Intraischemic hypothermia attenuates neutrophil infiltration in the rat neocortex after focal ischemia-reperfusion injury.
Intraischemic hypothermia attenuates neutrophil infiltration in the rat neocortex after focal ischemia-reperfusion injury.
复制标题
局灶性缺血再灌注损伤后，缺血内低温可减弱大鼠新皮质中的中性粒细胞浸润。
DOI：
10.1097/00006123-199612000-00024
复制
发表时间：
1996
期刊：
影响因子：
4.8
通讯作者：
Lee,KS
中科院分区：
文献类型：
--
作者：
Toyoda,T;Suzuki,S;Kassell,NF;Lee,KS
目的：低温影响化疗后疗效的机制仍有争议。一个被认为在缺血/再灌流后神经元损伤中起重要作用的机制是在受损的脑组织中积累多形核白细胞。为了更好地了解低温对这一损伤机制的潜在影响，本研究观察了缺血内低温对短暂性局灶性脑缺血后多形核白细胞聚集的影响。方法：通过测定大鼠大脑皮层髓过氧化物酶(MPO)活性，定量研究缺血内低温(30℃)对多形核白细胞聚集的影响。大鼠左侧大脑中动脉和双侧颈总动脉暂时阻断3h，造成可逆性局灶性脑缺血，再灌注后24小时处死动物。结果：与假手术组比较，常温动物脑梗塞核心(P<；0.05)和核周区(P<；0.05)MPO活性显著升高。体温过低的动物表现得很明显。与假手术组相比，核心区MPO活性增强(P<；0.05)，但核周区MPO活性不明显。亚低温组核周区MPO活性明显低于常温组(P<；0.01)。此外，低温组的脑梗塞体积减少了59%。结论：在低温条件下，缺血内低温可减轻短暂性局灶性脑缺血的炎症反应，即非梗死区。这一发现提出了这样一种可能性，即缺血/再灌流后炎症反应的减少可能参与了低温的神经保护作用。
OBJECTIVE:The mechanisms by which hypothermia influences postichemic outcome remain a matter of discussion. One mechanism thought to play an important role in neuronal damage after ischemia/reperfusion is the accumulation of polymorphonuclear leukocytes in compromised brain tissue. To better understand the potential impact of hypothermia on this injurious mechanism, the present study examined the effect of intraischemic hypothermia on polymorphonuclear leukocyte accumulation after transient focal ischemia.METHODS:The effect of intraischemic hypothermia (30 C) on the accumulation of polymorphonuclear leukocytes was quantified by measuring myeloperoxidase (MPO) activity in the neocortex of Sprague-Dawley rats. Reversible focal ischemia was created by subjecting rats to temporary occlusion of the left middle cerebral artery and both carotid arteries for 3 hours; animals were killed 24 hours after reperfusion.RESULTS:Normothermic animals exhibited significantly greater MPO activity in the infarction core (P< 0.05) and the pericore areas (P< 0.05), compared with corresponding areas in sham-operated animals. Hypothermic animals exhibited significantly. greater MPO activity in the core (P< 0.05) but not in the pericore region, compared with sham-operated animals. MPO activity in the pericore region of the hypothermic group was significantly less than that observed in the corresponding region of the normothermic group (P< 0.01). In addition, the total volume of cerebral infarction was reduced by 59% in the hypothermic group.CONCLUSION:These findings demonstrate that intraischemic hypothermia attenuates the inflammatory response to transient focal ischemia in the pericore region, ie, the region spared from infarction under hypothermic conditions. The findings raise the possiblity that a reduction in the inflammatory response after ischemia/reperfusion contributes to the neuroprotective effects of hypothermia.