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代谢型谷氨酸受体刺激对大鼠局灶性脑缺血期间脑氧消耗和血流的影响。

Effects of metabotropic glutamate receptor stimulation on cerebral O2 consumption and blood flow during focal cerebral ischemia in rats.

作者信息

Liu Xia, Chi Oak Z, Weiss Harvey R

机构信息

Department of Physiology and Biophysics, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, Piscataway, New Jersey 08854-5635, USA.

出版信息

Neurochem Res. 2003 Dec;28(12):1799-804. doi: 10.1023/a:1026159422237.

Abstract

This investigation was performed to evaluate the effects of ACPD [(1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid], a metabotropic glutamate receptor agonist, on cerebral O2 consumption during focal cerebral ischemia. Male Wistar rats were placed in control (n = 7) and ACPD (n = 7) groups under isoflurane anesthesia. Twenty minutes after middle cerebral artery (MCA) occlusion, gauze sponges with 10(-5) M ACPD or normal saline were placed on the ischemic cortex (IC) for a period of 40 min and were changed every 10 min. One hour after MCA occlusion, regional cerebral blood flow (rCBF) was determined using the C14-iodoantipyrine autoradiographic technique. Regional arterial and venous oxygen saturation were determined using microspectrophotometry. There were no statistical differences in vital signs, blood gases, and hemoglobin between the groups. In the control group, the cerebral blood flow and oxygen consumption of the IC were significantly lower than the contralateral cortex (rCBF: 45 +/- 11 vs. 110 +/- 11 ml/min/100 g, O2 consumption: 2.9 +/- 0.4 vs. 5.4 +/- 1.1 ml O2/min/100 g). ACPD did not change regional cerebral blood flow of the IC, but did significantly increase the oxygen extraction (7.8 +/- 0.2 vs. 6.9 +/- 0.3 ml O2/100 ml) and oxygen consumption of the IC (4.3 +/- 1.5 vs. 2.9 +/- 0.4) compared to the control IC. Our data demonstrated that topical application of 10(-5) M ACPD to the ischemic area worsened cerebral O2 balance. These data suggest that metabotropic glutamate receptors are not maximally activated during ischemia in the temporal cortex.

摘要

本研究旨在评估代谢型谷氨酸受体激动剂ACPD[(1S,3R)-1-氨基环戊烷-1,3-二羧酸]对局灶性脑缺血期间脑氧消耗的影响。将雄性Wistar大鼠在异氟烷麻醉下分为对照组(n = 7)和ACPD组(n = 7)。大脑中动脉(MCA)闭塞20分钟后,将含有10(-5)M ACPD或生理盐水的纱布海绵置于缺血皮质(IC)上40分钟,每10分钟更换一次。MCA闭塞1小时后,使用C14-碘安替比林放射自显影技术测定局部脑血流量(rCBF)。使用显微分光光度法测定局部动脉和静脉血氧饱和度。两组之间的生命体征、血气和血红蛋白无统计学差异。在对照组中,IC的脑血流量和氧消耗显著低于对侧皮质(rCBF:45±11 vs. 110±11 ml/min/100 g,氧消耗:2.9±0.4 vs. 5.4±1.1 ml O2/min/100 g)。ACPD并未改变IC区域的脑血流量,但与对照IC相比,确实显著增加了IC的氧摄取(7.8±0.2 vs. 6.9±0.3 ml O2/100 ml)和氧消耗(4.3±1.5 vs. 2.9±0.4)。我们的数据表明,向缺血区域局部应用10(-5)M ACPD会使脑氧平衡恶化。这些数据表明,在颞叶皮质缺血期间,代谢型谷氨酸受体未被最大程度激活。

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