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  • 1
    ISSN: 1432-0533
    Keywords: Subarachnoid hemorrhage ; Prostaglandin F2-alpha ; Hippocampus ; Purkinje cell ; Intracranial hypertension
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of subarachnoid hemorrhage (SAH) with various degrees of increase in intracranial pressure (ICP) on the staining of prostaglandin F2-alpha (PG F2α) were studied in rat brains. SAH was produced in 18 rats by injection of 0.18–0.20 ml of autologous arterial blood/100 g body weight into the cisterna magna. By changing the speed of injection, the ICP was transiently increased by 346±68 (mean±S.D.) mm Hg in eight rats (including three pretreated with indomethacin), by 200±42 mm Hg in five rats, and by 6±4 mm Hg in the other five. Three rats injected with the same volume of mock cerebrospinal fluid (CSF) with ICP increased by 217±67 mm Hg and five normal rats without injection served as controls. All animals were decapitated 15 min after injection. The cryosections were stained for PG F2α using an indirect immunofluorescence method. Positive staining for PG F2α was noted only in pial vessels in all normal and mock-CSF-injected rats. In SAH rats with ICP increased by 6±4 mm Hg, there was a positive reaction in hippocampal neurons and Purkinje cells as well as blood vessels. SAH rats with higher ICP showed stronger PG F2α staining in the above areas, as well as in cerebellar granule cells. All rats pretreated with indomethacin showed a smaller increase in staining. The above results indicate that subarachnoid blood clots per se produce a rapid increase of PG F2α in neurons and blood vessels of both cerebrum and cerebellum, and that this increase is augmented by intracranial hypertension.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0533
    Keywords: Prostaglandin F2-alpha ; Immunohistochemistry ; Transient increase ; Hippocampus ; Purkinje cell
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The changes in prostaglandin F2-alpha (PG F2α) staining over 3 days of recirculation in both fore-and hindbrains were studied. Five minutes of global ischemia was produced in 24 rats by Pulsinelli's method with hypotension around 50 mm Hg of mean arterial blood pressure. Eight rats (including three pretreated with indomethacin) were recirculated for 5 min, three for 1 h, five for 2 h and five for 3 days. Five normal rats without occlusion of vessels served as controls. The brains were snap frozen. Ten-micrometer cryosections were stained for PG F2α by the indirect immunofluorescence method after fixation in carbodiimide and in Zamboni's solution. Positive staining for PG F2α was noted in pial vessels in all normal and ischemic rats. Recirculated rats revealed the strongest reaction at 5 min after recirculation in blood vessels and in neuronal cytoplasm (especially in hippocampi and in Purkinje cells). The intensity of staining was markedly reduced after 1 h. Rats pretreated with indomethacin showed less increase in staining. The above results indicate that recirculation after ischemia produces a transient increase in PG F2α in blood vessels and neurons of both fore- and hindbrains.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Acta neurochirurgica 132 (1995), S. 26-31 
    ISSN: 0942-0940
    Keywords: Moyamoya disease ; adult ; peri-operative haemodynamic complications ; surgical factors ; non-surgical factors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The incidence and causes of peri-operative haemodynamic complications in adult Moyamoya disease were examined by reviewing 55 surgically treated adult patients. Ninety-nine craniotomies were performed in these patients, and eight peri-operative complications (four infarctions, two haemorrhagic infarctions and two reversible ischaemic neurological deficits without a new lesion) were seen. All of the eight haemodynamic complications arose in the initially affected hemispheres regardless of the side of operation. Some nonsurgical haemodynamic risk factors, i.e., hypercapnia, hypocapnia and hypotension/hypovolaemia, were noted in all of the eight cases, although the statistical analysis could not clarify the relevance of such factors to peri-operative complications. Surgical factors which might be responsible for the complications were noted in three cases. Sparing vital collateral vessels and minimum brain retraction as well as avoidance of non-surgical haemodynamic risk factors are considered to be essential to prevent peri-operative haemodynamic brain damage in adult Moyamoya disease.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 0942-0940
    Keywords: Cerebral vasospasm ; nicardipine ; papaverine ; subarachnoid haemorrhage
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The clinical effect of combination therapy with high doses of intravenous nicardipine and intra-arterial infusion of papaverine on symptomatic vasospasm after subarachnoid haemorrhage (SAH) was analysed retrospectively. In 66 of 122 patients who underwent early aneurysm surgery between 1990 and 1993, the intracranial haemodynamics were documented by transcranial Doppler (TCD) ultrasonography. 33 of these 66 patients received high dose nicar-dipine intravenously (Group I); the other 33 patients were not treated with calcium antagonists (Group II). Symptomatic vasospasm occurred in 6 Group I patients (18%) and in 13 (39%) in Group II patients. All 19 symptomatic patients received an intra-arterial infusion of papaverine; 15 patients (79%) responded well to this therapy and the symptoms were reversed quickly. Although the mean flow velocity (MFV) was not different between the two groups, it was reduced significantly after papverine infusion. Our retrospective analysis suggests that symptomatic vasospasm can be treated effectively with the combination of intravenous high dose nicardipine and intra-arterial infusion of papaverine, and that the correct timing of the infusions is crucial.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Acta neurochirurgica 141 (1999), S. 1353-1354 
    ISSN: 0942-0940
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 0942-0940
    Keywords: Cerebral vasospasm ; concentration ; papaverine ; subarachnoid haemorrhage
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We evaluated the effect of intra-arterially infused papaverine solutions of various concentrations on cerebral vasospasm following subarachnoid haemorrhage. A total of 90 vascular territories in 46 patients with symptomatic cerebral vasospasm after subarachnoid haemorrhage were treated with intra-arterial infusions of papaverine. In all patients, papaverine was infused at the top of the internal carotid artery (ICA). Of the 90 vascular territories, 30 vascular territories in 14 patients were treated with an infusion of 0.1–0.2% (weight/volume) papaverine (Group 1), 30 vascular territories in 16 patients were treated with a 0.4% (w/v) papaverine infusion (Group 2), and 30 vascular territories in 16 patients were treated with an infusion of 0.8–2.0% (w/v) papaverine (Group 3). Among the three groups, we compared the vasodilatory effects of papaverine by assessing the angiographical and clinical improvements following the treatment. When 0.4% (w/v) papaverine was infused, 24 vascular territories (80%) were successfully dilated and 7 patients (44%) showed a marked reversal of neurological deficits due to vasospasm. Therefore, 80 mg/20 ml (0.4% (w/v)) papaverine infused over a 10-minute period proved to be a beneficial concentration. Transient focal neurological deficits due to the infusion of papaverine occurred in 1 Group 1 patient (7%), 1 Group 2 patient (6%), and 7 Group 3 patients (44%). Highly concentrated papaverine had a higher risk of temporary deterioration. In conclusion, the papaverine concentration of 0.4% (w/v) infused at the top of the ICA was a safe and adequate concentration for treating cerebral vasospasm.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Acta neurochirurgica 62 (1982), S. 73-77 
    ISSN: 0942-0940
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Three cases with small traumatic haematomas in the midline structures of the brain are reported. The neurological examinations of these three patients showed decreased mental activity, and motor disturbances. In spite of their small size, the functional prognosis of these haematomas is very poor. The mechanisms of bleeding and the relevant literature are discussed.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Acta neurochirurgica 66 (1982), S. 55-59 
    ISSN: 0942-0940
    Keywords: Cerebral vertigo ; ischaemic carotid disease ; STA-MCA bypass operation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Three cases of transient vertigo, which was the only or initial symptom and supposed to be caused by ischaemia in the carotid artery distribution, are reported. All cases recovered from vertigo after a superficial temporal artery to middle cerebral artery (STA-MCA) bypass operation or after a completion of the MCA occlusion. The mechanism of so-called cerebral vertigo is discussed with some references.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 0942-0940
    Keywords: Substance P ; vasospasm ; subarachnoid haemorrhage ; isometric tension recording ; cyclic GMP ; rabbit
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The vasoactive effects of substance P (SP), as well as the content of cyclic guanine monophosphate (cGMP), were determined in the rabbit basilar artery after subarachnoid haemorrhage (SAH). Out of 47 rabbits, 24 were subjected to a SAH, induced by injecting 5ml of autologous arterial blood into the cisterna magna; 23 were used as controls. In 20 animals (10 SAH and 10 controls), isometric tension recording of isolated rings of the basilar artery — dissected 2 days after SAH — was employed to assess the dosedependent vasodilatation to SP (10−10 to 10−6M) after precontraction with serotonin (10−8 to 10−5M). In 15 animals (8 SAH and 7 controls), the basal cGMP content was measured in the basilar artery 2 days after SAH. In the other 12 animals (6 SAH and 6 controls), the increase in cGMP content was measured in the basilar artery after a 10-minute incubation with SP (10−6M). SP caused significantly less dilatation in animals subjected to SAH than in controls, especially for concentrations between 10−9 and 10−6M (p 〈 0.001). The cGMP content in the arteries 2 days after SAH was significantly lower than in control arteries (31.5 ± 7.3 against 57.3 ± 4.3 pmoles/g tissue). In the preparations incubated with SP, the increase of cGMP was 440 ± 115% in the control arteries, and only 97 ± 30% in the arteries after SAH. It is concluded that the vasodilator activity of SP is significantly impaired after SAH. Moreover, the changes in cGMP content after SAH suggest a link between impaired vasoactive response to SP and decreased production of cGMP after SAH.
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 0942-0940
    Keywords: Cytoskeleton ; delayed neuronal death ; nerve growth factor (NGF) ; neurofilament (NF)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We investigated the protective action of nerve growth factor (NGF) on delayed neuronal death, and we also studied the involvement of the 200 kDa neurofilament (NF 200) cytoskeletal proteins. Wistar rats were divided into three groups: Group I, in which transient forebrain ischaemia was produced; Group II, ischaemic group which received intraventricular administration of artificial cerebrospinal fluid (CSF); and Group III, ischaemic group which received intraventricular administration of 2 Μg of 2.5 S NGF. Forebrain ischaemia in these rats was produced by causing transient bilateral occlusion of the common carotid arteries and lowering the mean blood pressure to 50 mmHg for 8 minutes. On the 1st and 7th day after ischaemia we histologically examined neuronal death in the hippocampal CA1 sector. On the 7th day after ischaemia, mean cell death (degenerative cell number/total cell number) was 87±9% in group I (n=7), 51±36% in group II (n=7), and 14±16% in group III (n=8) (p〈0.05 vs. group II). The concentration of NF 200 in the hippocampal homogenate was measured by the Western blotting method on the 1st and 7th day after ischaemia. On the 1st day it was found to be 67±11% of that in the control group in group I (n=6), 73±21% in group II (n=6), and 84±7% in group III (n=6) (p〈0.05 vs. group II). The concentration of NF 200 in all groups remained at the same level until the 7th day after ischaemia (each group, n=6). These results suggest that 1) intraventricular NGF has a protective effect on delayed neuronal death, 2) these protective actions occur within one day after ischaemia, and 3) these effects may be mediated by the suppressed degradation and/or promoted restoration of neuronal cytoskeletal proteins.
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