全文获取类型
收费全文 | 60篇 |
免费 | 2篇 |
出版年
2021年 | 3篇 |
2018年 | 1篇 |
2017年 | 1篇 |
2014年 | 2篇 |
2012年 | 1篇 |
2011年 | 1篇 |
2009年 | 1篇 |
2008年 | 1篇 |
2007年 | 1篇 |
2006年 | 1篇 |
2004年 | 1篇 |
2003年 | 1篇 |
2001年 | 1篇 |
1999年 | 4篇 |
1998年 | 1篇 |
1997年 | 2篇 |
1996年 | 1篇 |
1995年 | 3篇 |
1994年 | 3篇 |
1993年 | 3篇 |
1992年 | 1篇 |
1991年 | 3篇 |
1990年 | 1篇 |
1989年 | 3篇 |
1988年 | 2篇 |
1987年 | 5篇 |
1986年 | 3篇 |
1985年 | 4篇 |
1984年 | 2篇 |
1981年 | 2篇 |
1980年 | 2篇 |
1979年 | 1篇 |
排序方式: 共有62条查询结果,搜索用时 390 毫秒
1.
Ethanol Administration in the Rat Decreases Prostacyclin Production by Isolated Brain Microvessels 总被引:1,自引:0,他引:1
The effects of short- and long-term ethanol administration to rats on basal levels and formation of prostacyclin (PGI2) measured as 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), and on lipid class content and fatty acid composition of isolated brain microvessels (BMV) were studied. After acute treatment (2 h, at the peak of plasma ethanol concentration) basal 6-keto-PGF1 alpha levels in BMV and release on incubation were reduced to 50% of control values. After chronic administration (15 days), PGI2 release was reduced to about 40% of control values, without changes in basal levels. Total lipid, phospholipid, and cholesterol levels in BMV, measured after prolonged administration of alcohol, were not modified. Also, only minor changes in the fatty acid composition of individual phospholipid classes were detected. The observed reduction of PGI2 synthesis in BMV thus could not be related to changes of the fatty acid precursor pool in the preparation. Precursor release and/or the biosynthetic pathways may be affected by ethanol administration. 相似文献
2.
Enhancement of ATPase Activity by a Lipid Peroxide of Arachidonic Acid in Rat Brain Microvessels 总被引:5,自引:5,他引:0
Tohru Koide Takao Asano Hiroshi Matsushita Kintomo Takakura 《Journal of neurochemistry》1986,46(1):235-242
The effects of 15-hydroperoxyarachidonic acid (15-HPAA) on Na+, K+- and Mg+-ATPase activities in the blood-brain barrier (BBB) were examined using rat brain microvessels (MV). 15-HPAA markedly stimulated these ATPase activities in MV at low concentrations whereas the synaptosomal Na+, K+-ATPase activity was inhibited in a dose-dependent manner. Further neurochemical analysis revealed that this stimulatory effect of 15-HPAA in MV was not due to a simple detergent-like action of the compound on the membranes but rather to stimulation of the phospholipase A2 and lipoxygenase activity within MV. In addition, it was shown that free radical reactions were involved in the mechanism. Since such anti-edema drugs as 1,2-bis(nicotinamido)propane were proved to be potent suppressors of the enhanced ATPase activity, further speculations on the role of this effect for ischemic brain edema are offered. 相似文献
3.
We studied the hexose transporter protein of the frontal and temporal neocortex, hippocampus, putamen, cerebellum, and cerebral microvessels (which constitute the blood-brain barrier) in Alzheimer disease and control subjects by reversible and covalent binding with [3H]cytochalasin B and by immunological reactivity. In Alzheimer disease subjects, we found a marked decrease in the hexose transporter in brain microvessels and in the cerebral neocortex and hippocampus, regions that are most affected in Alzheimer disease, but there were no abnormalities in the putamen or cerebellum. Hexose transporter reduction in cerebral microvessels of Alzheimer subjects is relatively specific because other enzyme markers of brain endothelium were not significantly altered. The low density of the hexose transporter at the blood-brain barrier and in the cerebral cortex in Alzheimer disease may be related to decreased in vivo measurements of cerebral oxidative metabolism. 相似文献
4.
Brain Micro vessel 12-Hydroxyeicosatetraenoic Acid Is the (S) Enantiomer and Is Lipoxygenase Derived
Steven A. Moore Michael J. Giordano Hee-Yong Kim Norman Salem Jr. Arthur A. Spector 《Journal of neurochemistry》1991,57(3):922-929
12-Hydroxyeicosatetraenoic acid (12-HETE) production from arachidonic acid by cerebral microvessels isolated from perfused adult murine brain was reduced by the lipoxygenase inhibitors baicalein, esculetin, gossypol, nordihydroguaiaretic acid, and quercetin. Except for quercetin and gossypol, the IC50 did not exceed 10 microM. Each inhibitor, except baicalein, also decreased microvessel prostaglandin production when present in concentrations above their IC50 value for 12-HETE. In contrast, inhibitors of the cytochrome P450 monooxygenase system, clotrimazole, metyrapone, and proadifen (SKF-525A), had little effect on microvessel 12-HETE production. Chiral phase HPLC analysis revealed that only the (S) enantiomer of 12-HETE was formed. The major microvessel metabolite of eicosapentaenoic acid co-eluted with 12-hydroxyeicosapentaenoic acid (12-HEPE) on reverse-phase HPLC and the (S) enantiomer of 12-HEPE on chiral phase HPLC. Furthermore, like 12-HETE, 12-HEPE production was blocked by lipoxygenase inhibitors. These studies demonstrate that brain microvessels produce only the (S) enantiomeric 12-hydroxy derivatives of both arachidonic acid and eicosapentaenoic acid by the action of a lipoxygenase that can be selectively inhibited by baicalein. Since arachidonic acid and eicosapentaenoic acid are available to cerebral blood vessels in certain pathological settings, these 12-hydroxy acid lipoxygenase products may mediate some of the cerebrovascular dysfunction that occurs following stroke, brain trauma, or seizures. 相似文献
5.
J. E. Hardebo P. C. Emson B. Falck Ch. Owman E. Rosengren 《Journal of neurochemistry》1980,35(6):1388-1393
The activities of tyrosine hydroxylase, aromatic L-aminoacid decarboxylase, monoamine oxidase, and catechol-O-methyltransferase were measured in microvessel (capillaries and venules), parenchymal arterioles, and pial vessels from rat brains, and the decarboxylase activity was compared in brain microvessels from rabbit, cat, dog, pig, cow, baboon, and man. Cranial sympathectomy was performed to estimate the neuronal contribution to the enzyme activities. All vascular regions had substantial activities of the various enzymes studied. The activity of aromatic L-aminoacid decarboxylase in cerebral microvessels was high in rat, dog, pig, cow, and man; intermediate in rabbit and cat; and low in baboon. In addition to this enzyme, cerebral microvessels also contained tyrosine hydroxylase and monoamine oxidase. Aromatic aminoacid decarboxylase and monoamine oxidase serve an enzymatic barrier function at the microvascular level, whereas the main function of tyrosine hydroxylase is probably to synthesize monoamines within nerve terminals that remain in close association with microvessels under the conditions used for preparation of the microvascular fraction. In larger intracerebral and pial vessels monoamine oxidase was present both in the wall itself and in perivascular sympathetic nerves; the remaining two enzymes had a primarily neuronal localization. The latter types of vessels also contained catechol-O-methyltransferase in their walls. 相似文献
6.
Using the model of glutathione (GSH) depletion, possible role of GSH in the maintenance of blood-brain barrier (BBB) integrity was evaluated in rats. Administration (ip) of GSH depletors, diethyl maleate (DEM, 1–4 mmol/kg), phorone (2–3 mmol/kg) and 2-cyclohexene-1-one (CHX, 1 mmol/kg), to male adults was found to deplete brain and liver GSH and increase the BBB permeability to micromolecular tracers (sodium fluorescein and [14C]sucrose) in a dose-dependent manner at 2h. However, BBB permeability to macromolecular tracers such as horseradish peroxidase and Evan's blue remained unaltered. It was also shown that observed BBB permeability dysfunction was associated with brain GSH depletion. A lower magnitude of BBB increase in rat neonates, as compared to adults, indicated a possible bigger role of GSH in the BBB function of mature brain. The treatment with N-acetylcysteine, methionine and GSH provided a partial to full protection against DEM-induced brain (microvessel) GSH depletion and BBB dysfunction; however, the treatment with -tocopherol, ascorbic acid and turmeric were not effective. Our studies showed that cerebral GSH plays an important role in maintaining the functional BBB integrity. 相似文献
7.
目的:观察黄芪注射液对2型糖尿病动物模型KKAy小鼠脑微血管病变的影响,探讨黄芪注射液对糖尿病脑血管病变的保护作用。方法:饲养至14周龄的雄性KKAy小鼠随机分成模型组和黄芪注射液治疗组(每日腹腔给药,剂量为3mL/kg),同龄雄性C57BL/6J小鼠作为对照组。血糖仪测量20、24、28周龄时各组小鼠的空腹血糖水平。28周龄时处死各组小鼠,放射免疫法检测血清6-酮-前列腺素-F1α(6-Keto-PGF1α)和血栓素B2(TXB2)的含量。透射电子显微镜观察脑组织超微结构变化。结果:模型组KKAy小鼠从20周龄开始血糖水平明显高于正常组小鼠(P〈0.01);黄芪治疗组小鼠从20周龄开始血糖水平明显高于正常组小鼠(P〈0.01),但低于模型组小鼠(P〈0.05或P〈0.01)。模型组小鼠血清6-Keto—PGF1α水平较正常组降低(P〈0.01),TXB2含量增高(P〈0.01);与模型组相比,黄芪注射液治疗组小鼠6-Keto—PGF1α水平升高(P〈O.01),TXB:含量下降(P〈0.01)。透射电镜显示模型组小鼠神经细胞胞核染色质疏松,线粒体肿胀,粗面内质网缩小,核糖体减少;治疗组小鼠以上病变明显改善。结论:黄芪注射液可以有效改善2型糖尿病动物模型KKAv小鼠脑微血管病变,保护神经细胞结构。 相似文献
8.
肾上腺髓质素对大鼠肠系膜微血管和微淋巴管的作用 总被引:5,自引:0,他引:5
应用活体显微电视录象技术,观察上腺髓质素对大鼠肠系膜微血管微淋巴管的作用及其对去甲肾上腺素,内皮素作用的是结果表明,ADM直接扩张肠系膜各级微血管和向一淋巴管,拮抗NE和ET引起的微血效及微循环血流液态的异常改变。ADM的上述作用可被一氧化氮生成抑制剂N^9-nitro-L-arginine(L-NNA)显著抑制。 相似文献
9.
Identification and quantification of blood–brain barrier transporters in isolated rat brain microvessels 下载免费PDF全文
Hajar Al Feteisi Zubida M. Al‐Majdoub Brahim Achour Narciso Couto Amin Rostami‐Hodjegan Jill Barber 《Journal of neurochemistry》2018,146(6):670-685
10.
Targeted unlabeled multiple reaction monitoring analysis of cell markers for the study of sample heterogeneity in isolated rat brain cortical microvessels 下载免费PDF全文
David Gomez‐Zepeda Catarina Chaves Méryam Taghi Philippe Sergent Wang‐Qing Liu Cérina Chhuon Michel Vidal Martin Picard Elizabeth Thioulouse Isabelle Broutin Ida‐Chiara Guerrera Jean‐Michel Scherrmann Yannick Parmentier Xavier Decleves Marie‐Claude Menet 《Journal of neurochemistry》2017,142(4):597-609