光化学法建立视网膜中央动脉阻塞模型

目的 通过光化学法建立一个新的和临床病理机制相似的视网膜中央动脉阻塞（central retial artery occlusion,CRAO）模型。方法 家猫静人注入光化学药物,激光照射视网膜动脉后形成模型,经眼底荧光素造影检查证实并做病理切片。结果 成功地建立了CRAO模型,病理切片证实阻塞的血管内有血栓形成。结论 光化学法可建立和临床病理机制相似的CRAO模型,此法操作简单,为临床研究CRAO的治疗提供了较好的动物模型。     

视网膜中央动脉阻塞性缺血对黄斑区视网膜神经上皮的影响

目的:应用光学相干断层扫描(OCT)探讨视网膜中央动脉阻塞(CRAO)性缺血对黄斑区视网膜组织结构的影响。方法:用OCT对单眼CRAO 2-3d,黄斑区视网膜血液循环未完全恢复的患者 14例(14眼 )和 11例(11眼 )对侧健眼进行经中心小凹的水平和垂直扫描,分别测量及计算中心小凹、中心凹及黄斑的平均视网膜神经上皮层(RNL)厚度。结果:正常眼中心小凹、中心凹及黄斑平均RNL厚度分别为(169.91± 10.96) μm、(176.36± 11.74) μm、(256.45± 16.95) μm;CRAO黄斑区RNL明显增厚,中心小凹、中心凹及黄斑平均RNL厚度分别为(235.64± 47.02) μm、(241.84± 49.36) μm、(401.57± 54.53) μm,与正常眼比较有显著性差异(P <0.05,P <0.01)。 结论:CRAO性缺血明显地改变了黄斑区正常视网膜组织结构,使视网膜神经上皮层细胞水肿.     

Intraarterial therapy for acute ischemic stroke: investigation of prognostic factors.

BACKGROUND: Intraarterial therapy (IAT) for acute cerebral infarction has been proven to be profitable. However, the criteria for the indications, the choice of the thrombolytic agents, and the use of adjunctive agents are controversial. We retrospectively analyzed the prognostic factors of IAT. MATERIALS AND METHODS: From 1994 to 2003, 28 patients underwent IAT due to middle cerebral artery occlusion (17 women and 11 men; median age, 69 years old). We evaluated the following prognostic parameters: institution of treatment, degree of paralysis at visit, size of high-intensity area on diffusion-weighted images, dose of intraarterial urokinase administration, elapsed time from symptom onset to completion of IAT, presence of penetration of embolus by microcatheter and microguidewire, recanalization after IAT, intracranial hemorrhage (ICH) within 24 hours after IAT, and intravenous heparin administration after IAT. The outcome was evaluated at discharge and was classified into the following categories according to the modified Rankin Scale: independence (0 to 2), dependence (3 to 5), and death (6). RESULTS: Seven patients were judged to be independent, 16 patients were judged to be dependent, and five patients died. Patients with recanalization after IAT had a better outcome than those without (p < 0.05); patients with intracranial hemorrhage had a worse outcome than those without (p < 0.05); and patients with intravenous heparin administration after IAT had a better outcome in activities of daily living than those without (p < 0.05). CONCLUSION: In addition to ICH and recanalization, our results suggested that intravenous heparin administration after IAT had a favorable effect on patient outcome.     

疏血通联合马来酸桂哌齐特治疗视网膜中央动脉阻塞的 疗效观察

目的 观察疏血通注射液联合马来酸桂哌齐特注射液治疗视网膜中央动脉阻塞的疗效。方法 本研究回顾性分析天津市静海区医院2012年12月~2017年2月收治的31例（31眼）CRAO患者的病历资料,所有患者均给予疏血通注射液联合马来酸桂哌齐特注射液等药物治疗,分析治疗1疗程（14 d）后视力恢复情况。结果 31眼CRAO中治愈3眼,显效7眼,有效17眼,无效4眼,总有效率87.10%。结论 疏血通具有抗凝、溶栓、清除自由基、减轻组织缺血/再灌注损伤的作用,马来酸桂哌齐特可缓解血管痉挛、降低血管阻力、增加血流量、降低氧耗,二者联合应用治疗CRAO疗效显著。     

头颅CT在缺血性眼病诊疗中的指导作用

目的探讨头颅CT在视网膜中央动脉阻塞（CRAO）、视网膜中央静脉阻塞（CRVO）和缺血性视神经病变（ION）等缺血性眼病（IOP）中应用的临床价值。方法100例IOP患者，其中CRAO20例，CRVO40例，ION40例：男性69例．女性31例，病程为1小时～8周，平均年龄为56．07岁（标准差8．05岁）。对照组为老年性白内障患者60例（60眼）．未发生缺血性眼病，平均年龄55．96岁（标准差7-39岁）．其中男性45例，女性15例。分析了行头颅CT检查的影像结果。结果在IOP患者中应用头颅CT检出颅脑病变18例，鼻窦黏液囊肿3例，上颌窦恶性肿瘤1例。对照组中检出颅脑病变5例，未检出鼻窦病变。IOP组颅脑病变阳性率明显高于对照组（P〈0．01）。IOP中各亚组颅脑病变阳性率均明显高于对照组（P〈0．01）；CRAO亚组、CRVO亚组及ION亚组两两之间颅脑病变阳性率的差异均有统计学意义（P〈0．05）。结论在缺血性眼病患者中应用头颅CT能检出部分颅脑病变和鼻窦病变．对该类疾病的诊疗具有一定指导作用。     

Small vessel involvement in Takayasu's arteritis

ObjectivesTo describe the small retinal and systemic vessel involvement in Takayasu's arteritis.MethodsWe described 3 patients with Takayasu's arteritis and small retinal vessel occlusion seen in our department between 2004 and 2011. We performed an extensive literature review and provided a global analysis of small retinal vessel involvement in Takayasu arteritis (i.e., total number of patients analyzed = 9).ResultsSeven patients had small retinal artery occlusion, and two had venous involvement. Four cases were inaugural of the disease (44.4%). Takayasu's arteritis was extended (Type V) in the majority of patients presenting with small retinal vessel occlusion (5/9, 55.6%), and 8/9 reported cases (88.9%) presented with involvement of the supra-aortic branches. Immunosuppressive regimen allowed an improvement in 5/9 patients and stabilization in 1/9, but the situation worsened in 3/9 patients. The visual outcome was severe, and 3/9 patients (33.3%) experienced irreversible blindness.ConclusionOcclusion of small retinal vessels is a rare and severe microcirculatory complication in Takayasu's arteritis, as well as necrotizing cutaneous vasculitis or myocarditis. Small retinal vessel involvement can be inaugural of the disease and seriously impact the visual prognosis in TA patients.     

Retinal protective effects of topically administered agmatine on ischemic ocular injury caused by transient occlusion of the ophthalmic artery

Agmatine, an endogenous polyamine and putative neuromodulator, is known to have neuroprotective effects on various neurons in the central nervous system. We determined whether or not topically administered agmatine could reduce ischemic retinal injury. Transient ocular ischemia was achieved by intraluminal occlusion of the middle cerebral artery of ddY mice (30-35 g) for 2 h, which is known to also induce occlusion of the ophthalmic artery. In the agmatine group (N = 6), a 1.0 mM agmatine-containing ophthalmic solution was administered four times daily for 2 weeks before occlusion. In the control group (N = 6), a 0.1% hyaluronic acid ophthalmic solution was instilled at the same times. At 22 h after reperfusion, the eyeballs were enucleated and the retinal sections were stained by terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL). Transient ocular ischemia induced apoptosis of retinal cells in the entire retinal layer, and topically administered agmatine can significantly reduce this ischemic retinal injury. The proportion of apoptotic cells was definitely decreased (P < 0.001; Kruskal-Wallis test). Overall, we determined that topical agmatine application effectively decreases retinal damage in an in vivo ocular ischemic injury model. This implies that agmatine is a good candidate as a direct neuroprotective agent for eyes with ocular ischemic diseases.     

Cerebral Angiographic Findings of Cosmetic Facial Filler-related Ophthalmic and Retinal Artery Occlusion

Cosmetic facial filler-related ophthalmic artery occlusion is rare but is a devastating complication, while the exact pathophysiology is still elusive. Cerebral angiography provides more detailed information on blood flow of ophthalmic artery as well as surrounding orbital area which cannot be covered by fundus fluorescein angiography. This study aimed to evaluate cerebral angiographic features of cosmetic facial filler-related ophthalmic artery occlusion patients. We retrospectively reviewed cerebral angiography of 7 patients (4 hyaluronic acid [HA] and 3 autologous fat-injected cases) showing ophthalmic artery and its branches occlusion after cosmetic facial filler injections, and underwent intra-arterial thrombolysis. On selective ophthalmic artery angiograms, all fat-injected patients showed a large filling defect on the proximal ophthalmic artery, whereas the HA-injected patients showed occlusion of the distal branches of the ophthalmic artery. Three HA-injected patients revealed diminished distal runoff of the internal maxillary and facial arteries, which clinically corresponded with skin necrosis. However, all fat-injected patients and one HA-injected patient who were immediately treated with subcutaneous hyaluronidase injection showed preserved distal runoff of the internal maxillary and facial arteries and mild skin problems. The size difference between injected materials seems to be associated with different angiographic findings. Autologous fat is more prone to obstruct proximal part of ophthalmic artery, whereas HA obstructs distal branches. In addition, hydrophilic and volume-expansion property of HA might exacerbate blood flow on injected area, which is also related to skin necrosis. Intra-arterial thrombolysis has a limited role in reconstituting blood flow or regaining vision in cosmetic facial filler-associated ophthalmic artery occlusions.     

Neurodegeneration and cellular stress in the retina and optic nerve in rat cerebral ischemia and hypoperfusion models

Experimental cerebral ischemia induces a stress response in neuronal and non-neuronal cells. In the present study we aimed to evaluate detailed cellular stress responses and neurodegenerative changes in the retinas in rat focal cerebral ischemia and hypoperfusion models involving invasive vascular manipulations. Independent groups of adult male Wistar rats were subjected to i) transient middle cerebral artery occlusion (tMCAO), ii) permanent middle cerebral artery occlusion (pMCAO), iii) cortical photothrombosis of the sensorimotor cortex using Rose Bengal dye or iv) bilateral common carotid artery occlusion (BCCAO). Rats were killed, and their eyes with the optic nerves enucleated and processed for histology, immunohistochemistry for neuronal nuclei (NeuN), glial fibrillary acidic protein (GFAP), hypoxia-inducible factor 1alpha (HIF-1alpha), c-fos, alphaB-crystallin, heat shock protein (HSP) 27, HSP60 and HSP70, and detection of DNA defragmentation. The total number of the retinal ganglion cell layer (RGCL) neurons and GFAP-immunoreactive astrocytes located in the nerve fiber layer were estimated using unbiased stereological counting. Our findings indicate that although permanent and transient MCAO does not cause detectable morphological alterations in the retina or optic nerve, it evokes ischemic stress as revealed by HIF-1alpha and HSPs expression in the RGCL neurons and reactive gliosis in the Müller cells. Severe neurodegenerative changes in the retina and optic nerve of the BCCAO rats are accompanied by a significant increase in immunoreactivities for the c-fos, HSP27 and HSP70 as compared with the sham-operated animals. The retinas from the ipsilateral side of the Rose Bengal model showed a significant decrease in the total number of NeuN-positive neurons in the RGCL as compared with the contralateral ones. However, these eyes did not differ between each other in the HSPs and HIF-1alpha expression or in the GFAP-immunoreactivity of the Müller cells. In conclusion, our data suggest differential expression of various HSPs in the retina and possibly their distinct roles in the cerebral ischemia-mediated stress response and neurodegeneration.     

OCCLUSION OF THE BASILAR ARTERY

The present report dealt with thirteen autopsied cases of basilar artery occlusion. The age of the patients ranged from fifty one to seventy six years with a mean age of fifty six years, and there were eleven males and two females. Basilar artery occlusion was found in one in every 160 autopsies. The average length of the clinical course of the disease was five months. Many patients had a history of hypertension, diabetes mellitus, and cerebrovascular attacks. The neurological signs and symptoms of basilar artery occlusion extremely varied and were complicated. In our series, occular bobbing, palatal myoclonus, Foville syndrome, and Millard-Gubler syndrome are significant. Arteriosclerotic thrombosis is the most important etiologic factor. The site of occlusion was most frequently encountered in the lower third of the basilar artery. Areas of softening were prominent in the midbrain and the pons. In the cerebellum, softenings were present particularly in the areas supplied by the superior cerebellar artery. Infarcts in the thalamus and the temporo-occipital lobes supplied by the posterior cerebral artery were observed very frequently. The distribution of softening was related to the site of occlusion of the basilar artery and the collateral circulation through the Willis ring.     

开颅减压治疗猫急性脑梗塞的实验研究

目的：探索开颅减压术对大面积脑梗塞的治疗效果及实施手术的时机。方法：家猫５０只,均行经左侧眼眶阻断左大脑中动脉造成局灶性脑梗塞。４０只动物再行左侧开颅减压术,另外１０只动物不行手术,手术组动物又分为４组,分别于血管阻断后６ｈ、１２ｈ、２４ｈ及３６ｈ行脑梗塞侧开颅减压术。４８ｈ后观察脑梗塞范围的大小。结果：手术组梗塞范围小于对照组（Ｐ〈０．０１）。手术组动物无死亡,而对照组死亡率为２０％（Ｐ〈０．０     

The use of antithrombotic drugs in artery disease

Evaluating the use of antithrombotic drugs in artery disease has been a long and difficult process, which is far from complete. The aims of treatment have ranged from the primary prevention of myocardial infarction or stroke, through the restoration of blood flow to ischaemic organs in order to salvage threatened tissue, to the prevention of recurrent vascular occlusion. Drugs studied in depth by clinical trial include the oral anticoagulants, antiplatelet drugs (especially aspirin), and thrombolytic agents. Their results are considered under the headings of coronary artery disease, cerebral ischaemia, and peripheral vascular disease. Aspirin, with or without dipyridamole, prevents progression of unstable angina to myocardial infarction or death, probably reduces long-term mortality after myocardial infarction, and prevents aortocoronary bypass graft occlusion. It decreases the risks of stroke or death in patients with transient cerebral ischaemia, diminishes cardiovascular morbidity after a thrombotic stroke, and may improve the outcome after some kinds of surgery for peripheral vascular disease. The benefits of oral anticoagulant treatment to prevent artery occlusion remain poorly defined. Oral anticoagulants prevent systemic embolism in many groups of high-risk patients, and probably reduce the risk of recurrence after embolism has occurred. Whether their long-term use to prevent reinfarction in patients with a previous myocardial infarct can be justified remains uncertain. They are of little or no proven value in patients with transient cerebral ischaemia or thrombotic stroke. On the other hand, there is increasing support for early thrombolytic treatment after myocardial infarction, especially since two multicentre trials have now shown reduced mortality in patients treated with intracoronary streptokinase within 4-6 hours of infarction and a further large multicentre study also demonstrated reduced mortality in patients treated with early intravenous streptokinase. In addition, the local infusion of streptokinase leads to recanalization in a high proportion of patients with a recent peripheral artery occlusion who are poor candidates for surgery.     

OCT测量分析视网膜中央静脉阻塞黄斑囊样水肿时 黄斑区视网膜厚度变化研究

目的 研究频域光学相干断层扫描仪Cirrus HD-OCT对视网膜中央静脉阻塞黄斑囊样水肿（CRVO-CME）时黄斑区视网膜厚度的变化情况。方法 纳入我院2017年11月~2019年2月收治的45例（60眼）CRVO-CME患者作为研究组,另选取45例（60眼）来我院进行体检的健康志愿者作为对照组。所有患者均行HD-OCT检查,根据早期糖尿病视网膜病变治疗研究（ETDRS）视力表对黄斑区进行分区,观察两组眼黄斑区视网膜厚度情况,分析黄斑区视网膜厚度与最佳矫正视力（BCVA）的关系。结果 研究组F、IT、II、IN、IS、OT、OI、ON以及OS黄斑区9个分区的视网膜厚度均大于对照组,差异有统计学意义（P＜0.05）。IT、II、IN、IS黄斑区4个内分区厚度组间比较,差异无统计学意义（P＞0.05）;OT、OI、ON以及OS黄斑区4个外分区厚度组组间比较,差异无统计学意义（P＞0.05）。CRVO-CME患者FT以及Fmax与BCVA存在负相关性（P＜0.05）。结论 CRVO-CME患者视网膜各分区均比正常人视网膜更厚,对CRVO-CME患者进行HD-OCT测量对视网膜厚度的判断较准确,为临床诊治CRVO-CME提供了有力依据。     

脑淋巴引流阻滞对缺血大鼠脑组织谷氨酸、Ca~(2+)含量和NMDAR1表达的影响

目的:探讨脑梗塞后给予大鼠颈淋巴管阻塞对缺血侧大脑皮质脑含水量、Ca2+和谷氨酸含量、脑梗塞体积以及N-甲基-D-天冬氨酸受体1(NMDAR1)表达水平等的影响。方法:用线栓法复制大鼠大脑中动脉阻塞(MCAO)模型,以及行大鼠大脑中动脉阻塞15min后摘除双侧颌下腺的颈浅和颈深淋巴结,制成脑梗塞后颈淋巴管阻塞(MCAO+CLB)模型,检测缺血侧大脑皮质脑含水量、Ca2+和谷氨酸含量、脑梗塞体积以及NMDAR1mRNA表达水平和免疫活性的变化。结果:在不同的时间点,MCAO+CLB组大鼠上述各指标要比MCAO组明显升高(P0.05)。结论:颈淋巴管阻塞通过提高脑含水量、Ca2+和谷氨酸含量、脑梗塞体积以及上调NMDAR1表达水平而加重脑梗塞。     

Traumatic carotid-cavernous fistula

Carotid-cavernous fistula is uncommon consequence of craniocerebral trauma. Earlier recognition of the patients with carotid-cavernous fistula and shorter time of delay in treatment could save patients from complications and vision loss. A 27-year-old man presented with severe craniocerebral injury after an car accident. He required emergent craniotomy for an open depressed cranial fractures, haemostasis and epidural hematoma. Three months later, the patient began to exhibit progressive chemosis and proptosis of left eye. Computed tomography and cerebral angiography revealed findings consistent with a carotid-cavernous fistula. Angiography revealed a fistula between carotid artery and the cavernous sinus. The patient was treated by transarterial embolization resulting in immediate and permanent occlusion of the fistula and improved visual acuity after six months follow-up. Posttraumatic carotid-cavernous fistula may be treated successfully with the use of transarterial coil embolization.     

上颌动脉显露技术在脑血管搭桥术中的应用

目的 观察上颌动脉翼状肌段的解剖特点,探讨上颌动脉显露技术在脑血管搭桥术中临床应用的可行性。方法 选取新鲜成人完整尸头标本12具,其中女3具、男9具,年龄50~80岁（平均64岁）。尸头标本经乳胶灌注后,采用翼点入路,切除颧弓,显露上颌动脉翼状肌段。观察记录两侧上颌动脉走行的特点、与翼外肌的位置关系,测量上颌动脉翼状肌段到颞下嵴的间距。 回顾性分析郑州大学第一附属医院神经外科2020年10月—2021年4月收治的2例脑血管搭桥患者的临床资料。男女各1例,年龄分别为62、38岁。1例患者诊断为基底动脉冗扩合并动脉瘤,一期行优势侧椎动脉介入闭塞术,二期行上颌动脉-桡动脉-小脑上动脉搭桥术;另1例患者诊断为脑梗死、前床突脑膜瘤、左侧颈内动脉末端重度狭窄,行上颌动脉-桡动脉-大脑中动脉搭桥术+脑膜瘤切除术。2例患者均经翼点入路、切除颧弓显露上颌动脉,完成血管搭桥手术。观察术后桥血管通畅情况,以及患者术后神经功能状态。结果 （1）尸头标本12具均成功暴露了两侧上颌动脉的翼状肌段,未发生颅神经损伤。上颌动脉经翼外肌外侧走行17侧,其翼状肌段到颞下嵴的长度为8.2~18.4（13.2±4.2）mm ;上颌动脉经翼外肌内侧走行7侧,其翼腭窝段均较短,无法上提至颞下嵴,故未记录其可游离长度。（2）2例患者均成功显露上颌动脉的翼状肌段,顺利完成脑血管搭桥手术。病例1患者,术后神经功能状态稳定;术后3个月复查头颅CT血管成像（CTA）,见桥血管通畅、基底动脉动脉瘤大小无明显变化。病例2术后左上肢肌力由术前2级下降至0级;术后3个月电话随访无再发脑缺血症状,患肢肌力恢复到4级,CTA显示桥血管闭塞。结论 翼点联合颧弓切除术可安全有效地显露上颌动脉翼状肌段。翼外肌外侧走行的上颌动脉相对长且表浅,是实施脑血管搭桥术的一种较好的供体血管。     

Neuroprotective effect of tyrosol on transient focal cerebral ischemia in rats

Tyrosol (2-(4-hydroxyphenyl)ethanol) is a well-known phenolic compound with antioxidant properties that is present in wine, olive oil, and other plant-derived products. The purpose of this study was to determine the neuroprotective effect of tyrosol in a stroke animal model. By using the transient middle cerebral artery occlusion rat model (2 h of occlusion, 22 h of reperfusion), we investigated the effects of tyrosol on infarct volume and sensory motor function deficit by performing 2,3,5-triphenyltetrazolium chloride staining and behavior tests after ischemia. Tyrosol showed a dose-dependent neuroprotective effect that peaked at 64.9% in rats treated with 30 mg/kg of tyrosol. In rotarod, beam balance, and foot fault tests, tyrosol exhibited protective effects against the sensory motor dysfunction. In conclusion, our results suggest that tyrosol is an appropriate candidate to be used in stroke therapy.     

Interleukin-1 receptor antagonist decreases the number of necrotic neurons in rats with middle cerebral artery occlusion.

Marked increases in the brain expression of interleukin (IL)-1 have been reported in rats after permanent occlusion of a large cerebral artery. Interactions between endothelial cells and leukocytes have been implicated in the pathogenesis of several types of ischemic injury to the myocardium and other organs. In this study we asked whether inhibiting the effects of IL-1 would affect the outcome of an experimental brain infarct. Adult male Wistar rats (n = 13) with permanent occlusion of the middle cerebral artery were given IL-1 receptor antagonist. A second group (n = 13) with the same type of brain injury was given a placebo. A third group, subjected to a sham operation, was given either IL-1 receptor antagonist (n = 2) or a placebo (n = 2). Experiments were terminated after either 24 hours or 7 days. Compared with the control group, animals treated with IL-1 receptor antagonist improved their neurological score (P < 0.05), experienced less pronounced changes in body weight (P < 0.05), and had fewer necrotic neurons (P < 0.001) and fewer leukocytes in the ischemic hemisphere (P < 0.001) as well as a smaller area of pallor (P < 0.05) in the ischemis hemisphere. The results suggest that inhibiting the proinflammatory effects of IL-1 with a receptor antagonist is an effective way of influencing the leukocyte responses elicited by an arterial occlusion. Such leukocyte inhibition seemingly attenuates the number of necrotic neurons resulting from the occlusion of a large brain artery.     

Integrin alphavbeta3 is expressed in selected microvessels after focal cerebral ischemia.

The endothelial and smooth muscle integrin alphaVbeta3, a receptor for vitronectin and fibrinogen, participates in angiogenesis associated with wound healing and tumorigenicity. The microvascular expression of alphavbeta3 and fibrin during experimental middle cerebral artery occlusion and reperfusion in a nonhuman primate model was examined by computer-assisted video imaging microscopy. No microvascular expression of alphavbeta3 was seen in the control subjects (n = 3) or the non-ischemic basal ganglia of subjects undergoing 2-hour MCA:O (middle cerebral artery occlusion) or 3-hour occlusion with 1-hour (n = 3), 4-hour (n = 3), and 24-hour (n = 3) reperfusion. In the ischemic territory, alphavbeta3 appeared initially at 2 hours of middle cerebral artery occlusion. Up-regulation of alphavbeta3 was confined to the media of 30.0- to 50.0-micron-diameter arterioles in the ischemic core and correlated significantly with fibrin deposition in those vessels (P < 0.0005). Integrin alphavbeta3 and its ligand fibrinogen appear in a subpopulation of microvessels after focal cerebral ischemia.     

Peroxisome proliferator-activated receptor-gamma ligands reduce inflammation and infarction size in transient focal ischemia

Newly developed insulin-sensitizing agents, which target the nuclear receptor peroxisome proliferator-activated receptor-gamma have recently been appreciated to exhibit potent anti-inflammatory actions. Since stroke is associated with an intense inflammatory response, we reasoned that these agents may ameliorate injury from stroke. We report that administration of troglitazone or pioglitazone 24 h before and at the time of cerebral infarction dramatically reduced infarction volume and improved neurological function following middle cerebral artery occlusion in rats. Furthermore, we find that delayed therapy also significantly reduced infarct volume. The brains of the drug-treated animals displayed reduced inflammation as evidenced by decreased immunoreactivity for microglial/macrophage markers and reduced protein and mRNA for interleukin-1beta, cyclooxygenase-2 and inducible nitric oxide synthase. We argue that the beneficial effects of these drugs are likely due to reduced expression of these inflammatory mediators, which are known to exacerbate ischemic injury following stroke. These results are of particular relevance to diabetic patients chronically treated with these agents who may benefit from the neuroprotective actions of these drugs.