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大鼠暴露于高氧压期间脑内的血流情况。

Blood flow in rat brain during exposure to high oxygen pressure.

作者信息

Torbati D, Parolla D, Lavy S

出版信息

Aviat Space Environ Med. 1978 Aug;49(8):963-7.

PMID:678247
Abstract

Total cerebral blood flow and blood flow in 10 brain structures of unanesthetized rats were measured by the indicator fractionation technique under different oxygen pressures. The first electrical discharge seen under high oxygen pressure was considered as an early sign of brain oxygen toxicity. It was found that the effect of high oxygen pressure on cerebral blood flow was time- and pressure-dependent. Exposure to 2 and 3.5 ATA of O2 led to vasoconstriction. Exposure to 5 ATA of O2 produced an initial vasoconstriction followed by a secondary vasodilatation to normal level. Cerebral blood flow was not reduced during exposure to 7 ATA of oxygen. Non-decreased blood flow preceded the appearance of the first electrical discharge in all investigated structures of the brain. There was no change in electrical activity of the brain as long as a decrease in cerebral blood flow was maintained. It is suggested that changes in electrical activity of the brain may be produced by toxic levels of brain tissue PO2. Vasoconstriction resulting in decreased cerebral blood flow was considered as a protective mechanism against the toxic effects of high tissue PO2.

摘要

采用指示剂分离技术,在不同氧分压条件下,测量了未麻醉大鼠的全脑血流量及10个脑结构的血流量。高氧分压下首次出现的放电被视为脑氧中毒的早期迹象。结果发现,高氧分压对脑血流量的影响具有时间和压力依赖性。暴露于2个和3.5个绝对大气压的氧气会导致血管收缩。暴露于5个绝对大气压的氧气会先出现血管收缩,随后继发血管舒张至正常水平。暴露于7个绝对大气压的氧气时,脑血流量并未降低。在所有研究的脑结构中,脑血流量未降低先于首次放电的出现。只要脑血流量持续降低,脑电活动就没有变化。提示脑组织氧分压的毒性水平可能导致脑电活动的改变。导致脑血流量降低的血管收缩被认为是一种针对高组织氧分压毒性作用的保护机制。

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