Division of Clinical Neurosciences, University of Edinburgh, Western General Hospital, Edinburgh, UK.
Int J Stroke. 2011 Oct;6(5):434-44. doi: 10.1111/j.1747-4949.2011.00659.x.
The spontaneously hypertensive stroke prone rat is best known as an inducible model of large artery stroke. Spontaneous strokes and stroke propensity in the spontaneously hypertensive stroke prone rat are less well characterized; however, could be relevant to human lacunar stroke. We systematically reviewed the literature to assess the brain tissue and small vessel pathology underlying the spontaneous strokes of the spontaneously hypertensive stroke prone rat. We searched systematically three online databases from 1970 to May 2010; excluded duplicates, reviews, and articles describing the consequences of induced middle cerebral artery occlusion or noncerebral pathology; and recorded data describing brain region and the vessels examined, number of animals, age, dietary salt intake, vascular and tissue abnormalities. Among 102 relevant studies, animals sacrificed after developing stroke-like symptoms displayed arteriolar wall thickening, subcortical lesions, enlarged perivascular spaces and cortical infarcts and hemorrhages. Histopathology, proteomics and imaging studies suggested that the changes not due simply to hypertension. There may be susceptibility to endothelial permeability increase that precedes arteriolar wall thickening, degeneration and perivascular tissue changes; systemic inflammation may also precede cerebrovascular changes. There were very few data on venules or tissue changes before hypertension. The spontaneously hypertensive stroke prone rat shows similar features to human lacunar stroke and may be a good spontaneous model of this complex human disorder. Further studies should focus on structural changes at early ages and genetics to identify factors that predispose to vascular and brain damage.
自发性高血压卒中易发性大鼠是一种广为人知的大动脉卒中诱导模型。自发性卒中及自发性高血压卒中易发性大鼠的卒中易发性特征还不太明确，但可能与人类腔隙性卒中相关。我们系统地回顾了文献，以评估自发性高血压卒中易发性大鼠自发性卒中的脑组织和小血管病理学基础。我们从 1970 年至 2010 年 5 月，系统地在三个在线数据库中进行了检索；排除了重复、综述和描述诱导性大脑中动脉闭塞或非脑病理学后果的文章；并记录了描述脑区和检查血管、动物数量、年龄、盐饮食摄入、血管和组织异常的数据。在 102 篇相关研究中，在出现类似卒中症状后被处死的动物显示出小动脉壁增厚、皮质下病变、扩大的血管周围间隙和皮质梗死和出血。组织病理学、蛋白质组学和影像学研究表明，这些变化不仅仅是由高血压引起的。可能存在内皮通透性增加的易感性，这种易感性先于小动脉壁增厚、变性和血管周围组织改变；全身炎症也可能先于脑血管变化。在高血压之前，关于小静脉或组织变化的数据非常少。自发性高血压卒中易发性大鼠具有与人类腔隙性卒中相似的特征，可能是这种复杂人类疾病的良好自发性模型。进一步的研究应集中在早期的结构变化和遗传学上，以确定易导致血管和脑损伤的因素。
