bluuebunny/crossref_metadata_2025_split huggingface dataset:
Circadian rhythmicity of stroke onset. Intracerebral and subarachnoid hemorrhage.
Authors: Sloan M A , Price T R , Foulkes M A , Marler J R , Mohr J P , Hier D B , Wolf P A , Caplan L R 
Published: June 2011

Our purpose was to describe and further understand the determinants of the time of onset of parenchymatous intracerebral hemorrhage and subarachnoid hemorrhage in patients enrolled in the Stroke Data Bank.
We analyzed the observed times of onset of intracerebral hemorrhage (n = 237 patients) and subarachnoid hemorrhage (n = 243 patients) compared with expected times of onset if the probability of onset was constant across all time intervals. We also analyzed the role of clinical features (if any) in explaining the findings.
For intracerebral hemorrhage, 52.5% of patients reported onset times between 0600 hours and 1400 hours, with peak onset between 1000 and 1200 hours (chi 2 = 62.94, df = 11, p less than 0.001). Patients with subarachnoid hemorrhage were more likely to lack a history of hypertension compared with patients who had intracerebral hemorrhage (chi 2 = 23.3, df = 1, p less than 0.001). Patients with subarachnoid hemorrhage were more likely to have more uniform onset time throughout the day (chi 2 = 12.92, df = 7, p = 0.074). However, subarachnoid hemorrhage patients with a history of hypertension were more likely to have peak onset times in mid-to-late morning compared with patients without such a history (chi 2 = 35.25, df = 10, p less than 0.001). The nonuniformity of onset times for intracerebral hemorrhage persisted even if patients with unknown onset times were treated as through their onset times were randomly distributed between 0000 and 0800 hours. Seasonal periodicity and the relation between initial systolic or diastolic blood pressure and time of onset for either type of hemorrhage were not observed.
Our data suggest that the time of onset for both intracerebral hemorrhage and subarachnoid hemorrhage patients with a history of hypertension is similar to the diurnal variation in blood pressure.
Relation between middle cerebral artery blood flow velocity and stump pressure during carotid endarterectomy.
Authors: Spencer M P , Thomas G I , Moehring M A 
Published: June 2011

Many patient monitoring techniques have been used for detecting cerebral hypoperfusion during carotid endarterectomy. We compared middle cerebral artery blood flow velocities with carotid artery stump pressures to evaluate the indications for common carotid artery cross-clamp shunting and the probable hemodynamic causes of cerebrovascular complications.
Blood flow velocities were monitored with transcranial Doppler ultrasound and carotid stump pressures were measured at the time of common carotid artery cross-clamping during 97 carotid endarterectomy procedures. Stump pressures measured with the gauge zero reference at the common carotid artery level were correlated with the percentage change of velocities.
Middle cerebral artery blood flow velocities usually decreased upon common carotid artery cross-clamping, depending on collateral availability and the autoregulation response. The best fit of the data was to an exponential function concave to the pressure axis, with velocity as a percentage of the pre-cross-clamp value reaching zero at 15 mm Hg stump pressure (r = 0.85 and p less than 0.001).
There is a less critical margin of error with percentage middle cerebral artery blood flow velocity decreases than with stump pressure measurements. This relation establishes changes in middle cerebral artery blood flow velocities as a reliable parameter for judging the effects of carotid cross-clamping on cerebral blood flow and providing an excellent indicator as to the necessity for shunting.
Beneficial effect of mild hypothermia and detrimental effect of deep hypothermia after cardiac arrest in dogs.
Authors: Weinrauch V , Safar P , Tisherman S , Kuboyama K , Radovsky A 
Published: June 2011

Mild cerebral hypothermia (34 degrees C) induced immediately after cardiac arrest improves outcome. Deep postarrest hypothermia (15 degrees C) has not been studied.
We used our dog model of normothermic ventricular fibrillation (no blood flow) of 12.5 minutes, reperfusion by brief cardiopulmonary bypass, controlled ventilation to 20 hours, and intensive care to 72 hours. Head surface cooling and bypass cooling were performed from start of reperfusion to 1 hour. Five groups of six dogs each were compared: group I, normothermic controls; group II, deep hypothermia (15 degrees C); group III, moderate hypothermia (30 degrees C); group IV, mild hypothermia (34 degrees C); and group V, mild hypothermia with head surface cooling begun during no flow.
In control group I, five dogs remained comatose (overall performance category [OPC] 4) and one severely disabled (OPC 3). In group II, four dogs achieved OPC 4 and two dogs OPC 3 (NS versus group I). Compared with group I, OPCs were better in group III (p less than 0.05), group IV (p less than 0.05), and group V (p less than 0.05). Neurological deficit scores were also better in groups III, IV, and V than in groups I or II (p less than 0.05). Total brain histological damage scores were better in group III (p = 0.02), group IV (p = 0.06), and group V (p less than 0.05) than in group I. In group II, OPC and neurological deficit scores were the same and histological damage scores numerically worse than in group I and all were worse than in groups III, IV, and V (p less than 0.05). Cardiovascular complications and myocardial morphological damage in groups II and III were worse than in groups I, IV, and V (p less than 0.05).
Mild or moderate cerebral hypothermia induced immediately after cardiac arrest improves cerebral outcome, more likely when initiated during arrest, whereas deep postarrest hypothermia can worsen cerebral and cardiac outcome.
Marked increase of stroke incidence in men between 1972 and 1990 in Frederiksberg, Denmark.
Authors: Jørgensen H S , Plesner A M , Hübbe P , Larsen K 
Published: June 2011

Stroke incidence declined until the end of the 1970s in the United States, and the decline continued into the 1980s in Japan. The purpose of this study was to determine possible temporal changes of stroke incidence in a European community.
A prospective stroke registry was established in the community of Frederiksberg (population, approximately 90,000), Denmark, in the two periods 1972-1974 and 1989-1990. All patients suspected of stroke were clinically evaluated by a neurologist. Only patients with first-ever stroke were included. Complete case ascertainment was ensured by registration of both hospitalized and nonhospitalized patients. Death certificates were also scrutinized.
A total of 927 patients with first-ever stroke was recorded. The annual stroke incidence rate per 1,000 increased by 18% from 2.6 in 1972-1974 to 3.1 in 1989-1990 (p < 0.01). This increase was due solely to a 42% increase in men, in whom stroke incidence rose from 2.1 to 3.0 (p < 0.0005). Incidence was unchanged in women at 3.0 and 3.1, respectively. The incidence rates from 1972-1974 were age and sex adjusted to the 1990 population. After adjustment to the Danish population, stroke incidence in Denmark was 2.0 for all, 2.3 for men, and 1.9 for women. In the second study period computed tomography or necropsy was performed in 85% of cases; 2.4/1,000 had cerebral infarction; 0.20/1,000 had intracerebral hemorrhage; and 0.02/1,000 had subarachnoid hemorrhage.
In a period when decline in stroke incidence has stopped in the United States and has continued in Japan, a marked increase of stroke incidence in Danish men was observed.
Selective brain cooling during and after prolonged global ischemia reduces cortical damage in rats.
Authors: Kuluz J W , Gregory G A , Yu A C , Chang Y 
Published: June 2011

Studies of the cerebroprotective effects of selective brain cooling have failed to show amelioration of ischemic injury in the cerebral cortex. This study was designed to test the hypothesis that mild-to-moderate selective brain cooling initiated after the onset of global brain ischemia in rats protects the cerebral cortex and improves neurological outcome.
Global forebrain ischemia for 30 minutes in 27 fasted adult male Wistar rats was achieved by bilateral carotid occlusion and hypotension. In group 1, brain temperature, measured in the temporalis muscle, was maintained at 37-38 degrees C throughout the experiment. In group 2, brain temperature fell spontaneously during ischemia to 34.7 +/- 0.1 degrees C and rose spontaneously to 36-37 degrees C after 10 minutes of recirculation. In group 3, brain temperature was lowered with ice packs placed around the head after 15 minutes of ischemia to 24.1 +/- 0.9 degrees C by the end of ischemia, maintained at 30.0 +/- 1.0 degrees C for the first hour of recirculation, then allowed to rise to 36-37 degrees C.
Seven-day survival was 0% (0 of 6) in group 1, 73% (8 of 11) in group 2, and 100% (6 of 6) in group 3. Severity of neuronal damage was less in group 2 than in group 1 in the cortex (p < 0.05) and hippocampal CA1 (p < 0.05) and CA3 regions (p < 0.05). Group 3 had less neuronal damage than group 2 in both cortex (p < 0.02) and striatum (p < 0.02). Furthermore, postischemic weight loss was less and neurobehavioral scores were significantly higher in group 3.
This study shows that selective brain cooling increases survival from prolonged global ischemia and reduces neuronal injury in the cerebral cortex as well as the striatum and hippocampus.
Extracellular alkalinity exacerbates injury of cultured cortical neurons.
Authors: Giffard R G , Weiss J H , Choi D W 
Published: June 2011

We have previously shown that extracellular acidity protects cultured fetal murine neocortical neurons from glutamate toxicity and combined oxygen-glucose deprivation injury, an action at least in part mediated by reduction in N-methyl-D-aspartate receptor activation. We now investigate the effect of extracellular alkalinity on both glutamate neurotoxicity and injury due to combined oxygen-glucose deprivation.
The effects of extracellular alkalinity during injury induced by exposure of murine neocortical cultures to glutamate (0.5 mM for 5 minutes) or oxygen-glucose deprivation are characterized morphologically and quantitated by efflux of lactate dehydrogenase from both neurons and glia to the bathing medium. Calcium accumulation is measured with calcium-45.
Moderate extracellular alkalinity is well tolerated by cortical cells but significantly potentiates both glutamate neuronal toxicity and oxygen-glucose deprivation neuronal injury. In contrast, glial viability in the face of combined oxygen-glucose deprivation is little affected by extracellular alkalinity. Increased accumulation of calcium-45 during oxygen-glucose deprivation in alkalotic medium and blockade of this increase by MK-801 is demonstrated.
These observations suggest that alkaline pH can exacerbate excitotoxic neuronal injury, most likely because of increased N-methyl-D-aspartate receptor activation. Metabolic alkalosis of any etiology may sensitize neurons to ischemic injury and potentiate reperfusion injury.
Lupus anticoagulant and anticardiolipin antibodies in young adults with cerebral ischemia.
Authors: Nencini P , Baruffi M C , Abbate R , Massai G , Amaducci L , Inzitari D 
Published: June 2011

Our study evaluates in an unselected young population with cerebral ischemia the frequency of antiphospholipid antibodies; the relationship of antiphospholipid antibodies to conventional risk factors for and pathological mechanisms of cerebral ischemia; and the risk of recurrence of cerebral ischemia or systemic thrombotic events in patients with antiphospholipid antibodies compared with those without.
We prospectively tested for antiphospholipid antibodies in 55 of 59 young (aged 15-44 years) adults consecutively examined for ischemic stroke (n = 44) or transient ischemic attack (n = 11). These patients underwent a complete clinical and laboratory assessment for cerebral ischemia and had a 3-year mean follow-up.
Ten patients (18%), all with stroke, had antiphospholipid antibodies. Antiphospholipid antibodies were significantly more frequent in women than in men (Fisher's test, p = 0.014). Two patients with antiphospholipid antibodies had a new diagnosis of systemic lupus erythematosus. On angiography, none of the patients with antiphospholipid antibodies had extracranial lesions. Patients with antiphospholipid antibodies had significantly more prior cerebral events (Fisher's test, p = 0.014), and, by survival analysis, higher probability of cerebral ischemic or systemic thrombotic events during follow-up than patients without (log rank test, p less than 0.005).
We conclude that the prevalence of antiphospholipid antibodies is rather high in young adults with cerebral ischemia; that patients with cerebral ischemia and antiphospholipid antibodies may have unrecognized systemic lupus erythematosus; and that, among young patients with cerebral ischemia, patients with antiphospholipid antibodies constitute a subgroup at high risk of cerebral ischemic or systemic thrombotic recurrence. Prevention in this latter group may require close follow-up and treatment.
Efflux of glutamate produced by short ischemia of varied severity in rat striatum.
Authors: Ueda Y , Obrenovitch T P , Lok S Y , Sarna G S , Symon L 
Published: June 2011

Evidence has accumulated suggesting that ischemia-induced neuronal damage may be linked to an extracellular overflow of glutamate. The purpose of this study was to provide new information about the time course of the increase in extracellular glutamate concentration associated with moderate and severe ischemia, and its relationship with electrical changes including anoxic depolarization.
Changes in the extracellular concentration of glutamate were continuously monitored in the rat striatum by microdialysis. Ischemia was induced by four-vessel occlusion for 3 or 5 minutes, and in some cases its severity was increased with a neck tourniquet. The severity of ischemia was assessed by electroencephalogram and direct current potential recording to detect anoxic depolarization.
In all experiments, the extracellular glutamate concentration began to increase shortly after the onset of ischemia and steadily rose throughout the ischemic period. Increases up to 35.0 mumol/l (2-3 mumol/l baseline; p less than 0.005) were observed when ischemia provoked the rapid occurrence of a large and sustained anoxic depolarization. Relatively smaller but still significant increases (6.9 mumol/l; p less than 0.005) were observed in penumbral conditions (electroencephalogram loss without anoxic depolarization). Glutamate began to be cleared immediately after reperfusion and 90% of released glutamate was cleared within 5 minutes, even when the preceding ischemia had been severe.
We propose that the extracellular glutamate concentration may not reach critical levels during short episodes of penumbral ischemia, but this might happen with a longer ischemic period.
Changes of neuronal transmission in the hippocampus after transient ischemia in spontaneously hypertensive rats and the protective effects of MK-801.
Authors: Suyama K 
Published: June 2011

I studied the mechanism of postischemic neuronal degeneration in the hippocampus by an electrophysiological method.
Sequential changes of field potentials evoked by perforant path stimulation in the dentate gyrus and the CA1 region of the hippocampus were evaluated in spontaneously hypertensive rats up to 7 days after transient global ischemia induced by bilateral occlusion of the carotid arteries for 20 minutes after electrocauterization of the vertebral arteries. Animals were treated with vehicle or the excitotoxin antagonist (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10 amine (MK-801, 2 mg/kg or 5 mg/kg) intraperitoneally 30 minutes before ischemia.
Complete recovery of the population spike was observed in the dentate gyrus within 24 hours after recirculation, followed by a gradual reduction of population spike amplitude. In contrast, population spike in the CA1 region showed partial recovery 24 hours after recirculation, and an abrupt reduction of population spike amplitude occurred on day 2. There was no significant enhancement of population spike amplitude in either region throughout the experiment. Interneuronal recurrent inhibition in the dentate gyrus was enhanced on day 4, and ischemic changes were apparent in the CA1 pyramidal cells on day 7. Pretreatment with 5 mg/kg MK-801 prevented field potential and pathological changes completely in the dentate gyrus and partially in the CA1 region.
My results indicate that pathological changes of the CA1 pyramidal neurons after transient ischemia may not be the result of postischemic overstimulation. However, neuronal transmission in the CA1 region may be persistently impaired during or after transient ischemia.
A new model of temporary focal neocortical ischemia in the rat.
Authors: Buchan A M , Xue D , Slivka A 
Published: June 2011

We describe a new rat model of temporary focal ischemia that produces neocortical ischemia without the need for prolonged anesthesia.
Temporary focal cerebral ischemia was initiated during halothane anesthesia, maintained for varying periods without anesthesia, and reversed by clip removal requiring brief anesthesia. Tandem carotid and middle cerebral artery occlusion for 1-4 hours and permanent occlusion were used to determine the duration and extent of ischemia necessary to produce predictable volumes of neocortical infarction in Wistar and spontaneously hypertensive rats.
In Wistar rats, occlusion of the right middle cerebral and both common carotid arteries resulted in cerebral blood flow reductions to approximately 8% of baseline. One hour of transient ischemia with 23 hours of reperfusion did not result in infarction. Three hours of ischemia followed by 21 hours of reperfusion resulted in infarction comparable to that caused by 24 hours of permanent ischemia. In spontaneously hypertensive rats, unilateral right middle cerebral and common carotid artery occlusion reduced cerebral blood flow to approximately 11% of baseline. Minimal damage was seen with 1 hour of reversible ischemia, but intervals of 2 and subsequently 3 hours followed by 22-21 hours of reperfusion produced progressively larger infarcts. Damage indistinguishable from that seen with 24 hours of permanent ischemia was seen with 3 or 4 hours of transient ischemia followed by 21 or 20 hours of reperfusion.
For unanesthetized normothermic rats, cerebral blood flow reductions to 10-20% of baseline resulted in maximal infarction once ischemic durations exceeded 2-3 hours. To be effective, experimental therapies aimed at lessening infarct size or restoring blood flow must be initiated within this critical time interval.
Dietary omega-3 fatty acids and endothelium-dependent responses in porcine cerebral arteries.
Authors: Kim P , Shimokawa H , Vanhoutte P M 
Published: June 2011

We sought to determine the effect of dietary omega-3 polyunsaturated fatty acids on cerebrovascular endothelium-dependent responses in studies performed on isolated porcine basilar arteries.
Male Yorkshire pigs (6-8 weeks old) were kept for 4 weeks on a standard diet (control group, n = 12) or on chow supplemented with polyunsaturated fatty acids (eicosapentaenoic acid, 3.5 g/day, or docosahexaenoic acid, 1.5 g/day; treated group, n = 12). Isometric tension recording of the basilar artery was carried out and responses were compared between the two groups.
The regimen resulted in a decrease in the plasma arachidonic acid level and an increase in eicosapentaenoic acid. Endothelium-dependent relaxations induced by bradykinin and adenosine diphosphate were augmented in the basilar arteries of the treated group. Incubation with indomethacin (10(-5) M) prevented the augmentation of the relaxations induced by bradykinin, but not those caused by adenosine diphosphate. The indomethacin-sensitive, endothelium-dependent contractions to arachidonic acid remained comparable in the two groups, indicating that the activity of cyclooxygenase was not affected by the diet.
Dietary supplementation with omega-3 polyunsaturated fatty acids enhances endothelium-dependent relaxations in the basilar artery by two mechanisms: 1) replacement of endogenous arachidonic acid and suppression of the concomitant release of vasoconstrictor prostaglandins from the endothelium, and 2) enhancement of the release of endothelium-derived relaxing factor.
Crossed hemispheric diaschisis in unilateral cerebellar lesions.
Authors: Rousseaux M , Steinling M 
Published: June 2011

We studied 12 patients with unilateral cerebellar hemorrhage to look at its effect on regional cerebral blood flow.
We used single-photon emission computed tomography by continuous inhalation of xenon-133. The blood flow was quantified in the cerebellum and in nine areas of interest on the slice passing through the basal ganglia.
The comparison of the blood flow values of the patients and control subjects showed a significant reduction in the contralateral hemisphere of the patients, predominantly in the frontal region and in the lenticular nucleus of the contralateral hemisphere but also in the anterointernal frontal area of the ipsilateral hemisphere. The analysis of the asymmetry indexes revealed in the same way significant differences between patients and control subjects in the frontal cortex and in the lenticular nucleus.
These results provided concordant evidence suggesting a blood flow reduction in the contralateral hemisphere. This phenomenon of "crossed hemispheric diaschisis" is probably related to the interruption of cerebellocortical tracts.
Partial protection from salt-induced stroke and mortality by high oral calcium in hypertensive rats.
Authors: Peuler J D , Schelper R L 
Published: June 2011

Repeated demonstration of an antihypertensive effect of high oral calcium in stroke-prone spontaneously hypertensive rats led us to determine whether it also protects such rats from premature mortality and stroke-related lesions.
Female stroke-prone rats (11-13 per diet) were fed high- and low-calcium (2.0% and 0.4%, respectively) diets with both high and low salt (7.0% and 0.3%, respectively) content from age 4 weeks until spontaneous death. In addition to life span, other variables measured included blood pressures, plasma chemistries, and histological characterization of stroke-related lesions.
Life span was increased from 51 +/- 4 to 68 +/- 1 weeks (p less than 0.05) by high versus low oral calcium in rats fed high-salt diets; it was further increased to greater than or equal to 82 weeks (p less than 0.05) in rats fed low-salt (+/- added calcium) diets. As seen previously, high oral calcium attenuated salt-induced hypertension but did not affect blood pressure in rats fed low-salt diets. High versus low oral calcium exerted contrasting effects (p less than 0.05) on brain lesions (hemorrhages and infarctions) in rats fed high-salt diets, decreasing lesion size (242 +/- 21 versus 712 +/- 276 microns per rat [diameters seen in histological sections]) but increasing lesion number (8.9 +/- 2.4 versus 3.4 +/- 2.2 per rat); it exerted little influence on the few brain lesions that appeared in rats fed low-salt diets.
High oral calcium may protect stroke-prone hypertensive rats from early salt-induced mortality at least partially by decreasing severity (size) of stroke-related lesions, an effect which may relate to decreased blood pressure. However, this protection may be limited by increased number (incidence) of such lesions, an effect which suggests that high oral calcium may increase the number of brain vessels susceptible to stroke-related injury independent of change in blood pressure.