Background: Spinally administered clonidine produces analgesia via [alpha]2-adrenergic receptors. The analgesic potency of clonidine and its dependency on muscarinic acetylcholine receptors increase in rats after nerve injury. The authors hypothesized that these changes reflect greater acetylcholine release from the spinal cord by clonidine, either through direct or indirect effects.
Methods: Male Sprague-Dawley rats were divided into two groups: no surgery or left L5 and L6 spinal nerve ligation (SNL). All experiments were performed 3 weeks after SNL. Crude synaptosomes were prepared from the spinal enlargement and loaded with [3H]choline. Samples were incubated with clonidine in the absence or presence of KCl depolarization. The authors also examined the effect of clonidine on KCl evoked acetylcholine release using perfusion of spinal cord slices, in which some spinal circuitry is maintained.
Results: In synaptosomes, clonidine alone induced minimal acetylcholine release, which was actually greater in tissue from normal rats than in tissue from SNL rats. In the presence of KCl depolarization, however, clonidine enhanced acetylcholine release in tissue from SNL rats but inhibited release in tissue from normal rats. Similarly, in spinal cord slices, clonidine enhanced KCl evoked acetylcholine release in tissue from SNL animals but inhibited such release in tissue from normal animals. The [alpha]2-adrenoceptor antagonist idazoxan inhibited the effects of clonidine in slices from SNL rats. 相似文献
Prosthetic valve endocarditis (PVE) caused by Candida species is associated with high morbidity and mortality. A combination
of surgical resection and antifungal drug therapy is the golden standard for treatment, yet surgical intervention is not possible
in all cases of Candida PVE. We report a case of PVE due to Candida albicans cured by medical treatment alone. This case suggests
that, in some instances, Candida PVE can be managed medically with antifungal therapy. Such a conservative approach should
be applied with caution and necessitates very close follow-up on a long-term basis. 相似文献
Two embryonal CNS tumors, atypical teratoid/rabdoid tumor (AT/RT) and primitive neuroectodermal tumor (PNET), may be confused with each other and misdiagnosed. Here we report an infant with a congenital supratentorial tumor, which was detected by fetal MRI at 37 weeks gestation. On routine histological examination, the tumor was composed mainly of small undifferentiated cells, among which many rhabdoid cells and occasional sickle‐shaped embracing cells were observed. No mesenchymal or epithelial areas were evident. Our impression was that the tumor was an atypical example of AT/RT. Immunohistochemically, almost all the tumor cells were strongly positive for vimentin. However, epithelial membrane antigen was notably negative, and most of the tumor cell nuclei were clearly positive for INI1. In addition, many tumor cells were positive for neurofilament protein. There were also occasional small areas containing many tumor cells positive for glial fibrillary acidic protein. Finally, a diagnosis of PNET, with a rhabdoid phenotype and expression of neuronal and glial markers, was made. In the present case, application of INI1 immunostaining was very helpful for distinguishing PNET from AT/RT. 相似文献
A 68‐year‐old man, who had no remarkable past medical history, was referred to a hospital because of disorientation and right‐sided hemiparesis. On magnetic resonance imaging, a contrast‐enhanced tumor in the left frontal lobe with perifocal edema was noted. He underwent left frontal lobectomy. Microscopic examination revealed infiltrative atypical astrocytes showing increased cellularity, distinct nuclear atypia, and many mitotic figures, while microvascular proliferation and necrosis were absent. Thus, the tumor was histologically diagnosed as anaplastic astrocytoma. It was of note that cytoplasmic eosinophilic granules were observed in approximately 25% of neoplastic cells. The granules were positively immunostained with anti‐αB‐crystallin antibody, and the other histochemical and immunohistochemical results also corresponded to Rosenthal fibers. The MIB‐1 labeling index of the highest area of the tumor was 22%, while that of granular cells was 2.1%. An ultrastructural study revealed amorphous electron‐dense structures attached to intermediate filament bundles, compatible with Rosenthal fibers. Such structures are relatively common in oligodendroglial tumors; however, they are extremely rare in astrocytic tumors. Fluorescence in situ hybridization targeted against chromosome 1 failed to demonstrate allelic loss of the short arm. The present case should also be discriminated from granular cell astrocytoma. We review related literature and discuss the significance of granules in gliomas. 相似文献
Binswanger’s disease is pathologically characterized by a combination of diffuse cerebrovascular white matter lesions and
lacunar infarcts in the basal ganglia and white matter. Although a blood-brain barrier (BBB) dysfunction has been implicated
in the pathogenesis of these white matter (WM) lesions, few authors have addressed this problem. In the present study, we
describe BBB dysfunction and its regional differences in the brains of Binswanger’s disease patients. Twelve brains from Binswanger’s
disease patients (group III) were examined and compared with those from five patients with non-neurological disease (group
I) and five cortical infarct patients without significant WM lesions (group II). Immunohistochemistry was performed for glial
fibrillary acidic protein and vimentin as astroglial cell markers, and for immunoglobulins, complements and fibrinogen as
extravasated serum protein markers. The grading scores for IgG extravasation were significantly higher in group III as compared
to group I, in both the periventricular WM and the subcortical WM (P < 0.01). In group III, the scores in the periventricular WM and subcortical WM were significantly higher than in the subcortical
U fibers and cerebral cortex (P < 0.01 for the periventricular WM; P < 0.001 for the subcortical WM), respectively. Clasmatodendritic astroglia, which had swollen cell bodies and large cytoplasmic
vacuoles with disintegrated processes, incorporated the serum components IgG, IgM, C3d, C1q and fibrinogen, both in the periventricular
WM and subcortical WM in 5 out of 12 (42%) Binswanger’s disease brains. These results indicate that WM lesions in Binswanger’s
disease are accompanied by BBB dysfunction, although it remains uncertain whether BBB dysfunction is secondary to either chronic
cerebral ischemia or arterial hypertension.
Received: 25 April 1997 / Revised, accepted: 21 July 1997 相似文献
A new mutant, the Eisai hyperbilirubinemic (EHB) rat, shows no inherent expression of the canalicular isoform of the multidrug
resistance protein (cMrp) in the liver. It has defective biliary secretion of organic anions such as bilirubin glucuronides,
bromosulfophthalein (BSP), cysteinyl leukotrienes, glutathione (GSH) and bile acid sulfate and glucuronides. When rats were
injected intravenously with CdCl2, biliary excretion of Cd over 30 min was 0.28% and 0.004% of the total dose in Sprague-Dawley (SD) and EHB rats, respectively.
Six SD rats and five EHB rats were fed a diet containing Cd. Bile Cd was detected at the level of 2 ng/20 min in SD rats,
but not in EHB rats. There was no significant difference of hepatic Cd concentration between SD and EHB rats. Furthermore,
there were no significant differences of renal and intestinal Cd, and hepatic and renal metallothionein (MT) concentrations
between the SD and EHB groups. Biliary excretion of reduced-GSH for 20 min was 1.3 ± 0.3 mg and 3.6 ± 0.9 μg in SD and EHB
rats, respectively. Our results suggest that hepatobiliary excretion of exogenous Cd is mediated mainly via carrier transport,
including a cMrp or GSH carrier, but that the lack of the transport pathway does not contribute to abnormal accumulation of
Cd in the liver.
Received: 12 August 1996 / Accepted 7 November 1996 相似文献
Abstract: Monoamine and their acid metabolites were determined in the CSF of 18 drug-treated chronic schizophrenic patients with the symptoms of tardive dyskinesia and neuroleptic-induced Parkinsonism (Parkinsonism). Six healthy volunteers were used as the control group. The norepinephrine (NE) levels were found to be significantly higher in the patients with tardive dyskinesia than in the controls. Furthermore, elevated CSF NE levels were also observed in the patients with Parkinsonism. Epinephrine (E) and Dopamine (DA) were not present in the CSF of the control group, whereas measurable levels of DA could be detected in 4 out of 9 and E was found in 8 out of 9 patients with tardive dyskinesia. The mean concentration of HVA was slightly but not significantly elevated in the patients with tardive dyskinesia and Parkinsonism. The mean values of CSF 5-HIAA were all within the normal range in both patient groups. From the above results, it was suggested that abnormal adrenergic activity rather than abnormal dopaminergic activity may play an important role as a mechanism in the etiopathogenesis of extrapyramidal disorders. Furthermore, in the patients with Parkinsonism, CSF neurochemical observations were similar to those of the patients with tardive dyskinesia in this study. It may help to explain the clinical coexistence of tardive dyskinesia and neuroleptic-induced Parkinsonism. 相似文献