MODERATE HYPOTHERMIA REDUCES BLOOD-BRAIN-BARRIER DISRUPTION FOLLOWING TRAUMATIC BRAIN INJURY IN THE RAT
MODERATE HYPOTHERMIA REDUCES BLOOD-BRAIN-BARRIER DISRUPTION FOLLOWING TRAUMATIC BRAIN INJURY IN THE RAT
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DOI：
10.1007/bf00304468
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发表时间：
1992-10-01
影响因子：
12.7
通讯作者：
POVLISHOCK, JT
中科院分区：
文献类型：
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作者：
JIANG, JY;LYETH, BG;POVLISHOCK, JT
研究了中度低温对大鼠中度创伤性脑损伤（TBI）后血脑屏障（BBB）通透性和急性高血压反应的影响。通过免疫细胞化学技术观察，TBI 使常温大鼠（37.5 摄氏度）的背侧皮质灰质和白质以及底层海马的血管通透性增加，对内源性血清白蛋白 (IgG) 的通透性增加。低温大鼠在受伤前冷却至 30 摄氏度（脑温度），血管通透性大大降低。在低温大鼠中，白蛋白免疫反应性仅限于皮质和海马之间的灰白色界面，不涉及上层皮质，并且大大减少了底层海马的参与。常温大鼠的急性高血压反应在 TBI 后 10 秒达到峰值（187.3 mm Hg），并在 50 秒内恢复到基线。相比之下，低温大鼠的急性高血压反应峰值显着降低（P < 0.05）（154.8 mm Hg，TBI 后 10 秒），并在损伤后 30 秒恢复到基线。这些结果表明，适度的低温大大减少了内源性血管蛋白示踪剂进入或可能穿过大脑的通道。这种降低可能部分与低温引起的全身血压对 TBI 反应的调节有关。
The effects of moderate hypothermia on blood-brain barrier (BBB) permeability and the acute hypertensive response after moderate traumatic brain injury (TBI) in rats were examined. TBI produced increased vascular permeability to endogenous serum albumin (IgG) in normothermic rats (37.5-degrees-C) throughout the dorsal cortical gray and white matter as well as in the underlying hippocampi as visualized by immunocytochemical techniques. Vascular permeability was greatly reduced in hypothermic rats cooled to 30-degrees-C (brain temperature) prior to injury. In hypothermic rats, albumin immunoreactivity was confined to the gray-white interface between cortex and hippocampi with no involvement of the overlying cortices and greatly reduced involvement of the underlying hippocampi. The acute hypertensive response in normothermic rats peaked at 10 s after TBI (187.3 mm Hg) and returned to baseline within 50 s. In contrast, the peak acute hypertensive response was significantly (P < 0.05) reduced in hypothermic rats (154.8 mm Hg, 10 s after TBI) and returned to baseline at 30 s after injury. These results demonstrate that moderate hypothermia greatly reduces endogenous vascular protein-tracer passage into and perhaps through the brain. This reduction may, in part, be related to hypothermia-induced modulation of the systemic blood pressure response to TBI.