bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effects of recombinant superoxide dismutase on manganese superoxide dismutase gene expression in gerbil hippocampus after ischemia.
Authors: Matsuyama T , Shimizu S , Nakamura H , Michishita H , Tagaya M , Sugita M 
Published: June 2011

We reported that recombinant human superoxide dismutase ameliorates delayed neuronal death in the postischemic gerbil hippocampus. Since postischemic induction of copper-zinc superoxide dismutase messenger RNA was abolished by this treatment, oxygen radicals generated on reperfusion may induce the expression of this gene. In the present study we examined whether oxygen radicals also induce the expression of manganese superoxide dismutase messenger RNA in the postischemic brain.
We induced transient cerebral ischemia by occluding the bilateral common carotid arteries of gerbils. Recombinant human superoxide dismutase (8 x 10(5) U/kg) or apo-superoxide dismutase was administered intravenously 1 minute before a 5-minute occlusion of the carotid arteries. We analyzed both copper-zinc and manganese superoxide dismutase RNA by in situ hybridization histochemistry and by Northern and dot blot analyses using radioisotope-labeled oligonucleotide probes.
Hybridization with the manganese superoxide dismutase messenger RNA occurred at the limit of detection in normal CA1 neurons. We observed striking increases in the labeling of CA1 up to 24 hours after 5 minutes of ischemia. The hybridization occurred anew in glial cells of the CA1 layer during 3 to 7 days. Pretreatment with recombinant human superoxide dismutase had no effect on the postischemic induction of manganese superoxide dismutase messenger RNA, whereas the same treatment significantly attenuated (P < .01) the increase in copper-zinc superoxide dismutase messenger RNA.
Our results demonstrated temporal postischemic induction of manganese superoxide dismutase messenger RNA. The inducer may not be superoxide radicals but may be other chemical mediators such as cytokines.
Effects of local reduction in pressure on endothelium-dependent responses of cerebral arterioles.
Authors: Baumbach G L , Faraci F M , Heistad D D 
Published: June 2011

The goal of this study was to examine effects of local reductions in intravascular pressure and dP/dt on endothelium-dependent responses of cerebral arterioles in normotensive Wistar-Kyoto rats (WKY) and stroke-prone spontaneously hypertensive rats (SHRSP).
WKY and SHRSP underwent clipping of one carotid artery at 1 month of age. At 6 months of age, responses of pial arterioles were examined in vivo in anesthetized rats. Bilateral craniotomies were performed to expose pial arterioles in the sham-operated and clipped cerebral hemispheres. Pressure (servo-null) was measured in sham-operated and clipped pial arterioles, and arteriolar diameter was measured before and during suffusion with bradykinin, A23187, and nitroprusside.
Carotid clipping normalized pial arteriolar pulse pressure but not mean pressure in SHRSP. Responses of sham-operated pial arterioles to bradykinin and A23187 were less in SHRSP than in WKY. Responses of sham-operated pial arterioles to nitroprusside were greater in SHRSP than in WKY. Carotid clipping in SHRSP normalized responses of pial arterioles to bradykinin but not A23187 and had no effect on responses to nitroprusside.
These findings suggest that elevated intravascular pressure per se may contribute to impairment of endothelium-dependent relaxation to at least some agonists in cerebral arterioles during chronic hypertension. Furthermore, the findings lead us to speculate that arteriolar pulse pressure may play a more important role than mean pressure in development of impaired endothelium dilatation during chronic hypertension.
Role of angiotensin receptor subtypes in the response of rabbit brain arterioles to angiotensin.
Authors: Haberl R L 
Published: June 2011

Angiotensin II has been reported to induce either constriction or dilation in the cerebral microcirculation. The goal of this study was to determine whether binding to different angiotensin II receptor subtypes may account for the divergent responses.
Pial arterioles ranging a diameter from 28 to 136 microns were observed through a microscope in a closed cranial window preparation in anesthetized rabbits. Arteriolar responses to topical application of 10(-5) mol/L angiotensin II or the vasoactive angiotensin II degradation products L-arginine/angiotensin-(3-8) were measured by videometry. The effect of the subtype 1 receptor antagonist losartan and the subtype 2 antagonist PD 123319 on these responses was examined in separate groups of animals.
Topical coapplication of 10(-5) mol/L losartan or 10(-5) mol/L PD 123319 produced 55% and 62% inhibition of the dilator response to 10(-5) mol/L angiotensin II, respectively. Combined application of the antagonists caused 79% inhibition. Each of the antagonists almost completely blocked the response to L-arginine/angiotensin-(3-8). Acetylcholine-induced dilation of rabbit brain arterioles was unaffected by the antagonists.
Both of the known angiotensin II receptor subtypes appear to be involved in angiotensin II-induced dilation of rabbit cerebral arterioles. These results argue against the assumption that vasodilation is a specific function of one of these receptor subtypes, which might have explained the equivocal effects of angiotensin II by predominance of a certain receptor subtype in a given vascular bed.
Endogenous angiotensin II inhibits production of cerebrospinal fluid during posthypoxemic reoxygenation in the rabbit.
Authors: Maktabi M A , Faraci F M 
Published: June 2011

The choroid plexus, the major source of cerebrospinal fluid (CSF), contains receptors for angiotensin II and a very high concentration of angiotensin converting enzyme. Circulating angiotensin II decreases blood flow to the choroid plexus and the production of CSF. During recovery from hypoxia, marked increases in circulating angiotensin II have been described in some studies. We tested the hypothesis that CSF production decreases during posthypoxemic reoxygenation and examined related changes in plasma concentrations of angiotensin II. We also determined whether effect of posthypoxic reoxygenation on production of CSF is due to endogenous release of angiotensin II.
We measured production of CSF in chloralose-anesthetized rabbits using ventriculocisternal perfusion of artificial CSF containing blue dextran. After control measurements, rabbits were subjected to one of the following interventions: (1) 30 minutes of hypoxia (PaO2 = 36 +/- 1 mmHg [mean +/- SE]) followed by 90 minutes of reoxygenation; (2) 30 minutes of hypoxia (PaO2 = 37 +/- 2 mmHg) followed by 90 minutes of reoxygenation in the presence of the angiotensin II antagonist saralasin; (3) hypoxia for 120 minutes (PaO2 = 35 +/- 1 mmHg); and (4) infusion of vehicle under normoxic conditions for 120 minutes (time control). Plasma concentrations of angiotensin II were also measured (radioimmunoassay) under control conditions, during hypoxia, and during posthypoxic reoxygenation (first intervention) and at corresponding time intervals in time control animals (fourth intervention).
Under control conditions, the rate of production of CSF averaged 6.7 +/- 0.1 microL.min-1. During posthypoxemic reoxygenation, production of CSF decreased by 31 +/- 4% (P < .05). In the presence of sarlasin, CSF production did not change significantly during posthypoxemic reoxygenation (-12 +/- 6%, P > .05). In time control animals and during prolonged hypoxia, CSF production did not change significantly (-12 +/- 5% [P > .05] and 9 +/- 7% [P > .05], respectively). Plasma concentrations of angiotensin were below the threshold of sensitivity of the assay under control conditions and during interventions in animals that were made hypoxic and then reoxygenated and in time control animals.
CSF production decreases during posthpoxemic reoxygenation. Since plasma concentrations of angiotensin II did not change during posthypoxic reoxygenation, this effect does not appear to be mediated by increases in circulating angiotensin II. We speculate that endogenous release of angiotensin II, perhaps in the choroid plexus epithelium, decreases production of CSF after hypoxic brain injury.
Spontaneous echo contrast and hemorheologic abnormalities in cerebrovascular disease.
Authors: Briley D P , Giraud G D , Beamer N B , Spear E M , Grauer S E , Edwards J M , Clark W M , Sexton G J , Coull B M 
Published: June 2011

Spontaneous echo contrast (SEC) is thought to represent a risk factor for cardioembolic stroke. In vitro studies suggest that SEC results from interaction between red cells and fibrinogen. To better understand the relation between SEC and stroke and to investigate the in vivo genesis of SEC, we examined the relation between SEC, the constituents of the blood, and plasma and serum viscosity in patients with acute stroke or chronic cerebrovascular disease.
Fifty patients with acute stroke or chronic cerebrovascular disease referred for transesophageal echocardiogram (TEE) were studied by transthoracic echocardiography and TEE. Complete blood count, fibrinogen, albumin, gamma-globulin, and plasma and serum viscosity determinations were made. Left atrial SEC was graded as absent, mild, or marked by means of TEE.
SEC was absent in 31 patients, mild in 10 patients, and marked in 9 patients. Higher grade of SEC was associated with a significantly greater percentage of patients with atrial fibrillation and larger left atrial dimension. Atrial fibrillation was present in 23% of the patients in the SEC absent group, 50% of the patients in the mild SEC group, and 78% of the patients in the marked SEC group (P < .01). Left atrial diameter averaged 3.8 +/- 0.6 cm in the SEC absent group, 4.3 +/- 1.1 in the mild SEC group, and 4.9 +/- 0.7 in the marked SEC group (P < .001). Hematocrit, white blood cell count, and platelet count did not differ among the three groups. Fibrinogen, gamma-globulin, plasma viscosity, and serum viscosity values were all significantly higher in the presence of SEC (P < .05). Fibrinogen values were 361 +/- 97 mg/dL in the SEC absent group and 427 +/- 135 mg/dL in the marked SEC group. gamma-Globulin levels were 0.75 +/- 0.23 g/dL in the SEC absent group and 1.06 +/- 0.48 g/dL in the marked SEC group. Both plasma viscosity (1.97 cp) and serum viscosity (1.64 cp) were higher in the marked SEC group than in the SEC absent group (1.77 and 1.50 cp, respectively).
In patients with acute stroke or chronic cerebrovascular disease, the severity of SEC was not related to albumin, hematocrit, white cell count, or platelet count but rather to elevated fibrinogen levels and concomitant increases in both plasma and serum viscosity. Moreover, increasing grade of SEC was associated with significantly increased left atrial diameter and a higher percentage of patients in atrial fibrillation.
Cerebrospinal fluid and therapy of isolated angiitis of the central nervous system.
Authors: Oliveira V , Póvoa P , Costa A , Ducla-Soares J 
Published: June 2011

Serial cerebral angiograms, computed tomography, and magnetic resonance imaging are among the proposed methods for monitoring disease activity and response to therapy in isolated angiitis of the central nervous system. Cerebrospinal fluid has not proved to be useful in monitoring clinical course.
We describe a 45-year-old man with histological diagnosis of isolated angiitis of the central nervous system that was treated with prednisone plus azathioprine and monitored for 2 years. Samples of the cerebrospinal fluid were obtained for cytological and routine chemical examination, as well as albumin and immunoglobulin content. Before treatment, cerebrospinal fluid showed marked plasmatic transudation of albumin and intrathecal synthesis of immunoglobulins. During the first year of immunosuppression no events were noticed, and the previously abnormal aspects of the cerebrospinal fluid showed improvement. During the weaning of azathioprine, a new stroke occurred in conjunction with a marked deterioration of cerebrospinal fluid parameters. Immunosuppression was resumed at previous levels, and during the following year no further events occurred. Once again, abnormal cerebrospinal fluid values improved significantly.
We report a case of isolated angiitis of the central nervous system in which the serial cerebrospinal fluid examinations (albumin and immunoglobulin content) showed a close correlation with clinical course. This method may be useful in monitoring response to therapy.
Ensuring reliability of outcome measures in multicenter clinical trials of treatments for acute ischemic stroke. The program developed for the Trial of Org 10172 in Acute Stroke Treatment (TOAST).
Authors: Albanese M A , Clarke W R , Adams H P , Woolson R F 
Published: June 2011

Ensuring the reliability and validity of outcome measures used in clinical trials is essential to the success of the trial. The Trial of Org 10172 in Acute Stroke Treatment (TOAST) is a multicenter clinical trial that is recruiting patients with acute ischemic stroke seen at medical centers across the United States.
This paper describes an approach to train physicians to use three clinical measures: the National Institutes of Health (NIH) Stroke Scale, a supplemental motor examination, and the Glasgow Outcome Scale. The program included education, certification, remediation when needed, monitoring, and reliability assessment. The goal was to ensure that interrater assessments were as equivalent to one another as possible.
Of the first 95 clinicians who began the certification process, 75 passed during the first evaluation. Eighteen of the other physicians were able to complete the process after remediation. The intraclass correlations of both the NIH Stroke Scale and supplemental motor examination exceeded 0.95. The kappa values for the Glasgow Outcome Scale were 0.61 and 0.62 for the first and second ratings of the videotape, respectively.
Our experience suggests that a program that includes educational and certification processes can be performed as part of the design of a multicenter clinical trial. The method of providing educational and testing videotapes to each site so that physicians can be trained and certified is an effective, inexpensive, and practical approach for enhancing and certifying the expertise of the large number of physicians involved in a multicenter study.
Incidence of stroke among inpatients in a large Italian hospital.
Authors: Azzimondi G , Nonino F , Fiorani L , Vignatelli L , Stracciari A , Pazzaglia P , D'Alessandro R 
Published: June 2011

The incidence of stroke among inpatients is not known. The aim of our study was to investigate the incidence of stroke not preceded by evident iatrogenic factors such as surgical or medical procedures in a cohort of inpatients in a large Italian general hospital.
From January 1, 1992, to December 31, 1992, we evaluated patients referred to our neurology department with a suspected diagnosis of stroke that occurred during hospitalization. Patients presenting with stroke as a complication of iatrogenic causes were excluded. We calculated the incidence rate of first-ever stroke in our cohort (crude and among patients aged older than 50 years), thereafter adjusting these rates for age to the general population of the city district of Bologna (Italy).
In 1992, 22 inpatients had a first-ever stroke with no evidence of iatrogenic factors. The crude stroke incidence rate was 11.08/1000 per year (95% confidence interval, 6.95 to 16.73). The age-adjusted rate was 5.46 (95% confidence interval 3.42 to 8.24).
The incidence rate of first-ever stroke among hospitalized patients is higher than those reported in community-based studies. Higher frequency of coronary artery disease among our patients could explain our findings. Further studies are needed to identify possible predisposing factors (individual or environmental) for stroke among inpatients.
Correlation of xenon-enhanced computed tomography-defined cerebral blood flow reactivity and collateral flow patterns.
Authors: Smith H A , Thompson-Dobkin J , Yonas H , Flint E 
Published: June 2011

A chronic compromise of cerebral hemodynamics has been shown to identify a group of patients at an increased risk for stroke. Because a "steal phenomenon" induced by a vasodilatory challenge has characterized the group at greatest risk, it was hypothesized that these individuals would also have a severe compromise of primary collaterals and an increased dependence on leptomeningeal collaterals.
Twenty-three patients with symptomatic cerebrovascular disease underwent angiography and xenon-enhanced computed tomographic cerebral blood flow studies before and after 1 g IV acetazolamide within 6 months of each other. Cerebral blood flow vasoreactivity was classified by whether cerebral blood flow increased (> 5%) or was unchanged (+/- 5%) (group 1) or fell by > 5% (group 2) in any vascular territory. Angiographic collateralization was classified into four types: normal (type 1), willisian (type 2), ophthalmic (type 3), and leptomeningeal (type 4).
Twenty percent (2/10) of group 1 patients and 69% (9/13) of group 2 patients (P = .0009) had leptomeningeal collaterals.
A negative flow reactivity is significantly associated with a dependence on leptomeningeal collaterals and implies a state of maximal hemodynamic compromise.
Magnetic resonance imaging study on the effect of levemopamil on the size of intracerebral hemorrhage in rats.
Authors: Elger B , Seega J , Brendel R 
Published: June 2011

Beneficial effects of calcium antagonists in cerebral ischemia and trauma have been attributed in part to improved cerebral blood flow. Enhancement of cerebral blood flow, however, could aggravate the pathological situation if brain injury is associated with intracerebral hemorrhage. In this study we used high-field magnetic resonance imaging in an animal model of intracerebral hemorrhage to determine noninvasively the effect of the calcium and serotonin antagonist levemopamil [international nonproprietary name for (S)-emopamil] when infused in a dose (6 mg/kg) that is known to increase cerebral blood flow.
Intracerebral hemorrhage was induced in rats by stereotaxic microinfusion of collagenase into the caudate putamen. Two series of experiments were performed. (1) Levemopamil was intravenously infused 30 minutes after intracerebral infusion of collagenase (0.05 U), which represents the time of intracranial bleeding. Another group of animals was given heparin (55 IU.kg-1.min-1) to evaluate the capability of this animal model to demonstrate drug-induced worsening of intracerebral hemorrhage. (2) The effects of hyperacute infusion of levemopamil (30 minutes after infusion of 0.5 U of collagenase) were compared with those of a 2-hour delayed administration. In both experimental settings, the extent of intracerebral hemorrhage was determined by T1-weighted magnetic resonance images (spin-echo; repetition time, 400 milliseconds; echo time, 23 milliseconds) taken in vivo in a coronal and a transverse brain plane 24 hours after collagenase infusion.
(1) Hemorrhagic brain areas measured 10.1 +/- 2.9 mm2, 8.5 +/- 2.1 mm2, and 18.8 +/- 2.5 mm2 in the coronal brain plane (10 mm anterior to the interaural line) of control, levemopamil-, and heparin-infused rats, respectively (8 animals per group, mean +/- SD). In the transverse brain plane (6 mm dorsal to the interaural line) the hemorrhagic area was 11.5 +/- 3.6 mm2, 9.7 +/- 2.4 mm2, and 19.9 +/- 3.3 mm2 in control, levemopamil-, and heparin-infused rats, respectively. (2) Animals with 2-hour delayed levemopamil infusion displayed intracerebral hemorrhage similar in size to that of control rats. (3) Neither small nor large hemorrhagic lesions were increased by levemopamil.
Aggravation of intracerebral hemorrhage was not observed by magnetic resonance imaging in levemopamil-infused animals. However, infusion of heparin caused a significant (P < .05), almost twofold increase in the size of intracerebral hemorrhage. These results justify clinical trials with levemopamil in cerebral disorders such as stroke, brain trauma, and peritumoral brain edema, which may be accompanied by intracerebral hemorrhage from the beginning or where transition to intracerebral hemorrhage may occur.
Arterial microsphere concentrations in cats are not affected by changes in hematocrit.
Authors: DeWitt D S , Prough D S , Deal D D , Hoen H M 
Published: June 2011

Acute anemia may lead to erroneously low arterial reference sample concentrations of radioactive microspheres, depending on the sampling rate and the size of the artery from which the reference samples are withdrawn. Because this error would lead to falsely high cerebral blood flow values in studies involving hemodilution caused by hemorrhage and fluid resuscitation, we studied the effects of hematocrit, withdrawal rate, and vessel location and size on arterial microsphere concentrations in anesthetized adult cats.
Cats were anesthetized with ketamine, isoflurane, and nitrous oxide; both brachial arteries were cannulated with polyethylene tubing, as was the abdominal aorta through the femoral artery. Sequential left atrial microsphere injections were made using several doses of each of five isotopes. The rate of reference sample withdrawal from the three sampling catheters was randomized to 1.03 mL.min-1 or 2.06 mL.min-1. We analyzed the ratio of the number of microspheres in paired reference samples using the factors hematocrit, rate of withdrawal, and site. A ratio less than 1 indicates an underestimation of arterial microsphere concentration, which would lead to erroneously high cerebral blood flow values. The procedure was repeated after isovolemic hemodilution with 10% hetastarch to hemoglobin levels approximating 85%, 70%, 55%, and 40% of baseline.
No significant effects of hematocrit on ratios of microsphere concentrations existed at any withdrawal rate or site. Ratios of microsphere concentrations in reference samples withdrawn slowly (1.03 mL.min-1) from the aorta and ratios of microsphere concentrations withdrawn either rapidly (2.06 mL.min-1) or slowly from the brachial arteries were significantly (P < .001) less than 1.
Hemodilution did not affect microsphere concentrations in arterial reference samples at any withdrawal site or rate and therefore does not affect the accuracy of microsphere blood flow determinations. However, slow withdrawal from a large vessel may underestimate actual microsphere concentrations.
I. Epidemiology For Stroke Facilities Planning
Authors: Stallones Reuel A. , Dyken Mark L. , Fang Harry C. H. , Heyman Albert , Seltser Raymond , Stamler Jeremiah 
Published: June 2011

The Major factors known to be associated with stroke include increasing age, hypertension, cardiovascular disease and diabetes. However, many additional data are required to substantiate the role of other risk factors.
The incidence, prevalence and mortality figures in this paper are presented in a form to be useful for palnning health facilities and manpower resources required in the proper management of stroke problems.
Continued Patency of Canine Lingual-Basilar System
Authors: Reichman O. Howard 
Published: June 2011

A canine lingual-basilar system has been helpful to study the use of extracranial vessels for perfusion of the cerebral circulation. This experimental system was patent in all nine long-term animals and enlarged with time.
The principles derived from this experimental investigation have been applied to six patients in whom the superficial temporal artery was used to enhance cerebral perfusion by anastomosis to a cortical branch of the middle cerebral artery. The first four patients have had follow-up arteriography which demonstrates patency of all five new vascular channels.