中風(fēng)是可卡因?yàn)E用引起的最嚴(yán)重的醫(yī)學(xué)風(fēng)險(xiǎn)。研究指出,，可卡因的血管作用能破壞大腦血流（CBF）,，從而促使可卡因?yàn)E用者發(fā)生中風(fēng)。因?yàn)閷煽ㄒ驗(yàn)E用性腦血管變化的基本機(jī)制缺乏認(rèn)識,，還沒有發(fā)現(xiàn)此類中風(fēng)的有效療法,。目前，神經(jīng)影像學(xué)方法,，包括磁共振成像和計(jì)算機(jī)斷層掃描血管造影，對于卡因誘導(dǎo)性限制性大腦血流的基本機(jī)制可以揭示一些有限的線索,。該研究報(bào)道的這種影像學(xué)方法是一種很有前途的方法，它能調(diào)查出中風(fēng)可能牽連的大腦小神經(jīng)血管網(wǎng)絡(luò)的結(jié)構(gòu)變化,。
該研究通過這種新神經(jīng)影像學(xué)技術(shù)，觀察到：濫用者常用劑量的可卡因可影響大腦動(dòng)脈,、靜脈和毛細(xì)血管,，甚至最小的血管，使它們收縮,，從而抑制不同時(shí)間內(nèi)的大腦血液流量,，在服用后短短的2-3分鐘內(nèi)大腦血流量明顯減少，在某些血管中,，腦血流量減少達(dá)到了70%，血管恢復(fù)時(shí)間各異,。在一些動(dòng)脈分支中,，可卡因中斷腦血流量超過45分鐘,，這種作用在重復(fù)使用可卡因后更為明顯。這些變化對腦組織氧輸送造成危害,，使其更易局部缺血和神經(jīng)死亡,。
要指出的是,，這些大腦模型中出現(xiàn)的可卡因誘導(dǎo)性微缺血性變化很可能就是神經(jīng)毒性作用的誘因,，它們可能隱含著可卡因?yàn)E用者常見的一些神經(jīng)并發(fā)癥，包括各種知覺改變,、面癱,、麻木、半癱或全癱及不可逆癱瘓,。(生物谷bioon.com)
doi:DOI: 10.1038/mp.2011.160
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Cocaine-induced cortical microischemia in the rodent brain: clinical implications.
H Ren, C Du, Z Yuan, K Park, N D Volkow, Y Pan
Cocaine-induced stroke is among the most serious medical complications associated with its abuse. However, the extent to which acute cocaine may induce silent microischemia predisposing the cerebral tissue to neurotoxicity has not been investigated; in part, because of limitations of current neuroimaging tools, that is, lack of high spatiotemporal resolution and sensitivity to simultaneously measure cerebral blood flow (CBF) in vessels of different calibers (including capillaries) quantitatively and over a large field of view. Here we combine ultrahigh-resolution optical coherence tomography to enable tracker-free three-dimensional (3D) microvascular angiography and a new phase-intensity-mapping algorithm to enhance the sensitivity of 3D optical Doppler tomography for simultaneous capillary CBF quantization. We apply the technique to study the responses of cerebral microvascular networks to single and repeated cocaine administration in the mouse somatosensory cortex. We show that within 2-3?min after cocaine administration CBF markedly decreased (for example, ~70%), but the magnitude and recovery differed for the various types of vessels; arterioles had the fastest recovery (~5?min), capillaries varied drastically (from 4-20?min) and venules showed relatively slower recovery (~12?min). More importantly, we showed that cocaine interrupted CBF in some arteriolar branches for over 45?min and this effect was exacerbated with repeated cocaine administration. These results provide evidence that cocaine doses within the range administered by drug abusers induces cerebral microischemia and that these effects are exacerbated with repeated use. Thus, cocaine-induced microischemia is likely to be a contributor to its neurotoxic effects.
