Okamoto T, Miyachi S, Yoshida J
Department of Neurosurgery, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Front Neurol Neurosci. 2005;20:1-11. doi: 10.1159/000088123.
We developed a canine model of arterial dissection and serially observed morphological changes angiographically and histopathologically to clarify the causes and mechanisms resulting in dissecting aneurysm formation or arterial occlusion. Intimal defects of various sizes and shapes were made on the arterial walls to provide an entry zone for dissection, so as to simulate the extent of arterial wall injury. Our experimental model showed angiographic and histopathological changes similar to those in clinical cases. As for our initial findings immediately after lesioning, either a double shadow (pseudolumen) or stenosis of the affected artery, due to compression from the subadventitial hematoma, was observed in the angiograms of all lesions. In some lesions with a pseudolumen, a dissecting aneurysm developed subsequently. Some arteries showing focal occlusion recanalized, and stenosis spontaneously improved. Very small dissections resulted in spontaneous healing, while a large intimal entry zone caused stenotic lesions. However, a medium-sized entry zone (4-6 mm) may induce aneurysm formation. The different features of dissection may be caused by the characteristics of flow into the subadventitial cavity and by thrombogenesis. Morphological changes after arterial dissection were closely related to the extent of intimal injury, suggesting that the size of the intimal entry zone may determine whether or not a dissecting aneurysm is formed.
我们建立了犬动脉夹层模型,并通过血管造影和组织病理学方法对其形态学变化进行了连续观察,以阐明导致夹层动脉瘤形成或动脉闭塞的原因和机制。在动脉壁上制造各种大小和形状的内膜缺损,作为夹层的入口区域,以模拟动脉壁损伤的程度。我们的实验模型显示出与临床病例相似的血管造影和组织病理学变化。在损伤后的最初观察结果中,所有损伤的血管造影均显示,由于外膜下血肿的压迫,出现了双影(假腔)或受累动脉狭窄。在一些有假腔的损伤中,随后形成了夹层动脉瘤。一些出现局灶性闭塞的动脉再通,狭窄也自行改善。非常小的夹层可自发愈合,而较大的内膜入口区域则导致狭窄性病变。然而,中等大小的入口区域(4-6毫米)可能会诱发动脉瘤形成。夹层的不同特征可能由流入外膜下腔的血流特性和血栓形成所致。动脉夹层后的形态学变化与内膜损伤程度密切相关,这表明内膜入口区域的大小可能决定是否会形成夹层动脉瘤。