Vasospasm in cerebral inflammation.
Vasospasm in cerebral inflammation.
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DOI：
10.1155/2014/509707
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发表时间：
2014
影响因子：
2
通讯作者：
Eisenhut M
中科院分区：
文献类型：
--
作者：
Eisenhut M
细菌性脑膜炎、脑疟疾、脑损伤和蛛网膜下腔出血中发现的所有形式的脑炎都与脑动脉和小动脉的血管痉挛有关。血管痉挛与蛛网膜下腔出血和细菌性脑膜炎的永久性神经功能障碍和死亡有关。IL-1水平升高可能通过钙依赖和独立激活肌球蛋白轻链激酶和释放血管收缩因子ET-1参与血管痉挛。脑血管痉挛发病机制的另一个关键因素可能是血管扩张剂一氧化氮的生物利用度降低。在人类蛛网膜下腔出血中与炎症相关的血管痉挛的治疗试验表明，通过钙拮抗剂、内皮素受体拮抗剂、他汀类药物和纤溶酶原激活剂可以减少血管痉挛。针对钙依赖和非依赖性血管痉挛、潜在炎症和一氧化氮耗竭的联合治疗方法值得在所有条件下与脑部炎症的双盲随机安慰剂对照试验中进一步研究。这些药物的辅助治疗可能能够减少与神经缺陷和死亡率增加相关的缺血性脑损伤。
All forms of cerebral inflammation as found in bacterial meningitis, cerebral malaria, brain injury, and subarachnoid haemorrhage have been associated with vasospasm of cerebral arteries and arterioles. Vasospasm has been associated with permanent neurological deficits and death in subarachnoid haemorrhage and bacterial meningitis. Increased levels of interleukin-1 may be involved in vasospasm through calcium dependent and independent activation of the myosin light chain kinase and release of the vasoconstrictor endothelin-1. Another key factor in the pathogenesis of cerebral arterial vasospasm may be the reduced bioavailability of the vasodilator nitric oxide. Therapeutic trials in vasospasm related to inflammation in subarachnoid haemorrhage in humans showed a reduction of vasospasm through calcium antagonists, endothelin receptor antagonists, statins, and plasminogen activators. Combination of therapeutic modalities addressing calcium dependent and independent vasospasm, the underlying inflammation, and depletion of nitric oxide simultaneously merit further study in all conditions with cerebral inflammation in double blind randomised placebo controlled trials. Auxiliary treatment with these agents may be able to reduce ischemic brain injury associated with neurological deficits and increased mortality.