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首页> 外文期刊>Neurological Research: An Interdisciplinary Quarterly Journal >A differential response of diffuse brain injury on the concentrations of endothelin and nitric oxide in the plasma and brain regions in rats.
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A differential response of diffuse brain injury on the concentrations of endothelin and nitric oxide in the plasma and brain regions in rats.

机译：弥漫性脑损伤对大鼠血浆和脑区域中内皮素和一氧化氮浓度的不同反应。

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In the present study, we hypothesized that acute diffuse brain injury (DBI) in rats would produce an increase in endothelin-1 (ET-1), a potent vasoconstrictor, and/or nitric oxide (NO), a potent vasodilator, in plasma and brain areas in rats. DBI was induced in anesthetized male Sprague-Dawley rats (350-400 g) using a 350 g weight dropped from 1 meter height impact through a device designed by Marmarou et al., 1994. Blood plasma and brain tissue (cerebral cortex, diencephalon and brain stem) samples were collected for estimation of ET-1 and NO at zero or 6 h from rats (n = 6) subjected to DBI as well as control rats (n = 6), i.e., not subjected to DBI. In a separate group of animals, cerebral blood flow (CBF) was recorded at 0, 5, 10, 15, 30, 60, 120, 240 and 360 min after induction of DBI or sham-DBI. Acute DBI produced a significant decrease in CBF at 120 min after induction of DBI. Plasma levels of ET-1 was found to be significantly increased (from 0.89 +/- 0.09 to 2.09 +/- 0.29 pg ml-1), at 6 h following DBI. DBI produced a significant decrease in the levels of ET-1 in diencephalon (from 70.97 +/- 9.47 to 57.64 +/- 2.65 pg g-1). In contrast to ET-1, DBI produced a significant increase in the concentrations of NO in the diencephalon, cerebral cortex and brain stem at 6 h post DBI. It appears that DBI-induced increase in the levels of NO in brain regions which might be down regulating the synthesis of ET-1 in diencephalon. It is concluded that ET and NO homeostatic mechanisms may play a role in the regional and vascular responses associated with acute DBI.
机译：在本研究中，我们假设大鼠的急性弥漫性脑损伤（DBI）在血浆中会产生内皮素-1（ET-1）（一种有效的血管收缩剂）和/或一氧化氮（NO）（一种有效的血管扩张剂）增加。和大鼠的大脑区域。在麻醉的雄性Sprague-Dawley大鼠（350-400 g）中，通过Marmarou等，1994设计的装置从1米高的撞击中掉落了350 g的重量，从而诱导了DBI。血浆和脑组织（大脑皮层，中脑和脑干）样本收集零和6小时时从接受DBI的大鼠（n = 6）和对照大鼠（n = 6）（即未进行DBI的大鼠）中估算ET-1和NO。在另一组动物中，诱导DBI或sham-DBI后第0、5、10、15、30、60、120、240和360分钟记录脑血流量（CBF）。急性DBI在诱导DBI后120分钟时CBF明显降低。发现在DBI后6小时，血浆ET-1水平显着增加（从0.89 +/- 0.09到2.09 +/- 0.29 pg ml-1）。 DBI使中脑的ET-1水平显着降低（从70.97 +/- 9.47 pg至57.64 +/- 2.65 pg g-1）。与ET-1相反，在DBI后6小时，DBI使中脑，大脑皮层和脑干中的NO浓度显着增加。看来DBI诱导的脑区域NO水平升高，可能下调了间脑中ET-1的合成。结论是，ET和NO稳态机制可能在与急性DBI相关的区域和血管反应中起作用。

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