Study on the Pathophysiology of Experimental Vascular Dementia in Gerbils using Magnetic Resonance Methods

在血管性痴呆患者中，大脑动脉通常变窄，脑血流量不断减少。为探讨动脉狭窄在血管性痴呆发病机制中的作用，采用沙土鼠双侧颈总动脉狭窄模型，观察动脉狭窄的慢性效应。实验一用直径0.1×1.0 mm、长2.0 mm的银夹狭窄颈总动脉。狭窄导致40%的动物血流量严重减少，低于0.20mI/g/min，其余60%动物血流量中度减少。40%的动物发生能量衰竭，在狭窄后4天内死亡。活体31P核磁共振波谱(31P核磁共振波谱)显示60%的动物没有能量损伤，也没有缺血症状。这些无症状动物的组织学检查在狭窄后1天没有发现缺血性改变。5天、4周和3个月的…狭窄后S较多，分别有40%、53%和60%的动物出现缺血性改变。缺血性改变包括大面积半球脑梗塞(1型)、多发性小脑梗塞(2型)和以神经细胞死亡为主的小片状改变(3型)。在狭窄后4周和3个月观察到3型缺血，最常见的是大脑皮层和大脑皮层。在狭窄后2周和3个月，这些都是缺血的。动物表现出明显的学习能力抑制。实验2用直径0.28~0.58 mm、长2.0 mm的聚乙烯管在双侧颈总动脉造成不同程度的狭窄。在严重狭窄组，继发血栓形成在颈动脉，导致能量受损和急性死亡。在中度狭窄组，30%的动物出现1或2型缺血的颈动脉血栓。在其余动物中，没有观察到颈动脉血栓，但经常观察到3型缺血。在中度至轻度狭窄组中，几乎没有发生缺血性改变。1型或2型缺血可能是由血栓形成的动脉阻塞或动脉间动脉栓塞引起的。3型缺血不太可能是这种机制造成的，可能是慢性低灌注所致。提示慢性低灌注性脑缺血可能在血管性痴呆的病理生理机制中起一定作用。较少

In patients with vascular dementia, cerebral arteries are usually narrowed, and cerebral blood flow is reduced constantly. In order to clarlfy the role of arterial stenosis In the pathophysiology of vascular dementia, both common carotld arteries were narrowed in gerbils, and chronic effects of arterial stenosls were studied. In experiment 1, the common carotid arteries were narrowed by silver clips wlth 0.1 x 1.0 mm in diameter and 2.0 mm in length. The stenosis caused severe blood flow reduction of below 0.20 mi/g/min in 40% of animals and moderate flow reduction in the remaining 60% of animals. 40% of animals developed energy failure and died within 4 days after the stenosis. The remalning 60% of animals had no energy impairments as judged by in vivo 31P nuclear magnetic resonance spectroscopy (MRS) and remained free from ischemic symptoms. Histological examinations in these asymptomatic animals exhibited no ischemic change at 1 day after the stenosis. At 5 days, 4 weeks and 3 month … More s after stenosis, 40%, 53% and 60% of animals showed ischemic changes. Ischemic changes included large hemisphric cerebral infarction (type 1), multiple small infarction (type 2) and small patchy changes consisting of neuronal cell death (type 3). Type 3 ischemia was observed at 4 weeks and 3 months after the stenosls and most commonly seen in the cerebral cortex and strlatum. At 2 weeks and 3 months after the stenosls, these ischemic. animals exhibited remarkable depresslon of learning ability. In experiment 2, flve different grades of stenosis was produced at both common carotid arteries using polyethylene tubes with 0.28-0.58 mm in diameter and 2.0 mm in length. In the group with severe stenosis, secondary thrombus formation occurred at the carotid arteries leading to energy impairments and acute death. In the group with intermediate grade stenosis, carotid thrombus was seen in 30% of animals which developed type 1 or 2 ischemia. In the remaining animals, no carotid thrombus was observed, yet, type 3 ischemia was frequently observed. In the groups with moderate to mild grade stenosis, little ischemic changes resulted. Type 1 or 2 ischemia is probably caused by thrombotic arterial obstruction or artery-to-artery embolism. Type 3 ischemia is unlikely to result from such mechanism and is presumably attributable to chronic low perfusion. The results suggest that chronic low perfusion may produce small patchy ischemia in the brain and may play a role in the pathophysiology of vascular dementia. Less