缺血诱导颅内外血运重建的基础研究与临床实践

Basic Research and Clinical Practice of Ischemia Induced Intracranial and Extracranial Revascularization

摘要: 目的：本研究旨在探讨缺血诱导的颅内外血运重建现象及其对神经功能恢复、脑梗死体积及相关因子表达的影响。方法：采用SD大鼠建立脑缺血并颅骨缺损模型，将大鼠分为实验组(脑缺血 + 去骨瓣减压手术、单纯去骨瓣减压、单纯脑缺血、脑缺血 + 去骨瓣减压术并硬脑膜切开反转)和对照组(假手术组)。观察术后14天和30天大鼠的脑梗死体积，并检测脑组织中血管内皮生长因子(VEGF)、血管内皮增殖细胞KI67及血小板–内皮细胞黏附分子(CD31)的表达。结果：实验组中，脑缺血结合去骨瓣减压手术显著减少了脑梗死体积，并促进了VEGF、KI67和CD31的表达。相比之下，单纯去骨瓣减压手术或单纯脑缺血对脑梗死体积和相关因子表达的影响较小。假手术组未发生脑梗死，相关因子表达水平较低。结论：缺血诱导的颅内外血运重建现象在脑缺血结合去骨瓣减压手术中尤为显著，该手术组合有助于促进血管新生和神经细胞增殖，减少脑梗死体积，从而改善神经功能。这些发现为临床上治疗脑梗死提供了新的思路和方法。

Abstract: Objective: This study aims to explore whether there is a phenomenon of intracranial and extracranial blood flow reconstruction after decom craniectomy for traumatic brain injury and its effects on the recovery of neurological function, the volume of cerebral infarction, and the expression of related factors. Methods: A rat model of cerebral ischemia with skull defect was established using SD rats. The rats were divided into an experimental group (cerebral ischemia decompressive craniectomy, decompressive craniectomy alone, cerebral ischemia alone, cerebral ischemia decompressive craniectomy with durotomy and dural flap) and a control group (sham surgery group). The volume of cerebral infarction was observed at 14 and 30 days after surgery, and the expression vascular endothelial growth factor (VEGF), vascular endothelial proliferating cell KI67, and platelet-endothelial cell adhesion molecule (CD1) in brain tissue was detected. Results: In the experimental group, cerebral ischemia combined with decompressive craniectomy significantly reduced the volume of cerebral infar and promoted the expression of VEGF, KI67, and CD31. In contrast, decompressive craniectomy alone or cerebral ischemia alone less effect on the volume of cerebral infarction and the expression of related factors. No cerebral infarction occurred in the sham surgery group, and the expression level related factors was low. Conclusion: The phenomenon of intracranial and extracranial blood flow reconstruction induced by ischemia is particularly significant in cerebral ischemia with decompressive craniectomy, and this surgical combination helps to promote angiogenesis and the proliferation of nerve cells, reduce the volume of cerebral infarction, and improve neurological function. These findings provide a certain basis for whether patients who have not undergone cranioplasty for a long time after decompressive craniectomy are suitable cranioplasty treatment in clinical practice, and whether it will cause secondary brain tissue damage leading to cerebral ischemia.