In a model of SAH-induced neurogenic fever, BAT thermogenesis is mediated by erythrocytes and blocked by agonism of adenosine A1 receptors.
In a model of SAH-induced neurogenic fever, BAT thermogenesis is mediated by erythrocytes and blocked by agonism of adenosine A1 receptors.
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DOI：
10.1038/s41598-021-82407-w
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发表时间：
2021-02-02
影响因子：
4.6
通讯作者：
Cetas JS
中科院分区：
文献类型：
--
作者：
Tupone D;Cetas JS
蛛网膜下腔出血（SAH）后的神经源性发热（NF）是发病率的主要原因，与预后不良和在神经重症监护病房（NICU）的住院时间延长有关。虽然在新生儿重症监护室中，SAH是比败血症更常见的发热原因，但它通常是一种排除性诊断，需要付出很大的努力来排除传染源。NF对COX抑制剂等标准的退热药物没有反应，并且缺乏良好的药物治疗导致引入外部冷却系统，这有其自身的相关问题。在鼠类SAH模型中，我们测量了注射全血、血浆或红细胞对棕色脂肪组织交感神经活动和发热产热的影响。我们证明，SAH后棕色脂肪组织的急性激活导致NF，不依赖于PGE2，蛛网膜下腔注射全血或红细胞，而不是单独的血浆，足以触发棕色脂肪组织产热，中枢神经系统中腺苷A1受体的激活可以阻断SAH后棕色脂肪组织产热成分。这些发现指出，与感染原因相比，NF的产生有一种独特的产热机制，并有望带来新的治疗方法。
Neurogenic fever (NF) after subarachnoid hemorrhage (SAH) is a major cause of morbidity that is associated with poor outcomes and prolonged stay in the neurointensive care unit (NICU). Though SAH is a much more common cause of fever than sepsis in the NICU, it is often a diagnosis of exclusion, requiring significant effort to rule out an infectious source. NF does not respond to standard anti-pyretic medications such as COX inhibitors, and lack of good medical therapy has led to the introduction of external cooling systems that have their own associated problems. In a rodent model of SAH, we measured the effects of injecting whole blood, blood plasma, or erythrocytes on the sympathetic nerve activity to brown adipose tissue and on febrile thermogenesis. We demonstrate that following SAH the acute activation of brown adipose tissue leading to NF, is not dependent on PGE2, that subarachnoid space injection of whole blood or erythrocytes, but not plasma alone, is sufficient to trigger brown adipose tissue thermogenesis, and that activation of adenosine A1 receptors in the CNS can block the brown adipose tissue thermogenic component contributing to NF after SAH. These findings point to a distinct thermogenic mechanism for generating NF, compared to those due to infectious causes, and will hopefully lead to new therapies.
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影响因子：
3.3
作者：
Cetas, J. S.;Lee, D. R.;Alkayed, N. J.;Wang, R.;Iliff, J. J.;Heinricher, M. M.
通讯作者：
Heinricher, M. M.
DOI：
10.1523/jneurosci.1240-11.2011
发表时间：
2011-07-27
期刊：
The Journal of neuroscience : the official journal of the Society for Neuroscience
影响因子：
--
作者：
Jinka TR;Tøien Ø;Drew KL
通讯作者：
Drew KL
影响因子：
6.1
作者：
COOPER, AL;FITZGEORGE, RB;ROTHWELL, NJ
通讯作者：
ROTHWELL, NJ
影响因子：
--
作者：
DERIJK, RH;STRIJBOS, PJLM;BERKENBOSCH, F
通讯作者：
BERKENBOSCH, F
影响因子：
3.5
作者：
Guth, James C.;Nemeth, Alexander J.;Maas, Matthew B.
通讯作者：
Maas, Matthew B.