Perivascular demyelination and intramyelinic oedema in reperfusion nerve injury.
Perivascular demyelination and intramyelinic oedema in reperfusion nerve injury.
复制标题
再灌注神经损伤中血管周围脱髓鞘和髓鞘内水肿。
作者：
Hitoshi Nukada;P. McMorran
神经缺血在各种神经病的病理学改变的发展中起主要作用，并且缺血的影响通过各种组织中的再灌注而放大。虽然急性缺血性神经的病理改变已经确立，但再灌注损伤引起的神经病理学尚未阐明。为了评估周围神经中哪些细胞类型受到缺氧事件后再氧合的影响，我们开发了一种短暂严重肢体缺血的动物模型。通过测量神经血流量证实，通过夹闭大鼠后肢的多个供应动脉实现了近完全缺血。在肢体缺血3、5或7小时后，释放血管夹以再灌注血流。再灌注7 d后取股下段坐骨神经、胫神经和腓神经行病理学检查。所有再灌注神经发展脱髓鞘神经纤维，特别是在血管周围区域。虽然3小时的缺血再灌注引起脱髓鞘，血管周围脱髓鞘是更突出的缺血再灌注时间较长后。观察到两种类型的神经水肿;神经内膜水肿，特别是在血管周围和神经束膜下腔，和髓鞘内水肿。髓鞘内水肿的神经纤维并不局限于血管周围区域。神经内膜血管内皮细胞也无一例外地出现肿胀。神经缺血本身，没有再灌注，没有引起这些病理变化。由于髓鞘似乎是特别容易受到活化的自由基，氧化应激，活化的中性粒细胞和细胞因子的形成似乎是重要的基础机制，在血管周围脱髓鞘和髓鞘内水肿的缺血/再灌注神经的发展。（250字处删节）
Nerve ischaemia plays a major role in the development of pathological alterations in various neuropathies, and the effects of ischaemia are amplified by reperfusion in various tissues. While pathological alterations in acutely ischaemic nerve have been established, nerve pathology resulting from reperfusion injury has never been elucidated. To evaluate what cell type in peripheral nerve is affected by reoxygenation following a hypoxic episode, we developed an animal model of transient severe limb ischaemia. Near-complete ischaemia, confirmed by the measurement of nerve blood flow, was achieved by clamping multiple arteries of supply to rat hindlimb. After 3, 5 or 7 h of limb ischaemia, vascular clips were released to reperfuse blood flow. Pathology in sciatic, tibial and peroneal nerves at the lower thigh level was examined at 7 d after reperfusion. All reperfused nerves developed demyelinated nerve fibres, particularly in perivascular regions. Although 3 h of ischaemia followed by reperfusion caused demyelination, perivascular demyelination was more prominent after a longer period of ischaemia with reperfusion. Two types of nerve oedema were observed; endoneurial oedema especially in perivascular and subperineurial spaces, and intramyelinic oedema. Nerve fibres with intramyelinic oedema were not confined to the perivascular region. Swollen endothelial cells in endoneurial vessels were also invariably observed. Nerve ischaemia per se, without reperfusion, did not induce these pathological changes. Because myelin appears to be particularly susceptible to activated free radicals, oxidative stress, activated neutrophils, and cytokine formation seem to be important underlying mechanisms in the development of perivascular demyelination and intramyelinic oedema in ischaemic/reperfused nerves.(ABSTRACT TRUNCATED AT 250 WORDS)
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影响因子：
--
作者：
HERNANDEZ, LA;GRISHAM, MB;GRANGER, DN
通讯作者：
GRANGER, DN
L-精氨酸-一氧化氮途径在心肌复氧损伤中的作用。
DOI：
10.1152/ajpheart.1992.262.2.h616
发表时间：
1992
期刊：
The American journal of physiology
影响因子：
--
作者：
Matheis,G;Sherman,MP;Buckberg,GD;Haybron,DM;Young,HH;Ignarro,LJ
通讯作者：
Ignarro,LJ
DOI：
--
发表时间：
1983-04
期刊：
The American journal of pathology
影响因子：
--
作者：
R. Engler;G. Schmid-Schönbein;R. Pavelec
通讯作者：
R. Engler;G. Schmid-Schönbein;R. Pavelec
DOI：
--
发表时间：
1984
期刊：
The American journal of pathology
影响因子：
--
作者：
Nukada,H;Dyck,PJ
通讯作者：
Dyck,PJ
影响因子：
14.5
作者：
TUCK, RR;SCHMELZER, JD;LOW, PA
通讯作者：
LOW, PA