Stroke-prone renovascular hypertensive rats

Purpose To summarized the methods for establishment, characteristics of vascular lesions in brain and heart and thc application of stroke-pronc renovascular hypertensive rats (RHRSP). Background Spontaneously hypcrtensivc rats (STR) and subtypes of SH R, especially stroke-prone spontaneously hypertensive rats (SHRSP) are considered as most important animal models at present for the studies of hypertension and its complications in heart and brain, evcn SHRSP arc considered as thc unique animal model in which prcvention of stroke can be studied cxperimentally Howcver, the applications of SHR and SHRSP are limited because of the effects of genetic deficits and thc difficulties with breeding Theretore, most of the researches on experimental stroke have been performed on the animal models with normotcnsion and normal structure of cerebral vessels. In fact, there are great differences in structure of cerebrovesscls, autoregulation of cerebral blood flow and extent of lesions in brain tissue, even the reaction to the medication after ischemia between the animals with extcnsive arteriosclerosis and with normal cerebral blood vessels. Obviously, thc relevancc of experimental stroke on normal animals to the stroke on cerebral arteriosclerotic patients clinically remains dubious. Data sources and methods Most published original articles about RHRSP in our laboratory were reviewed Results After the renal arteries were constricted bilaterally with ring-shape silver clips, the stroke-prone rcnovascular hypertensive rats were established. Hypertension was produced in all RHRSP(100%).The peak of blood pressure in RHRSP reached 29.1 ±3.0kPa. The lesions of cerebral arteries and arterioles and the damage of cerebral capillary structure by hypertension were observed in the RHRSP. The incidence of spontaneous stroke was 56.4% with in 40 weeks after the renal artery constriction. Left ventricular hypertrophy and small coronary arterial lesions in myocardium were discovered in all RHRSP. Myocardial infarction occurred spontaneously in 41.8% of RHRSP. The animal models have been used for the studies on mechanisms of stroke and myocardial infarction. Futhermore, RHlRSP with cercbrovascular basal pathological changes can be induced as cerebral thrombosis by thc photochemical method, which is quite similar to that of human being in evolution. Therefore. RHRSP with photochemical cerebral thrombosis can be used to appraised therapeutic effects of medication more objectively Conclusions Because the vascular lesions in cerebrum and heart in RHRSP are similar to that in human beings with hypertension, RHRSP can be used in the studies on mechanisms of hypertensive arterioscle-rotic stroke and cardiac lesions and on verifying the effects of different medications to complications of hypertension, and thc results might be more reliable than that in animal models without hypertension.     

肾性高血压大鼠脑梗死后期的基因表达谱分析

目的 利用基因芯片技术研究肾性高血压大鼠脑梗死后期梗死灶边缘区皮层基因表达谱的改变及其意义.方法 利用双肾双夹法复制肾性高血压大鼠模型,再采用线栓法复制成大脑中动脉闭塞模型,并设置假手术组,术后7 d取梗死灶边缘区域脑皮层,提取RNA,经过荧光标记后与含5705个基因的oligo芯片进行杂交、扫描,采集图像,经数据分析筛选出差异表达的基因.结果 差异表达基因共197个(包括表达序列标签12个),其中表达上调174个,下调23个.12类功能分组的基因均有上调,下调的基因仅包括运输、转录调控、信号、应激反应、代谢和细胞粘附组的基因.12类功能分组中有17个差异表达基因尚未有文献报道与脑缺血/梗死相关.结论 脑梗死后期基因表达仍然非常活跃,预示着损伤与修复的分子机制和可能的治疗靶点.     

Vascular perfusion differs in two distinct PDGFRβ-positive zones within the ischemic core of male mice 2 weeks following photothrombotic stroke

Stroke therapy has largely focused on preventing damage and encouraging repair outside the ischemic core, as the core is considered irreparable. Recently, several studies have suggested endogenous responses within the core are important for limiting the spread of damage and enhancing recovery, but the role of blood flow and capillary pericytes in this process is unknown. Using the Rose Bengal photothrombotic model of stroke, we illustrate blood vessels are present in the ischemic core and peri-lesional regions 2 weeks post stroke in male mice. A FITC-albumin gel cast of the vasculature revealed perfusion of these vessels, suggesting cerebral blood flow (CBF) may be partially present, without vascular leakage. The length of these vessels is significantly reduced compared to uninjured regions, but the average width is greater, suggesting they are either larger vessels that survived the initial injury, smaller vessels that have expanded in size (i.e., arteriogenesis), or that neovascularization begins with larger vessels. Concurrently, we observed an increase in platelet-derived growth factor receptor beta (PDGFRβ, a marker of pericytes) expression within the ischemic core in two distinct patterns, one which resembles pericyte-derived fibrotic scarring at the edge of the core, and one which is vessel associated and may represent blood vessel recovery. We find little evidence for dividing cells on these intralesional blood vessels 2 weeks post stroke. Our study provides evidence flow is present in PDGFRβ-positive vessels in the ischemic core 2 weeks post stroke. We hypothesize intralesional CBF is important for limiting injury and for encouraging endogenous repair following cerebral ischemia.     

短时间诱导高血压对急性脑缺血再灌注大鼠梗死体积的影响

目的探讨在不同缺血时间诱导高血压对急性局部脑缺血再灌注大鼠梗死体积的影响。方法61只年龄30～40周的SD大鼠,随机分为假手术组、缺血组、缺血再灌注组和升压组。通过静脉滴注新福林对升压组动物进行诱导高血压治疗。结果(1)缺血再灌注组的梗死体积大于相应的缺血组。(2)升压组的梗死体积小于缺血再灌注组和缺血4h组。(3)在缺血4h再灌注2h升压组中,再灌注前15min升压组的梗死体积小于再灌注后30min升压组。结论(1)诱导高血压治疗能有效地减少急性脑缺血再灌注大鼠梗死体积。(2)再灌注前升压疗效优于再灌注后升压。     

Cannabinoid CB(2) receptor activation decreases cerebral infarction in a mouse focal ischemia/reperfusion model.

Cannabinoid CB(2) Receptor (CB(2)) activation has been shown to have immunomodulatory properties without psychotropic effects. The hypothesis of this study is that selective CB(2) agonist treatment can attenuate cerebral ischemia/reperfusion injury. Selective CB(2) agonists (O-3853, O-1966) were administered intravenously 1 h before transient middle cerebral artery occlusion (MCAO) or 10 mins after reperfusion in male mice. Leukocyte/endothelial interactions were evaluated before MCAO, 1 h after MCAO, and 24 h after MCAO via a closed cranial window. Cerebral infarct volume and motor function were determined 24 h after MCAO. Administration of the selective CB(2) agonists significantly decreased cerebral infarction (30%) and improved motor function (P<0.05) after 1 h MCAO followed by 23 h reperfusion in mice. Transient ischemia in untreated animals was associated with a significant increase in leukocyte rolling and adhesion on both venules and arterioles (P<0.05), whereas the enhanced rolling and adhesion were attenuated by both selective CB(2) agonists administered either at 1 h before or after MCAO (P<0.05). CB(2) activation is associated with a reduction in white blood cell rolling and adhesion along cerebral vascular endothelial cells, a reduction in infarct size, and improved motor function after transient focal ischemia.     

Induced hypertension treatment to improve cerebral ischemic injury after transient forebrain ischemia

The effect of induced hypertension treatment on cerebral ischemia is still controversial. We investigated the preferred blood pressure manipulation level and pressor agent required to reduce cerebral ischemic injury following transient forebrain ischemia induced by bilateral occlusion of the common carotid arteries in anesthetized gerbils. Following 60-min cerebral ischemia, we evaluated the preferred blood pressure manipulation level and pressor agent required to treat cerebral ischemic injury after reperfusion by examining the effects of different levels of mean arterial blood pressure (MABP), increased with phenylephrine or angiotensin II or decreased by blood withdrawal, on cerebral blood flow (CBF), survival ratio, cerebral edema, and brain energy metabolism following transient forebrain ischemia in gerbils. Mild phenylephrine-induced hypertension treatment (21+/-4 mmHg) during post-cerebral ischemia-reperfusion improved the survival ratio and reduced cerebral edema, which was also associated with an increase in local CBF and a recovery of brain energy metabolism. However, intense phenylephrine-induced hypertension, angiotensin II-induced hypertension, or hypotension worsen the survival rate and produced extra cerebral edema, that were also associated with deterioration of brain energy metabolism. These results demonstrate that a mild induced hypertension with phenylephrine (21+/-4 mmHg above the baseline level) results in reduction of the cerebral edema and improves the survival ratio and brain energy metabolism. Furthermore, angiotensin II may have neurotoxic effect to use as the pressor agent for induced hypertension after cerebral ischemia.     

Cerebral vasoconstriction in response to hypocapnia is maintained after ischemia/reperfusion injury in newborn pigs.

BACKGROUND AND PURPOSE: Hypocapnic cerebral vasoconstriction is used therapeutically to reduce elevated intracranial pressure caused by cerebral edema. Because cerebral ischemia/reperfusion injury causes a selective loss of prostanoid-dependent responses, including vasodilation to hypercapnia, we designed these experiments to examine the effect of ischemia/reperfusion on hypocapnic cerebral vasoconstriction. METHODS: Microvascular responses were studied in 10 newborn pigs (closed cranial window) in response to hyperventilation-induced hypocapnia (PaCO2, 22 +/- 2 mm Hg) both before and 45 minutes after 20 minutes of global cerebral ischemia. Responses to hypercapnia (PaCO2, 63 +/- 3 mm Hg), topical isoproterenol (10(-7) M), and norepinephrine (10(-4) M) were also studied before and after ischemia in the same animals for comparison. RESULTS: Before ischemia/reperfusion, pial arterioles vasoconstricted to hypocapnia (-17 +/- 2%) and norepinephrine (-35 +/- 4%) and vasodilated to CO2 (37 +/- 7%) and isoproterenol (25 +/- 2%). After ischemia/reperfusion, the constriction of pial arterioles to hypocapnia (-19 +/- 2%) was similar to that before ischemia. This is in contrast to the loss of dilation to hypercapnia. Dilation to isoproterenol and constriction to norepinephrine were not affected by ischemia. CONCLUSIONS: Hypocapnic cerebral vasoconstriction is maintained after ischemia/reperfusion. Since prostanoid-dependent responses, such as hypercapnic dilation, are lost following cerebral ischemia, these data suggest that hypocapnic constriction is not dependent on an intact prostanoid system and that cerebral vascular responses to CO2 involve multiple mechanisms, depending on whether CO2 is increasing or decreasing from baseline.     

一种氯化铁诱导血栓生成的小鼠大脑中动脉远端缺血模型

目的 建立稳定的小鼠大脑中动脉远端氯化铁血栓模型,评价其造成的脑损伤及神经功能损伤程 度。 方法 C57BL6/J雄性小鼠随机分为脑缺血组和假手术组。脑缺血组用10%氯化铁（ferric chloride, FeCl3）溶液诱导右侧大脑中动脉远端形成血栓。在术前、术后10 mi n、术后1 d和7 d观测术侧脑血流 和手术动脉血流量的变化。术后1 d观察脑组织梗死率。术后1 d、3 d、5 d、7 d用3种神经学评分[改良 加西亚评分（modified Garcia score,mGS）、改良神经损伤严重程度评分（modified neurological severity scores,mNSS）和15分神经学评估表（15-point neurological evaluation scale,NES）]和胶黏纸测试评价小 鼠神经功能。术后7 d免疫荧光染色标记神经细胞核观察脑组织损伤,标记CD16/32、CD206和Iba1观 察胶质细胞表达。 结果 与假手术组相比,脑缺血组术后10 mi n、1 d、7 d脑表面血流和手术动脉血流下降,术后1 d脑 皮层梗死明显,术后7 d仍有明显脑组织损伤;脑缺血组术后1 d、3 d、5 d和7 d时3种神经学评分及胶 黏纸测试均提示小鼠神经功能不同程度损伤。术后7 d脑缺血组梗死周围皮层M1和M2型胶质细胞表 达增加。 结论 FeCl3溶液可诱导形成稳定的小鼠脑缺血模型,该模型可造成手术侧大脑中动脉远端及脑表 面血流量降低,皮层脑梗死,小鼠神经功能受损,梗死周围胶质细胞表达上调。本研究建立了稳定 氯化铁诱导血栓形成的小鼠脑缺血模型,为脑血栓形成和抗栓药物治疗提供了一种可靠的研究工 具。     

Review: cerebral microvascular pathology in ageing and neurodegeneration

This review of age-related brain microvascular pathologies focuses on topics studied by this laboratory, including anatomy of the blood supply, tortuous vessels, venous collagenosis, capillary remnants, vascular density and microembolic brain injury. Our studies feature thick sections, large blocks embedded in celloidin, and vascular staining by alkaline phosphatase. This permits study of the vascular network in three dimensions, and the differentiation of afferent from efferent vessels. Current evidence suggests that there is decreased vascular density in ageing, Alzheimer's disease and leukoaraiosis, and cerebrovascular dysfunction precedes and accompanies cognitive dysfunction and neurodegeneration. A decline in cerebrovascular angiogenesis may inhibit recovery from hypoxia-induced capillary loss. Cerebral blood flow is inhibited by tortuous arterioles and deposition of excessive collagen in veins and venules. Misery perfusion due to capillary loss appears to occur before cell loss in leukoaraiosis, and cerebral blood flow is also reduced in the normal-appearing white matter. Hypoperfusion occurs early in Alzheimer's disease, inducing white matter lesions and correlating with dementia. In vascular dementia, cholinergic reductions are correlated with cognitive impairment, and cholinesterase inhibitors have some benefit. Most lipid microemboli from cardiac surgery pass through the brain in a few days, but some remain for weeks. They can cause what appears to be a type of vascular dementia years after surgery. Donepezil has shown some benefit. Emboli, such as clots, cholesterol crystals and microspheres can be extruded through the walls of cerebral vessels, but there is no evidence yet that lipid emboli undergo such extravasation.     

Chronic cerebral hypoperfusion protects against acute focal ischemia, improves motor function, and results in vascular remodeling

Atherosclerosis may cause severe stenosis of the arteries supplying the brain, which induces chronic cerebral hypoperfusion. Although an infarction often occurs in this area, it is uncertain how brain vessels respond to the chronic hypoperfusion or how the vascular responses are related to stroke severity when the area has been subjected to severe ischemia. To address these uncertainties, we induced chronic cerebral hypoperfusion in Sprague-Dawley rats with a bilateral common carotid artery ligation (BCAL). A middle cerebral artery occlusion/reperfusion (MCAO/R) was introduced with a nylon suture four weeks after either BCAL (BCAL-MCAO) or a sham operation (Sham-MCAO). Motor disability scores and infarct sizes, based on 2,3,5-triphenyltetrazolium chloride staining, were significantly reduced with BCAL-MCAO treatment compared with sham-MCAO treatment (P<0.01). The diameters of the posterior cerebral, posterior communicating, and basilar arteries on the brain surface were larger and more tortuous in BCAL-treated rats (P<0.01). The density of large capillary- and arteriole-sized vessels in the brain parenchyma also increased in BCAL-treated rats (P<0.05). Strokes were less severe when the vicinity subjected to infarction was preconditioned with chronic cerebral hypoperfusion. Increasing the vascular reserve with adaptive vascular remodeling may have contributed to this response.     

Leukotriene constriction of mouse pial arterioles in vivo is endothelium-dependent and receptor-mediated

The diameters of pial arterioles of mice were monitored in vivo with an image-splitting technique and television microscopy. Concentrations of leukotriene C4 as low as 10(-7) M constricted the arterioles. The leukotriene C4-D4 receptor blocker ICI 198615 (10(-8) M) inhibited the response. Endothelial injury by helium-neon laser/Evans blue technique eliminated the constriction and unmasked a slight but consistent relaxation that was not inhibited by 10(-8) M ICI 198615. Since leukotrienes are produced by the brain and enter the cerebrospinal fluid in ischemia, head trauma, and subarachnoid hemorrhage, the possibility that leukotrienes C4 and D4 contribute to decreases in cerebral blood flow during these conditions should be considered. However, the present data makes such a possibility far less likely because the endothelium is frequently injured in these conditions, and therefore the ability of leukotrienes to constrict vessels would be severely curtailed.     

胰岛素对局灶性脑缺血再灌注损伤的作用

目的　观察胰岛素对脑缺血再灌注损伤的治疗作用。方法　制备易卒中型肾血管性高血压大鼠（ Ｒ Ｈ Ｒ Ｓ Ｐ） ,用线栓法复制大脑中动脉阻塞（ Ｍ Ｃ Ａ Ｏ） ,造成缺血６ ｈ 再灌注１８ ｈ ,术后立即及６ 小时后即时使用胰岛素,测定神经功能障碍评分及脑梗死体积的变化。结果　胰岛素可使神经功能障碍评分显著减低,梗死灶体积及其占全大脑体积比值,两半球体积差值显著减小。结论　胰岛素能减轻脑缺血再灌注损伤,早期用药效果更好。     

血管内皮生长因子治疗性血管生成作用与缺血性脑血管病

血管内皮生长因子是血管特异性生长因子,能特异性地作用于血管内皮细胞,诱导血管生成,在血管发生和血管形成过程中起重要作用。传统观念认为,成年脑部血管内皮细胞是不能增殖的,但近期的动物实验发现局灶性脑缺血后可诱导缺血半暗带区的新生血管形成。这种脑血管生成是通过血管生长因子与内皮细胞上表达的酪氨酸受体结合而调控的。但是这种血管形成数量有限,并不足以挽救血液灌注不足引起的损害。新近的研究已经证实,外源性给予血管生长因子能刺激侧枝循环形成和增加局部血流,并且已在外周动脉闭塞性疾病和心肌缺血中成功应用,这种新的刺激和诱导新生血管形成新颖方法—治疗性血管生成,为治疗缺血性脑血管病提供了一条全新的思路。     

一种氯化铁诱导血栓生成的小鼠大脑中动脉远端缺血模型

目的 建立稳定的小鼠大脑中动脉远端氯化铁血栓模型，评价其造成的脑损伤及神经功能损伤程
度。
方法 C57BL6/J雄性小鼠随机分为脑缺血组和假手术组。脑缺血组用10%氯化铁（ferric chloride，
FeCl3）溶液诱导右侧大脑中动脉远端形成血栓。在术前、术后10 mi n、术后1 d和7 d观测术侧脑血流
和手术动脉血流量的变化。术后1 d观察脑组织梗死率。术后1 d、3 d、5 d、7 d用3种神经学评分[改良
加西亚评分（modified Garcia score，mGS）、改良神经损伤严重程度评分（modified neurological severity
scores，mNSS）和15分神经学评估表（15-point neurological evaluation scale，NES）]和胶黏纸测试评价小
鼠神经功能。术后7 d免疫荧光染色标记神经细胞核观察脑组织损伤，标记CD16/32、CD206和Iba1观
察胶质细胞表达。
结果 与假手术组相比，脑缺血组术后10 mi n、1 d、7 d脑表面血流和手术动脉血流下降，术后1 d脑
皮层梗死明显，术后7 d仍有明显脑组织损伤；脑缺血组术后1 d、3 d、5 d和7 d时3种神经学评分及胶
黏纸测试均提示小鼠神经功能不同程度损伤。术后7 d脑缺血组梗死周围皮层M1和M2型胶质细胞表
达增加。
结论 FeCl3溶液可诱导形成稳定的小鼠脑缺血模型，该模型可造成手术侧大脑中动脉远端及脑表
面血流量降低，皮层脑梗死，小鼠神经功能受损，梗死周围胶质细胞表达上调。本研究建立了稳定
氯化铁诱导血栓形成的小鼠脑缺血模型，为脑血栓形成和抗栓药物治疗提供了一种可靠的研究工
具。     

Ischemic axonal injury and its recovery after focal cerebral ischemia

After focal cerebral infarction by occluding the middle cerebral artery (MCA) of the rat, the neuronal death occurred in the ipsilateral thalamic neurons, because axons of the thalamic neurons were injured by infarction and retrograde degeneration occurred in the thalamic neurons. However, cortical neurons adjacent to the infarction survived despite their axons injured by ischemia. We employed immunohistochemical staining for 200 kilodalton (kD) neurofilament (NF), in order to study those responses of cortical and thalamic neurons against axonal injury caused by focal cerebral infarction. In the sham operated rats the immunoreactivity to the anti-200 kD NF antibody was only detected in the axon but not in the cell bodies and dendrites. At 3 days after MCA occlusion, axonal swelling proximal to the site of ischemic injury was found in the caudoputamen and internal capsule of the ipsilateral side. At 7 days after occlusion, cell bodies and dendrites of the neurons in the ipsilateral cortex and thalamus were strongly stained with anti-NF antibodies. At 2 weeks after occlusion these responses disappeared in the cortex, but lasted in the thalamus. These phenomena are caused by stasis of the slow axonal transport, because the NF is transported by slow axonal transport. In the cortical neurons impairment of slow axonal transport recovered in the early phase after injury, but in the thalamic neurons the impairment prolonged up to 3 weeks after occlusion. The early recovery of axonal transport from ischemia seemed to be essential for survival of neurons after ischemic axonal injury.     

Clinical restitution following cerebral ischemia in hypo-, normo- and hyperglycemic rats

Rats with different levels of blood glucose concentration were exposed to 10 min of complete brain ischemia achieved by compression of neck vessels by a pneumatic cuff. All normoglycemic rats survived the ischemic period and made the best clinical recovery. Hyperglycemic rats died within 12 h. Seizure activity was observed in all animals in this group. Three of eight hypoglycemic rats died between 3 and 16 days. The clinical recovery was less complete than in the control group. Thus, recovery from cerebral ischemia depends upon preischemic blood glucose concentration. Hyper- and hypoglycemia hamper the clinical recovery after transient cerebral ischemia.     

Increased permeability to horseradish peroxidase across cerebral vessels,evoked by electrically induced seizures in the rat

Summary Under normal conditions a slight vesicular transfer of intravenously injected horseradish peroxidase (HRP) occurs across the endothelium of cerebral vessels, especially short segments of arterioles. The vesicular transport can be notably increased by chemically induced acute hypertension.In the present investigation 4 groups of animals received HRP, and the permeability of the cerebral endothelium was studied semimacroscopically, light microscopically and electron microscopically.The rats in group 1 were given 10 electroshocks. This caused a significant rise in the blood pressure (BP). Furthermore, a noticeable extravasation of HRP was observed, especially across the endothelium in cerebral arterioles. From the basement membranes of the vessels reaction product could be followed into the extracellular spaces of the neighbouring neuropil.Group 2 comprises rats that were given 10 electroshocks preceded by transection of the cervical part of the spinal cord. The BP remained at normal level and the permeability was unaltered.The animals in group 3 received only 1 electroshock. Usually, the BP was markedly increased and this was accompanied by enhanced permeability across the vessels of the brain.Group 4 consists of control animals, injected with HRP and treated as groups 1 and 3 with the difference that electrical stimulation was not performed.A general feature was that no endothelial damage was observed and that reaction product was not found between neighbouring endothelial cells from the first luminal to the first abluminal tight junction.Based on the observations it seems reasonable to assume that the increased permeability of tracer that occurs after 10 electroshocks or only one is caused by the acute hypertension evoked by the electrical stimulation; furthermore, the transfer is concluded to be vesicular transport.     

Mitochondrial angiopathy in cerebral blood vessels of mitochondrial eneephalomyopathy

Summary We studied cerebral blood vessels of two autopsied patients with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS). All the main cerebral arteries in the proximal portion at the brain base and more distal portion at the cortical surface, as well as within the brain parenchyma were examined by electron microscopy. There was a striking increase in number of mitochondria in the smooth muscle and endothelial cells, which were most prominent in the pial arterioles and small arteries up to 250 m in diameter and less frequent and severe in the larger pial arteries and intracerebral arterioles and small arteries. These vascular changes have not hitherto been described in MELAS, or in other disorders affecting blood vessels of the brain and other organs. It is suggested that the vascular changes are caused by primary mitochondrial dysfunction in the vascular smooth muscle and endothelial cells of the brain and that they constitute the pathogenic base of the brain lesions and their unusual distribution pattern in MELAS.Supported in part by a grant from the Ministry of Health and Welfare of Japan     

老年糖尿病颅内动脉流速异常与脑血管事件发生关系的研究

目的 评价经颅多普勒超声(TCD)检测老年糖尿病患者颅内动脉血流异常的预后价值。方法 对86例60-85岁老年2型糖尿病患者进行TCD检测并前瞻性随访69个月。结果本组老年糖尿病患者血流速度异常率较高,占60.5％,且以流速异常增高为主;随访期间,6例发生非脑血管病死亡,17例发生非致死性脑梗死,1例发生非致死性脑出血,2例发生一过性脑缺血发作(TIA)。所有20例发生脑血管事件的患者进入研究时,颅内动脉血流速度异常者脑血管事件发生率显著高于颅内动脉血流速度正常者(P<0.01)。在流速异常患者中2支或2支以上血管病变者较单支血管病变者更易发生脑血管病变(P<0.01)。结论老年糖尿病患者经颅多普勒超声检测颅内动脉血流速度异常对随后脑血管事件的发生有预测价值。