bluuebunny/crossref_metadata_2025_split huggingface dataset:
Free protein S deficiency in acute ischemic stroke. A case-control study.
Authors: Mayer S A , Sacco R L , Hurlet-Jensen A , Shi T , Mohr J P 
Published: June 2011

Deficiency of free protein S, a naturally occurring anticoagulant, may be acquired in the setting of acute illness and increasingly has become recognized as a possible stroke risk factor. We sought to determine whether free protein S deficiency is associated with acute cerebral infarction among older individuals at risk for stroke.
Free protein S was measured by Laurell rocket immunoelectrophoresis in 94 adults admitted for acute cerebral infarction and in 94 hospitalized control subjects of similar age, sex, and race. Patients with a history of cerebrovascular disease, acute thrombotic or hematologic diseases, or medical conditions known to cause free protein S deficiency were excluded from the control group.
The percentage of patients with free protein S deficiency (< 20% normal total protein S) was similar in the case and control groups (21% versus 20%, respectively). Among all subjects, free protein S deficiency was more common in blacks than nonblacks (34% versus 13%, p = 0.001). A very low free protein S (< 15% normal total protein S) was more frequent among case patients than control subjects (11% versus 5%), but this trend failed to reach statistical significance.
Free protein S deficiency is common among hospitalized patients, even in the absence of a recognized predisposing condition. Our findings indicate that acquired deficiency of free protein S is not a major risk factor for ischemic stroke.
Interaction of endothelium with dilation produced by inhibitors of cyclic nucleotide diesterases in mouse brain arterioles in vivo.
Authors: Rosenblum W I , Shimizu T , Nelson G H 
Published: June 2011

In vitro evidence gathered from extracerebral conductance vessels suggests interaction between the endothelium-derived relaxing factor for acetylcholine (EDRFACh) and cyclic nucleotide action in vascular smooth muscle. The purpose of this study was to examine this interaction in vivo in pial arterioles. As had been done in vitro, we used phosphodiesterase inhibitors that elevate cyclic nucleotide levels in vascular smooth muscle.
Pial vessels of mice were observed with television microscopy. Diameter of the arterioles was monitored with an image-splitting technique. The responses to topically applied phosphodiesterase inhibitors were tested before and after focal endothelial injury or before and during application of N-guanidino-L-monomethyl arginine (L-NMMA). Both treatments are known to eliminate the endothelium-dependent response to acetylcholine in this preparation.
Phosphodiesterase inhibitors dilated pial arterioles. This was true for phosphodiesterase inhibitors elevating levels of both adenosine 3',5'-cyclic monophosphate (cAMP) and guanosine 3',5'-cyclic monophosphate (cGMP) as well as for inhibitors thought to selectively affect either nucleotide. The dilation was inhibited by endothelial injury and by L-NMMA.
The data suggest that brain arterioles are dilated by both cAMP and cGMP but that this action is impaired if EDRFACh levels are reduced. Since EDRFACh elevates cGMP levels, these data support the hypothesis that the relaxing actions of cGMP and cAMP depend upon adequate basal levels of cGMP in vascular smooth muscle. This hypothesis, originally introduced in studies of extracerebral conductance arteries in vitro, can now be applied to brain resistance vessels in vivo.
Middle cerebral artery occlusion without craniectomy in rats. Which method works best?
Authors: Laing R J , Jakubowski J , Laing R W 
Published: June 2011

Our purpose was to assess the effectiveness of middle cerebral artery occlusion in producing acute focal ischemia in the rat by the use of Koizumi's and Longa's methods, in which occlusion is achieved by passing a nylon thread into the internal carotid artery.
Cerebral blood flow was measured by using the hydrogen clearance method, and the brains were examined histologically to assess ischemic damage.
By Koizumi's method profound reduction in cerebral blood flow was achieved in 28 of 30 rats (93%). The mean cerebral blood flow in the middle cerebral artery territory was 10.7 (95% confidence interval, 9.9-11.5) ml/100 g per minute. By Longa's method reduction in cerebral blood flow was achieved in only 29 of 52 rats (56%), and in these animals mean cerebral blood flow was 33 (95% confidence interval, 28.3-33.7) ml/100 g per minute (p < 0.001 compared with Koizumi's method). Cerebral blood flow was reduced to < 16 ml/100 g per minute in only seven animals (24%).
By Koizumi's method the depth of ischemia is more profound, occlusion is achieved in a much higher proportion of cases, and the incidence of perforation of the intracranial internal carotid is much less frequent than by Longa's method.
A prospective study of cerebral ischemia in the young. Analysis of pathogenic determinants. The National Research Council Study Group.
Authors: Carolei A , Marini C , Ferranti E , Frontoni M , Prencipe M , Fieschi C 
Published: June 2011

The etiology of stroke in the young is different from that in older patients and remains unknown in almost one third of the cases. To gain further insight into both pathogenic and etiologic determinants, we prospectively studied a large number of consecutive young adults with focal cerebral ischemia.
Three hundred thirty-three patients aged 15-44 years with transient ischemic attack or ischemic stroke within the 8 weeks before hospital admission were recruited and investigated by using a standardized protocol of clinical evaluation, blood tests, electrocardiography, echocardiography, chest roentgenography, and brain computed tomography. Presumed etiology was diagnosed by prospectively applied criteria.
Women predominated (61%) among patients under 35 years of age, mainly due to the frequency of cerebral ischemia related to oral contraceptive use, while men outnumbered women (60%) among patients over that age because of a higher prevalence of atherothrombotic disease. Potential cerebral embolism of cardiac origin was the presumed cause of stroke in 23.7%, but conventional sources of emboli were found only in 7.5% of cases. There was a low prevalence of atrial fibrillation among young patients with cerebral ischemia. Mitral valve prolapse was found in 8.4%, as expected, predominantly (71.4%) among the younger patients. The prevalence of stroke over transient ischemic attack was proportional to the likelihood of cardiac embolism. Acute alcohol intoxication was considered a precipitating factor in only three patients. The percentages of cerebral ischemia attributed to arterial dissection (0.3%), oral contraceptive use in women (8.1%), migraine (1.2%), and other associated medical diseases (1.5%) were lower than reported in recent clinical series.
Two different groups of pathogenic determinants predominate in younger women and in older men, supporting public health measures aimed at strict medical control of the recognized cerebrovascular risk factors.
Causes of urinary incontinence after acute hemispheric stroke.
Authors: Gelber D A , Good D C , Laven L J , Verhulst S J 
Published: June 2011

We prospectively studied bladder function in stroke patients to determine the mechanisms responsible for poststroke urinary incontinence.
Fifty-one patients with recent unilateral ischemic hemispheric stroke admitted to a neurorehabilitation unit were enrolled. The presence of urinary incontinence was correlated with infarct location, neurological deficits, and functional status. Urodynamic studies were performed on all incontinent patients.
Nineteen patients (37%) were incontinent. Incontinence was associated with large infarcts, aphasia, cognitive impairment, and functional disability (p < 0.05) but not with age, sex, side of stroke, or time from stroke to entry in the study. Urodynamic studies, performed on all 19 incontinent patients, revealed bladder hyperreflexia in 37%, normal studies in 37%, bladder hyporeflexia in 21%, and detrusor-sphincter dyssynergia in 5%. All of the patients with normal urodynamic studies were aphasic, demented, or severely functionally impaired. All of the patients with hyporeflexic bladders had underlying diabetes or were taking anticholinergic medications. Forty-six percent of incontinent patients treated with scheduled voiding alone were continent at discharge compared with 17% of patients treated pharmacologically.
There are three major mechanisms responsible for poststroke urinary incontinence: 1) disruption of the neuromicturition pathways, resulting in bladder hyperreflexia and urgency incontinence; 2) incontinence due to stroke-related cognitive and language deficits, with normal bladder function; and 3) concurrent neuropathy or medication use, resulting in bladder hyporeflexia and overflow incontinence. Urodynamic studies are of benefit in establishing the cause of incontinence. Scheduled voiding is a useful first-line treatment in many cases of incontinence.
Absence of elevation of big endothelin in subarachnoid hemorrhage.
Authors: Hamann G , Isenberg E , Strittmatter M , Schimrigk K 
Published: June 2011

Endothelin peptides are potent vasoconstrictors and thus are seen as potential cause of cerebral vasospasm after subarachnoid hemorrhage (SAH). Earlier reports showed elevated or normal endothelin levels in plasma and cerebrospinal fluid in patients suffering from SAH. The present study was designed to determine whether endothelin is a causal factor in SAH.
We studied 11 patients with acute SAH. Seven of these 11 patients had a proven aneurysm and six had experienced vasospasm. Big endothelin levels were determined by a radioimmunoassay recognizing the C-terminal peptide (normal range, 1-11 fmol/ml).
There were no elevations of big endothelin in the 59 plasma samples and the 17 simultaneously estimated cerebrospinal fluid samples. Differences between plasma and cerebrospinal fluid did not reach significant levels. Big endothelin values between patients with and without vasospasm showed no significant differences.
Our findings suggest that plasma elevation of the endothelins is not reproducible in SAH and that big endothelin is unlikely to be a causal plasma factor in the complex multifactorial development of vasospasm after SAH.
Subarachnoid hemorrhage and endothelial L-arginine pathway in small brain stem arteries in dogs.
Authors: Katusić Z S , Milde J H , Cosentino F , Mitrović B S 
Published: June 2011

Experiments were designed to determine the effect of subarachnoid hemorrhage on endothelium-dependent relaxations in small arteries of the brain stem. A "double-hemorrhage" canine model of the disease was used, and the presence of vasospasm in the basilar artery was confirmed by angiography.
Secondary branches of both untreated basilar arteries (inner diameter, 324 +/- 11 microns; n = 12) and arteries exposed to subarachnoid hemorrhage for 7 days (inner diameter, 328 +/- 12 microns; n = 12) were dissected and mounted on glass microcannulas in organ chambers. Changes in the intraluminal diameter of pressurized arteries were measured using a video dimension analyzer.
In untreated arteries, 10(-11) to 10(-7) M vasopressin, 10(-10) to 10(-6) M bradykinin, and 10(-9) to 10(-6) M calcium ionophore A23187 caused endothelium-dependent relaxations. At 10(-6) and 3 x 10(-4) M the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME) abolished relaxations to vasopressin and produced small but significant rightward shifts of the concentration-response curves to bradykinin and A23187. At 10(-3) M L-arginine prevented the inhibitory effect of L-NAME. Subarachnoid hemorrhage abolished relaxations to vasopressin but did not affect relaxations to bradykinin or A23187.
These studies suggest that in small arteries of the brain stem vasopressin causes relaxations by activation of the endothelial L-arginine pathway. This mechanism of relaxation is selectively inhibited by subarachnoid hemorrhage. Preservation of endothelium-dependent relaxations to bradykinin and A23187 is consistent with the concept that small arteries are resistant to vasospasm after subarachnoid hemorrhage.
Cerebral autoregulation during moderate hypothermia in rats.
Authors: Verhaegen M J , Todd M M , Hindman B J , Warner D S 
Published: June 2011

Little is known about the effects of hypothermia on cerebral autoregulation. The present study was designed to examine cerebral blood flow responses to controlled hemorrhagic hypotension in normothermic and hypothermic rats.
Cortical blood flow was measured with a laser-Doppler flowmeter in halothane-anesthetized rats assigned to one of three groups: normothermic group 1 (n = 8) with a pericranial temperature of approximately 36.5 degrees C or hypothermic group 2 (n = 8) or group 3 (n = 8) with a pericranial temperature of approximately 30.5 degrees C. In group 2, a PaCO2 of approximately 40 mm Hg was maintained without correction for body temperature. To evaluate the role of PaCO2, in group 3 animals PaCO2 was kept at approximately 40 mm Hg as corrected for body temperature. In all animals, the mean arterial blood pressure was reduced by hemorrhage in increments of 10 mm Hg every 2 minutes.
In group 1 animals, a typical autoregulatory curve was observed with cerebral blood flow first falling at or below 75% of baseline at a mean arterial pressure of 57 +/- 15 mm Hg (mean +/- SD). Absolute normotensive cerebral blood flow in group 2 fell to < or = 75% of baseline at a mean arterial pressure of 73 +/- 21 mm Hg. In group 3, no evidence of autoregulation was seen. Cerebral blood flow reached values < or = 75% of baseline at a mean arterial pressure of 82 +/- 14 mm Hg, whereas calculated cerebrovascular resistance failed to show any compensatory vasodilation as the mean arterial pressure decreased.
Different PaCO2 management schemes used during hypothermia may have profound effects on cerebral blood flow and on autoregulation. If PaCO2 is maintained at 40 mm Hg after correction for temperature, autoregulation is abolished. If uncorrected PaCO2 is maintained at approximately 40 mm Hg, some degree of autoregulation is preserved, albeit with a right-shifted "knee."
Potentiation by hypoxia of contractions caused by angiotensin II in dog and monkey cerebral arteries.
Authors: Yoshida K , Okamura T , Toda N 
Published: June 2011

Hypoxia alters the responsiveness to endogenous substances of cerebral arteries, possibly resulting in the modulation of blood supply to ischemic brain regions. The present study was undertaken to analyze the mechanism of potentiation by hypoxia of angiotensin II-induced cerebroarterial contractions.
Monkey and dog cerebral arterial strips with endothelium were suspended for isometric tension recording in Ringer-Locke solution aerated with 95% O2-5% CO2 (partial pressure, 570-600 mm Hg) or 95% N2-5% CO2 (approximately 10 mm Hg).
Contractions induced by angiotensin II and substance P were potentiated by exposure to hypoxia, whereas contractile responses to prostaglandin F2 alpha were not influenced. Treatment with cyclooxygenase inhibitors abolished the peptide-induced contraction but did not alter the prostaglandin F2 alpha-induced contraction. Relaxations induced by arachidonic acid were suppressed by indomethacin and hypoxia, whereas those caused by a prostaglandin I2 analogue were unaffected.
The potentiation by hypoxia of cerebroarterial contractions caused by angiotensin II and substance P appears to be due to an interference with the synthesis of prostaglandin I2 from arachidonic acid and a resultant increase in the production of vasoconstrictor prostaglandins.
Angiographic evaluation of brain infarction limited to the anterior cerebral artery territory.
Authors: Kazui S , Sawada T , Naritomi H , Kuriyama Y , Yamaguchi T 
Published: June 2011

Brain infarction localized in the anterior cerebral artery territory is rather uncommon, and its etiology has not yet been fully elucidated.
Based on computed tomographic findings, 17 patients with solitary anterior cerebral artery territory infarction were selected from among 3,619 patients admitted consecutively to our institute. Patients without angiographic examinations were excluded. The angiographic findings and clinical category of stroke were analyzed in each patient.
Angiographic abnormalities were revealed in all patients. These consisted of occlusive changes (n = 10) or reversible segmental dilatation (n = 3) of the anterior cerebral artery, A1 hypoplasia (n = 5), and occlusive changes of the carotid artery (n = 3). In one patient with anterior cerebral artery occlusion, the occluded artery was reopened and subsequently became reoccluded. The clinical category of stroke was classified as atherothrombotic in 10 patients, cardioembolic in three, and undetermined in the remaining four. In eight of the 10 patients with atherothrombotic infarction, the anterior cerebral artery was narrowed or occluded. In all patients with cardioembolic infarction, the A1 segment contralateral to the infarction was hypoplastic.
In our series, solitary anterior cerebral artery territory infarction was attributable most commonly to local atherothrombosis and occasionally to cardiogenic embolism. A hypoplastic A1 segment may facilitate the occurrence of embolism in the anterior cerebral artery. Reversible dilatatory and occlusive changes of this artery may be another important cause of infarction.
Cerebral blood flow alterations in a rat model of cerebral sinus thrombosis.
Authors: Ungersböck K , Heimann A , Kempski O 
Published: June 2011

Outcome from sinus vein thrombosis is very variable, with symptoms from headache to coma. Experimental findings suggest that an involvement of cortical veins is necessary to affect the cerebral microcirculation. Laser Doppler flowmetry was used to investigate the regional and temporal changes in local cortical blood flow after experimental occlusion and thrombosis of the superior sagittal sinus and tributary cortical veins in rats.
Thrombosis was induced by slow injection of kaolin-cephalin suspension after frontal and caudal ligation of the sagittal sinus in rats. Local cerebral blood flow was measured by laser Doppler flowmetry and correlated with parenchymal damage found 24 hours after induction of thrombosis.
Local cerebral blood flow 1 hour after sinus occlusion and induction of thrombosis had decreased to 60.92 +/- 29.05% (p < 0.01); however, there was a large variability among individual animals. Only five of 12 rats showed histological damage and intracerebral hemorrhages 24 hours after induction of thrombosis. A subgroup analysis revealed that parenchymal damage occurred in concurrence with reduced blood flow values after sinus ligation and injection of the thrombogenic material. Sinus thrombosis alone, without alteration of blood flow, did not cause tissue necrosis.
The data support the contention that sinus vein thrombosis evolves gradually, with major symptoms occurring only if the thrombus expands from the sinus into bridging and cortical veins. Collateral venous outflow pathways are thereby occluded, and local blood flow may become reduced to and below the ischemic threshold.
The role of bradykinin in mediating ischemic brain edema in rats.
Authors: Kamiya T , Katayama Y , Kashiwagi F , Terashi A 
Published: June 2011

We investigated the hypothesis that bradykinin generation may induce ischemic brain edema in spontaneously hypertensive rats.
Cerebral ischemia lasting 3 hours was produced by bilateral common carotid artery occlusion in 67 rats. After the ischemic period, the rats were reperfused. Cerebral water content and energy metabolites (adenosine triphosphate, lactate, and pyruvate), as well as plasma and tissue bradykinin, were measured. Additionally, using the same experimental paradigm, bradykinin synthesis inhibitors (aprotinin [n = 7] and soybean trypsin inhibitor [n = 7]) were administered immediately after ischemia induction to determine the relation of bradykinin generation to the progression of ischemic brain edema.
Cerebral water content increased during the 3-hour ischemic period, peaked at 30 minutes of reperfusion, and declined thereafter. Bradykinin levels in plasma and tissue rose markedly 30 minutes after reperfusion and fell thereafter. The progressive loss of adenosine triphosphate was mirrored by the rise in lactate. In the treated groups, aprotinin and soybean trypsin inhibitor administration significantly attenuated cerebral edema (p < 0.01 and p < 0.05, respectively). The treated groups also showed less lactate accumulation and more adenosine triphosphate preservation than did the controls.
These results demonstrate that bradykinin levels in plasma and tissue corresponded to cerebral edema progression and that bradykinin suppression decreased edema formation. These novel findings indicate that bradykinin activation augments the progression of ischemic brain edema.
Isolated or predominant ocular motor nerve palsy as a manifestation of brain stem stroke.
Authors: Kim J S , Kang J K , Lee S A , Lee M C 
Published: June 2011

There have been few reports of strokes producing isolated or predominant ocular motor nerve palsies as a clinical manifestation.
We studied seven patients with brain stem stroke who had ocular motor palsies as the only or the predominant neurological manifestation, and we correlated their clinical features with radiological findings.
Five patients had small strokes in the area of oculomotor nuclei or fascicles and showed various combinations of oculomotor disturbances. Three of these patients showed vertical gaze paresis of the opposite eye. One patient with a small hemorrhage near the aqueduct of Sylvius showed fourth nerve palsy on the contralateral side, and a patient with a small infarct in the pontine tegmentum showed isolated sixth nerve palsy. Nonocular minor neurological signs included trigeminal sensory changes in four patients and clumsy arm in two. Ocular and nonocular dysfunctions generally improved within several months. Radiological findings of the brain stem correlated well with the ocular signs.
We conclude that acute brain stem stroke should be included in the differential diagnosis of isolated ocular motor nerve palsies and that appropriate diagnostic investigations should be performed in these cases.
Cigarette smoking and alcohol consumption as risk factors for aneurysmal subarachnoid hemorrhage.
Authors: Juvela S , Hillbom M , Numminen H , Koskinen P 
Published: June 2011

Aneurysmal subarachnoid hemorrhage is a serious disease despite recent improvements in medical and surgical treatment. Hence, identification of modifiable risk factors for subarachnoid hemorrhage is important.
We compared the smoking and drinking habits of 278 consecutive patients with aneurysmal subarachnoid hemorrhage, aged 15-60 years (145 men and 133 women) with those of 314 hospitalized control patients (164 men and 150 women) who did not differ in regard to age, day of onset of symptoms, and acuteness of disease onset.
Multiple logistic regression analysis showed that recent alcohol intake and smoking, but not hypertension, were significant independent risk factors for hemorrhage. After adjustment for age, hypertension, and smoking status, men who had consumed 1-40, 41-120, or > 120 g of alcohol within the 24 hours preceding the onset of illness had a relative risk of hemorrhage of 0.3 (95% confidence interval [CI], 0.1-0.8), 2.5 (95% CI, 1.1-5.5), and 4.5 (95% CI, 1.5-12.9), respectively, compared with men who had consumed 0 g. Women who had consumed 1-40 or > 40 g of alcohol had a risk of hemorrhage of 0.4 (95% CI, 0.2-0.8) and 6.4 (95% CI, 2.3-17.9), respectively, compared with women without use of alcohol. Heavily smoking (> 20 cigarettes per day) men and currently smoking women had adjusted relative risks of hemorrhage of 7.3 (95% CI, 3.8-14.3) and 2.1 (95% CI, 1.2-3.6), respectively, compared with men who had never smoked and with women who were not current smokers. Higher levels of erythrocyte mean corpuscular volume in patients with subarachnoid hemorrhage than in control subjects supported the notion of different smoking and drinking habits.
Recent heavy alcohol intake and current smoking seem to be independent risk factors for aneurysmal subarachnoid hemorrhage.