死亡率低大鼠模型的实验性蛛网膜下腔出血后迟发性脑血管痉挛评估
Summary
动脉瘤性蛛网膜下腔出血（SAH）出血，进入蛛网膜下腔动脉瘤破裂时发生的。虽然此事件的发病率和死亡率一直在下降，由于更好的治疗方法，血管痉挛的风险蛛网膜下腔出血后仍然是相同的，因为它是几年前的。建立一个全面的和可再生的动物模型来确定启动事件，脑血管痉挛的重要性一直是研究的重点，因为在第一次使用的一个实验性血管痉挛大鼠模型于1979年由巴里<em>等。</em早期的工作表明，在大鼠急性单次注射自体血枕大池（几分钟内），但不迟发性脑血管痉挛<sup> 3，6，14</sup>。在这里，我们描述SAH大鼠模型死亡率低，可复制的延迟血管痉挛的结果。
Abstract
目的：描述并建立一个可重复的模型，演示了在大鼠动脉瘤性蛛网膜下腔出血（SAH）后迟发性脑血管痉挛，以确定始发事件，病理生理变化和潜在的治疗目标。
方法：对28只雄性SD大鼠（250 – 300克）任意分配给其中的两个群体 – 蛛网膜下腔出血或生理盐水对照组。 SAH组（n = 15）的大鼠蛛网膜下腔出血引起的双注射自体血液，相隔48小时，枕大池。同样，生理盐水组（n = 13）被注入到小脑延髓池的盐水对照组。 5天处死大鼠后，第二次注血和被保存下来的大脑进行组织学分析。血管痉挛的程度，测定使用的基底动脉的部分，通过测量使用NIH图像J软件的内部管腔的横截面面积。的意义测试使用的杜克/克莱默的统计分析。
结果：组织切片分析后，基底动脉管腔截面积较生理盐水组在SAH，脑血管痉挛，前一组一致的。在SAH组，基底动脉的内部面积（0.056微米±3）从血管痉挛5天之后，第二次血液注射液（七天后的初始注血），较生理盐水对照组的内部区域（0.069 ±3，P = 0.004）。有没有脑血管痉挛死亡率。
结论：双SAH模型大鼠诱导温和的，生存能力，基底动脉血管痉挛，在小动物模型，可用于研究脑血管痉挛的病理生理机制。低和可接受的死亡率是一个重要的标准，需要满足的一个理想的SAH动物模型，使血管痉挛的机制可以elucidated 7，8。进一步修改的模型可以进行调整日益严重的血管痉挛和神经系统检查。
Protocol
Representative Results
Discussion
灵长类动物，具有更相似的遗传组成和解剖特征的人，更紧密地模仿迟发性脑血管痉挛的事件，可以更容易地进行非侵入性成像（MRI和血管造影），以监测动脉的变化，比啮齿类动物8。然而，灵长类动物模型的成本过高，与更复杂的护理和道德问题，不是小动物模型。已开发的小动物SAH模型以前主要集中在诱导SAH的三种方法：1）血管内动脉的颅内动脉使血液进入蛛网膜下腔逃脱，周围动…
Disclosures
The authors have nothing to disclose.
Acknowledgements
在写这篇稿子，我们要感谢的努力，玛丽娄医生，神经科学和生理学系，Vallano的宝贵意见。
Materials
| Name of equipment / reagent | Company | Catalogue Number |
| Male SD rats (250-300 g) | Taconic | SD-M |
| 26 G Catheters | Webster | 8416683 |
| 25 G Needles | Buffalo | 305122 |
| 1 cc Syringes | Central stores | 54245 |
| Ketamine/Xylazine cocktail | Animal Care (SUNY)* | – |
| Betadine | Central stores | 51458 |
| Sucrose | Sigma | S9378-1kg |
| Paraformaldehyde | Sigma | P6148-500G |
| Phosphate buffer solution | Fisher | BP-399-4 |
| Surgical Table | Harvard | PY2 72-2590 |
| OCT Compound (cryoprotection) | VWR | 25608-930 |
| Superfrost Slides | Fisher | 12-550-15 |
* Synthesized at Department of Laboratory Animal Care, SUNY Upstate Medical University. Add 1 cc [100 mg/ml] of Xylazine to 10 ml [100 mg/ml] of Ketamine.
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