背景:亚低温已作为治疗重型颅脑损伤的常规措施之一,但对亚低温治疗的指征、时程和疗效仍存在争论.继发性颅脑损伤尤其是血脑屏障破坏所致血管源性脑水肿相当普遍,亚低温如何保护血脑屏障及降低其通透性等诸问题迫切需要进一步研究.目的:观察颅脑损伤后早期亚低温治疗对脑毛细血管内皮细胞紧密连接开放的影响,阐明亚低温降低伤后血脑屏障通透性的可能机制.设计:随机对照的实验研究.单位:汕头大学医学院第一附属医院神经外科.对象:实验于2002-05/2002-12在汕头大学医学院中心实验室完成,选择90只Wistar大鼠(常温对照组10只、常温损伤组40只、亚低温治疗组40只,常温损伤组和亚低温治疗组分为伤后3,24,48,72 h 4个时相点,每个时相点10只大鼠).方法:镧示踪电镜法和干-湿重法.主要观察指标:颅脑损伤后内皮细胞紧密连接的开放及其程度,颅脑损伤后不同时相脑组织含水量.结果:常温损伤组伤后3 h紧密连接初步开放,24～48 h紧密连接开放达高峰,72 h紧密连接仍大量开放.亚低温治疗组紧密连接仅轻度开放;亚低温治疗组脑组织含水量[伤后3 h:(78.94 ±0.38)%,伤后24 h:(79.13±0.56)%,伤后48 h:(79.41±0.71)%,伤后72 h:(79.20±0.44)%]较常温损伤组[伤后3 h:(79.56±0.51)%,伤后24 h:(79.80±0.49)%,伤后48 h:(80.46 ±0.47)%,伤后72 h:(79.83±0.44)%]明显减少,伤后3,24,72 h差异有显著性意义(t=3.127 5,2.206 9,2.465 4,P＜0.05),伤后48 h差异有非常显著性意义(t=2.272 7,P＜0.01).结论:亚低温有减轻颅脑损伤后血脑屏障毛细血管内皮细胞紧密连接的开放程度及减轻脑水肿的作用,亚低温减轻伤后内皮细胞紧密连接开放是降低伤后血脑屏障通透性机制之一.%BACKGROUND: Subhypothermia has been a routine treatment measure for severe brain injury. However, there is much debate on the therapeutic indicator, course and effects of it. The vascular edema caused by secondary brain injury especially damaged blood brain barrier is very common so that it needs further research on subhypothermia for certain problems such as how to protect blood brain barrier and reduce its permeability and so on.OBJECTIVE: To observe the effects of early intervention of subhypothermia treatment to the opening of tight junctions of vascular endothelium of brain capillary vessels in brain injury and elaborate the possible mechanism of subhypothermia on reducing permeability of blood brain barrier.DESIGN: A randomized and controlled experiment.SETTING: Department of Neurosurgery, First Hospital, Medical College of Shantou University.SUBJECTS: The experiment was completed in the Central Laboratory,Medical College of Shantou University during May 2002 to December2002. Totally 90 Wistar rats were chosen and divided into normal temperature control group(n= 10), normal temperature damaged group(n=40)and subhypothermia treatment group( n =40) . The damaged group and treatment group were divided into 4 subgroups according to 3 hours, 24hours, 48 hours and 72 hours time points with each of 10 rats.METHODS: Lanthanum tracer electronic microscope method and drying-wet method.MAIN OUTCOME MEASURES: The opening and its extent of tight junctions of endothelial cells after head injury and water content in brain tissue at different time points.RESULTS: In normal temperature damage group, the tight junctions started to open at the 3rd hour and reached peak during 24th to 48th hour and still opened at 72th hour. In subhypothermia treatment group, the tight junctions only slightly opened. The measured water content of brain in subhypothermia group was(78.94 ±0. 38)% at the 3rd hour, (79. 13 ±0.56)% at the 24th hour, (79.41 ±0.71 )% at the 48th hour and (79.20 ± 0. 44)% at the 72th hour while in normal temperature damage group, (79. 56 ±0. 51)% at the3rd hour, (79. 80±0.49)% at the 24th hour, (80.46±0.47)% at the 48th hour and(79. 83 ±0.44)% at the 72th hour. Compared with damage group,the water content of subhypothermia group was lower and there was significant difference between the 3rd, 24th and 72th hour ( t = 3. 127 5, 2. 206 9,2. 465 4, P ＜ 0.05). There was very significant difference at 48th after injury(t =2.272 7, P ＜ 0.01).CONCLUSION: Subhypothermia can reduce the opening of tight junctions of endothelial cells of capillary vessels of blood brain barrier and cerebral edema after head injury happens. It is one of the mechanisms for subhypothermia to reduce the permeability of blood brain barrier by reducing the fight junctions of endothelial cells.
展开▼
