Kang Y
Department of Neurosurgery, Faculty of Medicine, Kyoto University.
Nihon Geka Hokan. 1990 Jan 1;59(1):10-26.
Under the hypothesis that cerebral aneurysms develop partly because of defective or decreased healing process at the site of intimal injury, namely at the site of cerebral arterial bifurcation, following experiments were performed. Experiment (1): Rats were treated with ligation of one common carotid artery and ligation of posterior branches of renal artery on both sides to induce cerebral aneurysms. Three months after the treatment, the contralateral carotid artery was ligated. Two months after the ligation, they were sacrificed and examined under light and electron microscopes. In 7 of 11 bifurcations which developed small cerebral aneurysms, prominent intimal thickening with proliferated smooth muscle cells and collagen was observed in the lumen of aneurysms. In 3 of 7 bifurcations which showed no aneurysmal development, apparent intimal thickening was also found at the site where aneurysms were expected to grow. In the group treated for inducing cerebral aneurysms but not ligated the contralateral carotid artery, none of 12 bifurcations with or without aneurysms showed such intimal thickening. Experiment (2): Rats were treated for inducing cerebral aneurysms. Three months after the treatment, reserpine was injected (0.75 mg/Kg B.W./day intraperitoneally) for 2 weeks. At the next day of the last injection, they were sacrificed and examined under the light microscope. In 6 of 12 bifurcations which developed small cerebral aneurysms, prominent intimal thickening was observed in the lumen of aneurysms. In 2 of 3 bifurcations which showed no aneurysmal development, apparent intimal thickening was also found at the site where aneurysms were expected to grow. In the group treated for cerebral aneurysms but not injected reserpine, none of 10 bifurcations with or without aneurysms showed such intimal thickening. Experiment (3): Rats were treated for inducing cerebral aneurysms. Two weeks after the treatment, FSF (fibrin stabilizing factor, known as blood coagulation factor XIII) was injected (10 U/100 g B.W./day, intravenously) for 5 days. Twelve days after the start of injection, they were sacrificed and examined under light and electron microscopes. In 11 of 20 bifurcations which developed small cerebral aneurysms, prominent intimal thickening was observed in the lumen of aneurysms. In the most advanced cases, the lumen of aneurysms were completely filled with proliferated smooth muscle cells and collagen. In 5 of 10 bifurcations which showed no aneurysmal development, apparent intimal thickening was found at the site where aneurysms were expected to grow. In the group treated for inducing cerebral aneurysms but not given FSF, none of 15 bifurcations with or without aneurysms showed such intimal thickening.
基于脑动脉瘤部分是由于内膜损伤部位（即脑动脉分叉处）愈合过程存在缺陷或减弱这一假设，进行了以下实验。实验（1）：对大鼠进行一侧颈总动脉结扎及双侧肾动脉后支结扎以诱导脑动脉瘤形成。处理3个月后，结扎对侧颈动脉。结扎2个月后，处死大鼠并进行光镜和电镜检查。在11个形成小脑动脉瘤的分叉中，有7个在动脉瘤腔内观察到明显的内膜增厚，伴有平滑肌细胞和胶原增生。在7个未发生动脉瘤的分叉中，有3个在预期动脉瘤生长的部位也发现了明显的内膜增厚。在接受诱导脑动脉瘤处理但未结扎对侧颈动脉的组中，12个有或无动脉瘤的分叉均未显示出这种内膜增厚。实验（2）：对大鼠进行诱导脑动脉瘤处理。处理3个月后，腹腔注射利血平（0.75mg/Kg体重/天），持续2周。在最后一次注射的次日，处死大鼠并进行光镜检查。在12个形成小脑动脉瘤的分叉中，有6个在动脉瘤腔内观察到明显的内膜增厚。在3个未发生动脉瘤的分叉中，有2个在预期动脉瘤生长的部位也发现了明显的内膜增厚。在接受脑动脉瘤处理但未注射利血平的组中，10个有或无动脉瘤的分叉均未显示出这种内膜增厚。实验（3）：对大鼠进行诱导脑动脉瘤处理。处理2周后，静脉注射纤维蛋白稳定因子（FSF，即凝血因子XIII，10U/100g体重/天），持续5天。注射开始12天后，处死大鼠并进行光镜和电镜检查。在20个形成小脑动脉瘤的分叉中，有11个在动脉瘤腔内观察到明显的内膜增厚。在最严重的病例中，动脉瘤腔完全被增生的平滑肌细胞和胶原填充。在10个未发生动脉瘤的分叉中，有5个在预期动脉瘤生长的部位发现了明显的内膜增厚。在接受诱导脑动脉瘤处理但未给予FSF的组中，15个有或无动脉瘤的分叉均未显示出这种内膜增厚。
