窦汇区球囊加压法制备急性弥漫性脑肿胀动物模型

Establishment of posttraumatic acute diffuse brain swelling with sinus balloon compression method in rabbits

目的利用窦汇区球囊加压法建立兔外伤性急性弥漫性脑肿胀（PADBS）模型，为探讨PADBS的发生机制提供依据。方法新西兰兔50只按随机数字表法分为对照组（10只）和模型组（40只）。使用颅内压探头，制备窦汇区球囊压迫模型，模型组又分为加压1．5h组、解压后1．5h组、解压后3h组和解压后4．5h组4个亚组（每组各10只），动态监测各组颅内压、脑含水量、病理及超微结构等变化。结果加压1．5h组死亡1只，解压后1．5h组死亡1只，解压后3h组死亡2只，解压后4．5h组死亡3只，模型制备成功率为83％（33／40）。对照组、加压1．5h组、解压后1．5h组、解压后3h组、解压后4．5h组颅内压分别为（4．9±0．8）mmHg、（50．1±4．3）mmHg、（45．2±1．7）mmHg、（48．6±2．2）mmHg、（59．1±2．5）mmHg（P〈0．05）。对照组、加压1．5h组、解压后1．5h组、解压后3h组、解压后4．5h组脑含水量分别为（75．0±0．6）％、（76．7±0．8）％、（77．3±0．5）％、（78．5±0．6）％、（79．4±0．7）％（P〈0．05）。解压后1．5h组出现血管源性脑肿胀；解压后3h组脑组织细胞破坏明显，细胞毒性脑肿胀形成；解压后4．5h组高颅压和细胞缺血缺氧的恶性循环形成。结论颅内压探头监测可保证稳定的球囊压力，建立的PADBS动物模型具有良好的可靠性和稳定性，为进一步探索PADBS的可能机制和治疗策略提供依据。

Objective To establish a rabbit posttraumatic acute diffuse brain swelling （PADBS） model and investigate the mechanism of action. Methods Fifty New Zealand rabbits were assigned to control group （n = 10） and model group （n =40） according to random number table. The animal model of sinus balloon compression was established under intracranial pressure monitoring by using intracranial pressure probe. The model group was subdivided equally at 1.5 hours after compression, 1.5 hours after decompression, 3 hours after decompression and 4.5 hours after decompression, for which intracranial pressure, brain water content, pathological mechanism and uhrastructure were measured dynamically. Results The success rate of modeling was 83% （33/40）. Intracranial pressure was （4.9± 0.8 ） mmHg in control group, （ 50.1 ± 4.3 ） mmHg in 1.5 hours after compression group, （45.2 ±1.7 ） mmHg in 1.5 hours after decompression group, （ 48. 6 ± 2.2 ） mmHg in 3 hours after decompression group, and （59.1 ±2.5 ）mmHg in 4.5 hours after decompression group （P 〈 0.05 ）. Brain water content was （75.0 ± 0. 6 ） % in control gorup, （76.7 ± 0.8 ） % in 1.5 hours after compression group, （77.3 ± 0.5 ） % in 1.5 hours after decompression group, （78.5 ± 0. 6 ） % in 3 hours after decompression group, and （ 79.4 ± 0. 7 ） % in 4.5 hours after decompression group （ P 〈 0.05 ）. Vasogenic brain oedema was seen 1.5 hours after decompression. Cytotoxicity brain swelling generated with brain tissue destroyed 3 hours after decompression. The vicious cycle of high intracranial pressure and brain tissue destruction occurred 4.5 hours after decompression. Conclusion Under intracranial pressure probe monitoring, the rabbit model of PADBS by sinus balloon compression has stable pressure of the sinus balloon and has good reliability and repeatability, which provides a reliable evidence for further study on the possible mechanism and treatment methods of PADBS.