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HEPES prevents edema in rat brain slices.

机译:HEPES可防止大鼠脑片浮肿。

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摘要

Brain slices gain water when maintained in bicarbonate-buffered artificial cerebro-spinal fluid (ACSF) at 35 degrees C. We previously showed that this edema is linked to glutamate receptor activation and oxidative stress. An additional factor that may contribute to swelling is acidosis, which arises from high CO2 tension in brain slices. To examine the role of acidosis in slice edema, we added N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid (HEPES) to osmotically balanced ACSF (HEPES-ACSF), thereby increasing buffering capacity beyond that provided by bicarbonate/CO2. Water gain was markedly inhibited in HEPES-ACSF. After 3 h incubation in HEPES-ACSF at 35 degrees C, water gain was limited to that of fresh slices after 1 h recovery in ACSF at room temperature. The effect of HEPES in decreasing slice water gain was concentration dependent from 0.3 to 20 mM. The inhibition of water gain by HEPES suggests that tissue acidosis is a contributing factor in brain slice edema.
机译:当在35摄氏度的碳酸氢盐缓冲的人工脑脊髓液(ACSF)中保持脑切片时,水分会增加。我们之前的研究表明,这种水肿与谷氨酸受体激活和氧化应激有关。可能导致肿胀的另一个因素是酸中毒,这是由于脑片中高的CO2张力引起的。为了检查酸中毒在切片水肿中的作用,我们在渗透平衡的ACSF(HEPES-ACSF)中添加了N-2-羟乙基哌嗪-N'-2-乙磺酸(HEPES),从而使缓冲能力超出了碳酸氢盐/ CO2所提供的缓冲能力。 HEPES-ACSF显着抑制了水分获取。在35摄氏度的HEPES-ACSF中孵育3小时后,室温下在ACSF中恢复1小时后,水分的获取仅限于新鲜切片的水分。 HEPES在降低切片水分获取中的作用取决于浓度0.3到20 mM。 HEPES对水分获取的抑制作用表明组织酸中毒是脑切片水肿的一个促成因素。

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