Toyoda T, Suzuki S, Kassell N F, Lee K S
Department of Neurological Surgery, Virginia Neurological Institute, University of Virginia, Charlottesville, USA.
Neurosurgery. 1996 Dec;39(6):1200-5. doi: 10.1097/00006123-199612000-00024.
The mechanisms by which hypothermia influences postischemic 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.
The effect of intraischemic hypothermia (30 degrees 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.
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.
These findings demonstrate that intraischemic hypothermia attenuates the inflammatory response to transient focal ischemia in the pericore region, i.e., the region spared from infarction under hypothermic conditions. The findings raise the possibility that a reduction in the inflammatory response after ischemia/reperfusion contributes to the neuroprotective effects of hypothermia.
低温影响缺血后转归的机制仍存在争议。一种被认为在缺血/再灌注后神经元损伤中起重要作用的机制是多形核白细胞在受损脑组织中的积聚。为了更好地理解低温对这种损伤机制的潜在影响，本研究检测了缺血期低温对短暂性局灶性缺血后多形核白细胞积聚的影响。
通过测量Sprague-Dawley大鼠新皮质中的髓过氧化物酶（MPO）活性，定量缺血期低温（30℃）对多形核白细胞积聚的影响。通过暂时阻断大鼠左大脑中动脉和双侧颈动脉3小时造成可逆性局灶性缺血；动物在再灌注24小时后处死。
与假手术动物的相应区域相比，正常体温动物在梗死核心区（P<0.05）和核心周围区（P<0.05）的MPO活性显著更高。与假手术动物相比，低温动物在核心区的MPO活性显著更高（P<0.05），但在核心周围区则不然。低温组核心周围区的MPO活性显著低于正常体温组相应区域（P<0.01）。此外，低温组脑梗死总体积减少了59%。
这些发现表明，缺血期低温减轻了核心周围区对短暂性局灶性缺血的炎症反应，即低温条件下未发生梗死的区域。这些发现提示，缺血/再灌注后炎症反应的减轻可能是低温神经保护作用的机制之一。
