bluuebunny/crossref_metadata_2025_split huggingface dataset:
Between-method correlation in quantifying internal carotid stenosis.
Authors: Sitzer M , Fürst G , Fischer H , Siebler M , Fehlings T , Kleinschmidt A , Kahn T , Steinmetz H 
Published: June 2011

The degree of internal carotid stenosis has emerged as the most important predictor of ischemic stroke in extracranial carotid artery disease. The purpose of this study was to assess the validity of the noninvasive techniques for quantifying internal carotid stenosis with respect to the accepted standard of intra-arterial angiography.
We measured the maximum percentage reduction in luminal diameter on the intra-arterial digital subtraction angiograms of 56 symptomatic patients with extracranial internal carotid stenosis (n = 77) or occlusion (n = 20). These data were compared with independent measurements based on continuous-wave Doppler ultrasonography, pulsed-wave Doppler spectrum analysis, color Doppler-assisted duplex imaging, and magnetic resonance angiography.
Correlations with intra-arterial angiography were equally strong (r > .90) for magnetic resonance angiography, continuous-wave Doppler, and color duplex analysis. Positive and negative predictive values for (therapeutically relevant) 70% to 99% stenosis were higher for continuous-wave Doppler (.82, .97) and color duplex (.84, .98) than for magnetic resonance angiography (.79, .81). Also, accuracy in quantifying high-grade stenosis was better for both of these ultrasonographic techniques, mainly due to the frequent occurrence of a "flow gap" on the magnetic resonance angiograms. Continuous-wave Doppler and magnetic resonance angiography, but not color duplex, failed to detect slow residual arterial flow in one and two cases of symptomatic "pseudo-occlusion" of the internal carotid, respectively.
(1) Several noninvasive methods compare well with intra-arterial angiography in identifying and quantifying high-grade internal carotid stenosis; (2) the use of these noninvasive methods may suffice for treatment decisions; and (3) because residual between-method disagreement is partly explained by principles of physics, the validity of continuous-wave Doppler and color duplex in quantifying 60% to 99% stenosis is likely to be underestimated by correlation with intra-arterial angiography.
Impairment of anti-platelet-aggregating activity of endothelial cells after experimental subarachnoid hemorrhage.
Authors: Ohkuma H , Ogane K , Fujita S , Manabe H , Suzuki S 
Published: June 2011

Serial changes of anti-platelet-aggregating activity in the endothelial cells after experimental subarachnoid hemorrhage were studied in 30 feline two-hemorrhage models.
One hour or 2, 4, 7, or 14 days after mimic subarachnoid hemorrhage, ADP (40 mg/kg) was infused into the basilar artery via the right vertebral artery to activate circulating platelets. Immediately after ADP infusion, the basilar artery was fixed by intra-arterial perfusion with 1.5% glutaraldehyde in 0.1 mol/L phosphate buffer and was removed. The luminal surface was examined under a scanning electron microscope.
One hour after subarachnoid hemorrhage, no platelets adhered or aggregated on the luminal surface. However, 4 to 7 days after subarachnoid hemorrhage, many platelets were observed adhering or aggregating on the luminal surface.
These findings suggest the impairment of anti-platelet-aggregating activity of endothelial cells after subarachnoid hemorrhage. This impairment may be involved in inducing cerebral ischemia during cerebral vasospasm by causing platelet adhesion and aggregation.
Effects of flunarizine on neurological recovery and spinal cord blood flow in experimental spinal cord ischemia in rabbits.
Authors: Johnson S H , Kraimer J M , Graeber G M 
Published: June 2011

The lipophilic calcium channel antagonist flunarizine has been demonstrated to be neuroprotective in several models of cerebral ischemia. Ischemic spinal cord injury may have a similar pathophysiology and hence may respond in a similar fashion. This study was designed to investigate the effects of pretreatment with flunarizine on systemic hemodynamics, spinal cord blood flow, and neurological recovery in a rabbit model of ischemic spinal cord injury.
New Zealand White rabbits were anesthetized with ketamine and xylazine and instrumented for systemic blood pressure monitoring and spinal cord blood flow measurements using the microsphere method. After pretreatment with flunarizine or vehicle, ischemic spinal cord injury was created selectively in the caudal regions of the spinal cord by cross-clamping the abdominal aorta for a period of 25 minutes. Spinal cord blood flow was measured before, during, and 15 minutes after cross-clamp removal. Animals were allowed to recover and were graded neurologically at 18 and 24 hours after ischemia.
Flunarizine injection was associated with hypotension that was both transient and dose related. Animals pretreated with flunarizine 0.4 mg/kg had significantly improved neurological recovery scores at 18 hours after ischemia (P = .017) compared with vehicle controls. At 24 hours this effect was lessened (P = .095); however, 60% of flunarizine-treated animals retained their ability to hop, whereas all of the vehicle-treated animals were nonambulatory.
Flunarizine has a protective effect on neurological recovery after experimental ischemic spinal cord injury. The therapeutic window is narrow, and dosing is limited by untoward hypotension. The mechanism of protection likely involves inhibition of pathological cytosolic calcium accumulation rather than a direct effect on vascular smooth muscle.
Angiotensin converting enzyme inhibitors attenuate ischemic brain metabolism in hypertensive rats.
Authors: Sadoshima S , Fujii K , Ooboshi H , Ibayashi S , Fujishima M 
Published: June 2011

Angiotensin converting enzyme (ACE) inhibitors are expected to modulate neuronal activities. The present study was designed to examine the beneficial effects of ACE inhibitors on microcirculation and metabolism in the ischemic brain.
Cerebral ischemia was developed for 60 minutes in spontaneously hypertensive rats (SHR, n = 35) by bilateral carotid artery occlusion. ACE inhibitor (0.1 or 10 mg/kg SQ 29,852 or captopril) were intravenously injected 15 minutes before cerebral ischemia. Cerebral blood flow to the parietal cortex was measured with the H2 clearance technique. Lactate, pyruvate, and ATP in the brain were estimated by the enzymatic method.
Before cerebral ischemia, high doses of both SQ 29,852 and captopril significantly decreased mean arterial pressure by 15 to 25 mm Hg and reduced cerebral vascular resistance by 13% to 17% of the resting values. Cerebral blood flow and arterial pressure during ischemia were not altered by these ACE inhibitors. After 60 minutes of cerebral ischemia, tissue lactate in vehicle-treated SHR increased 6.6-fold and ATP decreased to 65% of the control values. Administration of SQ 29,852 or captopril significantly reduced the lactate levels to 1.6- to 3.1-fold and well preserved the ATP levels to 82% to 93% of the control.
These results suggest that inhibition of ACE activities may be protective for cerebral metabolism against ischemic insult.
Fructose-1,6-bisphosphate reduces infarct volume after reversible middle cerebral artery occlusion in rats.
Authors: Kuluz J W , Gregory G A , Han Y , Dietrich W D , Schleien C L 
Published: June 2011

We tested the hypothesis that fructose-1,6-bisphosphate, when administered 10 minutes before the end of 2 hours of reversible middle cerebral artery occlusion, reduces ischemia-reperfusion injury and infarct volume measured after a 3-day survival period in rats.
After 1 hour and 50 minutes of middle cerebral artery occlusion by the intraluminal suture method, fructose-1,6-bisphosphate, 500 mg/kg in group 1 and 350 mg/kg in group 2 (or an equivalent volume of 1.8% saline as placebo in each group), was given intravenously for a period of 15 minutes to fasted adult Sprague-Dawley rats. After 2 hours of ischemia, the suture was withdrawn and the rats allowed to survive for 3 days. The areas of infarction in 10 hematoxylin-eosin-stained coronal sections of the brain were measured and used to calculate infarct volume.
In group 1, fructose-1,6-bisphosphate decreased total cerebral hemispheric infarct volume by 43% (from 199.6 +/- 11.2 to 114.2 +/- 35.8 mm3, P < .04; mean +/- SEM). Cerebral cortical and subcortical infarct volumes were decreased by 46% (from 137.3 +/- 7.5 to 74.1 +/- 28.6 mm3, P < .04) and 36% (from 62.3 +/- 5.1 to 40.0 +/- 8.3 mm3, P < .04), respectively. In group 2, fructose-1,6-bisphosphate had no effect on infarct volume in rats that developed mild intraischemic hyperthermia, but in rats kept normothermic during ischemia, fructose-1,6-bisphosphate reduced subcortical infarct volume from 53.7 +/- 8.1 to 18.4 +/- 8.0 mm3 (P < .03).
Fructose-1,6-bisphosphate improves functional neurological outcome and reduces infarct volume after reversible middle cerebral artery occlusion in rats.
Mild hypothermia after cardiac arrest in dogs does not affect postarrest multifocal cerebral hypoperfusion.
Authors: Oku K , Sterz F , Safar P , Johnson D , Obrist W , Leonov Y , Kuboyama K , Tisherman S A , Stezoski S W 
Published: June 2011

Although mild resuscitative hypothermia (34 degrees C) immediately after cardiac arrest improves neurological outcome in dogs, its effects on cerebral blood flow and metabolism are unknown.
We used stable xenon-enhanced computed tomography to study local, regional, and global cerebral blood flow patterns up to 4 hours after cardiac arrest in dogs. We compared a normothermic (37.5 degrees C) control group (group I, n = 5) with a postarrest mild hypothermic group (group II, n = 5). After ventricular fibrillation of 12.5 minutes and reperfusion with brief cardiopulmonary bypass, the ventilation, normotension, normoxia, and mild hypocapnia were controlled to 4 hours after cardiac arrest. Group II received (minimal) head cooling during cardiac arrest, followed by systemic bypass cooling (to 34 degrees C) during the first hour of reperfusion after cardiac arrest.
The postarrest homogeneous transient hyperemia was followed by global hypoperfusion from 1 to 4 hours after arrest, with increased "no-flow" and "trickle-flow" voxels (compared with baseline), without group differences. At 1 to 4 hours, mean global cerebral blood flow in computed tomographic slices was 55% of baseline in group I and 64% in group II (NS). No flow (local cerebral blood flow < 5 mL/100 cm3 per minute) occurred in 5 +/- 2% of the voxels in group I versus 9 +/- 5% in group II (NS). Trickle flow (5 to 10 mL/100 cm3 per minute) occurred in 10 +/- 3% voxels in group I versus 16 +/- 4% in group II (NS). Cerebral blood flow values in eight brain regions followed the same hyperemia-hypoperfusion sequence as global cerebral blood flow, with no significant difference in regional values between groups. The global cerebral metabolic rate of oxygen, which ranged between 2.7 and 4.5 mL/100 cm3 per minute before arrest in both groups, was at 1 hour after arrest 1.8 +/- 0.3 mL in normothermic group I (n = 3) and 1.9 +/- 0.4 mL is still-hypothermic group II (n = 5); at 2 and 4 hours after arrest, it ranged between 1.2 and 4.2 mL in group I and between 1.2 and 2.6 mL in group II.
After cardiac arrest, mild resuscitative hypothermia lasting 1 hour does not significantly affect patterns of cerebral blood flow and oxygen uptake. This suggests that different mechanisms may explain its mitigating effect on brain damage.
Familial cerebrovascular accidents due to concomitant hyperhomocysteinemia and protein C deficiency type 1.
Authors: Franken D G , Vreugdenhil A , Boers G H , Verrips A , Blom H J , Novakova I R 
Published: June 2011

Hyperhomocysteinemia and protein C deficiency are risk factors for thromboembolism. Hyperhomocysteinemia has been reported to inhibit the expression of thrombomodulin and to inactivate both thrombomodulin and protein C irreversibly, leading to decreased protein C activity.
In a 16-year-old girl, who developed a sinus sagittalis thrombosis, and in her father, who experienced a transient ischemic attack, both hyperhomocysteinemia and protein C deficiency type 1 were present. Protein C deficiency alone was found in one of the two sisters, who was without any clinical vascular history.
In this family with independently inherited hyperhomocysteinemia and protein C deficiency, clinical cerebrovascular disease occurred only in those members with a combination of both risk factors, suggesting a synergistic interaction between these thrombogenic risk factors.
Headache in stroke.
Authors: Vestergaard K , Andersen G , Nielsen M I , Jensen T S 
Published: June 2011

The etiology of headache in stroke is not known, and its relation to migraine and tension-type headache is unclear. The aim of our study was to investigate and classify headache appearing in stroke patients prospectively, using the new headache classification as determined by the Headache Classification Committee of the International Headache Society (1988).
Two hundred eighty consecutively admitted patients aged younger than 81 years with acute stroke were examined and questioned about headache and prior headache complaints; 238 (85%) were able to communicate.
Sixty-five (27%) of the 238 patients experienced headache from 3 days before to 3 days after stroke. Headache occurred in 50% of patients with intracerebral hemorrhage, in 26% with infarction, and in 15% of patients with lacunar infarction. Headache was more common when stroke occurred in posterior circulation than anterior circulation (P < .02). Fifty-six patients were able to give further information about headache characteristics. The headache in thromboembolic stroke was classified as tension-type headache (25 patients), migraine-like headache (14 patients), and other headache (12 patients). Migraine was more frequent in vertebrobasilar stroke. Headache was lateralized in 33% of cases. In patients with unilateral headache and unilateral stroke lesion, the headache was ipsilateral in 14 of 17 cases. In infarction, severity of headache showed no relation to lesion size or lesion localization. Patients with previous tension-type headache and migraine experienced reactivation of known headache equally often.
(1) Headache occurs in one fourth of patients with acute stroke. (2) Unilateral headache is usually ipsilateral to stroke lesion. (3) Headache severity is not related to size of ischemic stroke lesion.
Impact of early surgery on outcome after aneurysmal subarachnoid hemorrhage. A population-based study.
Authors: Fogelholm R , Hernesniemi J , Vapalahti M 
Published: June 2011

Population-based patient materials have not been used earlier in assessing the effects of neurosurgical treatment on survival and functional outcome of subarachnoid hemorrhage. Moreover, the proportion of all subarachnoid hemorrhage patients who might be candidates for neurosurgical treatment has not been estimated.
We compared the survival and functional outcome of two population-based patient materials from Central Finland in 1976 through 1978 (n = 146) and 1980 through 1987 (n = 351). The most important basic characteristics of both materials were similar. In the 1970s, only patients aged < 60 years with carotid territory aneurysms were operated on after an interval of 2 weeks from the bleeding. In the 1980s, early surgery was attempted, and the other exclusion criteria were abandoned. Allocation to medical or surgical treatment was not randomized.
During the 1970s, only 14% of the patients had surgical treatment, with a median delay of 15 days after the bleeding; in the 1980s, the corresponding figures were 46% and 4 days. Despite these fundamental changes in the treatment policy, the survival up to 3 years in the 1980s was only marginally improved compared with the 1970s. Conversely, the functional outcome at 4 years after the bleeding was significantly better in the 1980s than the 1970s, with 82% and 64% of the survivors, respectively, being independent in the activities of daily living (P = .002). We estimated that 60% of all patients with subarachnoid hemorrhage might be candidates for neurosurgical treatment, provided that there are no delays in admission or evaluation.
An active treatment policy of subarachnoid hemorrhage including early surgery only marginally improves survival, but the quality of life of the survivors is significantly better. Only 60% of all patients in the population with subarachnoid hemorrhage can, at least theoretically, benefit from surgical treatment.
Activation of healthy hemisphere in poststroke recovery. A transcranial Doppler study.
Authors: Silvestrini M , Caltagirone C , Cupini L M , Matteis M , Troisi E , Bernardi G 
Published: June 2011

The possible involvement of the healthy hemisphere in functional recovery in stroke hemiplegia is still controversial. This study of patients who had suffered ischemic stroke assessed circulatory changes in the healthy hemisphere by transcranial Doppler ultrasonography during opposition exercise of fingers that had recovered movement.
Measurements of flow velocity in the middle cerebral arteries were recorded in 12 recovered hemiplegic stroke patients and 12 healthy sex- and age-matched control subjects during a 2-minute sequential thumb-to-finger opposition task, alternatively performed with normal and recovered fingers. The effects of the motor task on heart rate, blood pressure, and end-tidal PCO2 were also evaluated.
With respect to the basal values, a comparable increase of flow velocity (%mean +/- SD) in the contralateral middle cerebral artery occurred in patients during movement of normal (9.7 +/- 2.7%) and recovered fingers (10.4 +/- 5.1%) and in controls (11.3 +/- 4.9%). However, in the middle cerebral artery ipsilateral to the hand performing the motor task, the increase of flow velocity was significantly higher (P < .001, two-way analysis of variance) during movement of the recovered hand in patients (10.5 +/- 4.6%) than during the movement of the normal hand in both patients (1.7 +/- 3.7%) and controls (1.8 +/- 4.5%). No significant difference of changes in heart rate, blood pressure, and end-tidal PCO2 was observed for patients or normal control subjects during the various phases of the study.
Our data suggest that activation of the healthy hemisphere contributes toward functional recovery of motor deficit after stroke and confirms the ability of transcranial Doppler ultrasonography to correlate cerebral artery flow dynamics with selective cerebral activation.
Nitric oxide production during focal cerebral ischemia in rats.
Authors: Kader A , Frazzini V I , Solomon R A , Trifiletti R R 
Published: June 2011

Nitric oxide has been implicated as a mediator of glutamate excitotoxicity in primary neuronal cultures.
A number of indicators of brain nitric oxide production (nitric and cyclic guanosine monophosphate [cGMP] concentrations and nitric oxide synthase activity) were examined after bilateral carotid ligation and right middle cerebral artery occlusion in adult rats.
Brain nitrite was significantly increased in the right versus left cortex 5, 10, and 20 minutes after middle cerebral artery occlusion (P < .05), with a return to baseline at 60 minutes. There were no significant changes in cerebellar concentrations. Cortical levels of cGMP were increased at 10, 20, and 60 minutes after occlusion, with significant right-to-left differences (P < .05). Cerebellar concentrations of cGMP were also increased but without significant side-to-side differences. Nitric oxide synthase activity increased approximately 10-fold from baseline 10 minutes after occlusion in the right cortex but decreased markedly by 60 minutes from its peak at 10 minutes. The right-to-left difference in nitric oxide synthase activity was significant at 20 minutes (P < .05). Pretreatment of rats with NG-nitro-L-arginine, a nitric oxide synthase inhibitor, abolished the rise in nitrite and cGMP.
These results suggest that a sharp transient increase in the activity of nitric oxide synthase occurs during the first hour of cerebral ischemia, which leads to a burst in nitric oxide production and activation of guanylate cyclase.
Effect of nitric oxide synthase inhibition on cerebral blood flow and injury volume during focal ischemia in cats.
Authors: Nishikawa T , Kirsch J R , Koehler R C , Bredt D S , Snyder S H , Traystman R J 
Published: June 2011

We tested the hypothesis that inhibition of nitric oxide synthase activity in brain before ischemia alters cerebral blood flow and decreases brain injury after 4 hours of middle cerebral artery occlusion in cats.
Halothane-anesthetized cats underwent 4 hours of left middle cerebral artery occlusion after they were randomly assigned to receive either intravenous N omega-nitro-L-arginine methyl ester, at a dose that completely inhibited cortical nitric oxide synthase activity (10 mg/kg, n = 10), or an equal volume of diluent (10 mL saline, n = 10). Serial blood flow measurements were made with radiolabeled microspheres, and injury volume was measured by triphenyltetrazolium staining.
Blood flow to caudate nucleus and inferior temporal cortex decreased to the same extent in both groups during middle cerebral artery occlusion. Somatosensory evoked potential amplitude was reduced to less than 10% of baseline values in both groups. Injury volume of ipsilateral caudate nucleus in cats pretreated with nitroarginine (52 +/- 5%, mean +/- SE) was less (P < .05) compared with the saline group (80 +/- 4%), whereas ipsilateral cerebral hemispheric injury volume was similar between the two groups (30 +/- 6% and 32 +/- 4% of hemisphere in saline and nitroarginine groups, respectively).
These results suggest that inhibition of nitric oxide synthase decreases caudate injury volume at 4 hours of middle cerebral artery occlusion without an alteration in distribution of cerebral blood flow.
Mice expressing a bovine basic fibroblast growth factor transgene in the brain show increased resistance to hypoxemic-ischemic cerebral damage.
Authors: MacMillan V , Judge D , Wiseman A , Settles D , Swain J , Davis J 
Published: June 2011

Cerebral intraventricular infusion of acidic or basic fibroblast growth factor has been shown to attenuate ischemic damage to hippocampal CA1 neurons in the gerbil. The purpose of the present study was to determine if the basic fibroblast growth factor transgenic mouse has an enhanced ability to resist the effects of severe cerebral hypoxemia-oligemia.
Mice that were transgenic for bovine basic fibroblast growth factor were exposed to right carotid artery ligation, hyperglycemia, and 20 minutes of 1% carbon monoxide. After 5 days' recovery, brains were examined for histological damage.
Counts of CA1 neurons in the right hippocampus showed a significantly higher number of neurons per millimeter CA1 in hypoxic-ischemic transgenic mice compared with nontransgenic controls (transgenic, 260 +/- 33; nontransgenic, 151 +/- 37 neurons per millimeter CA1; P < .05).
The results indicate that basic fibroblast growth factor transgenic mice, as judged by CA1 hippocampal neuronal survival, have an enhanced ability to resist the effects of a complex hypoxic-ischemic cerebral insult.