolic stroke patients if such predisposing factors are demonstrated.
Evaluation times for patients with in-hospital strokes.
Authors: Alberts M J , Brass L M , Perry A , Webb D , Dawson D V 
Published: June 2011

Each year at least 35,000 people suffer a stroke while hospitalized, but little is known about the clinical characteristics of such patients or how rapidly they are identified and evaluated. With a recent emphasis on the very early treatment of stroke, in-hospital stroke patients may be candidates for some early interventions.
This was a retrospective study using the stroke registries at two academic medical centers. Data were collected about the clinical characteristics of patients with an in-hospital stroke and who recognized the stroke. Detailed time data were analyzed to determine the time of stroke recognition, medical evaluation, and neurological evaluation. These specific time epochs were analyzed to determine which were responsible for any delays in stroke identification and assessment. Data were analyzed using nonparametric methods, including the Wilcoxon rank sum and Kruskal-Wallis procedure.
Sixty-three patients were identified with in-hospital strokes and adequate time data. In-hospital stroke patients were recognized most frequently by nurses (63%) and by the patient (16%). Patients on a cardiology service and general surgery service accounted for 48% of all in-hospital strokes. The mean and median times from stroke recognition to a neurology evaluation were 14.5 and 2.5 hours, respectively. Total delays differed significantly with service and locale (P = .004). Patients on the Duke neurology service were evaluated significantly sooner (median delay, 0.5 hour) than patients on the Duke medical (median delay, 5.8 hours) or Duke surgical (median delay, 20.5 hours; P < .01 by Wilcoxon rank sum) services. Patients on the Yale surgical service were evaluated significantly sooner than patients on the Duke medical (P = .0006) or surgical (P = .0001) services. The time between physician notification and calling for a neurology evaluation accounted for > 60% of the total time delay for patients not on a neurology service.
A substantial number of in-hospital stroke patients experience a long delay between symptom recognition and a neurological evaluation. While medical personnel are usually notified very soon after an in-hospital stroke is recognized, such patients often do not receive a rapid neurological evaluation. Additional education of hospital staff may reduce these time delays.