17beta-estradiol pretreatment prevents the global ischemic injury-induced decrease of Akt activation and bad phosphorylation in gerbils

Estradiol acts as a neuroprotective factor against ischemic brain injury. This study investigated whether estradiol modulates neuroprotective mechanism through the activation of Akt and its downstream target such as Bad in global ischemic injury. Adult female gerbils were ovariectomized and treated with estradiol prior to ischemic injury. Transient cerebral ischemia was accomplished by bilateral clipping of the common carotid artery for 5 min. Brains were collected on 1, 3, 5 day after injury. In hippocampal CA1 region of non-treated gerbils, most of neuronal cells exhibited pyknotic nuclei and showed the positive reaction of TUNEL staining on 5 day after injury. However, estradiol significantly reduced the neuronal cell death. Potential activation was measured by phosphorylation of Akt at Ser473 and Bad at Ser136 using western blot analysis. The levels of pAkt and pBad were significantly decreased in non-treated gerbils on 1-5 day after injury. However, estradiol prevents the global ischemic injury-induced decrease of pAkt and pBad. Our findings suggest that estradiol prevents cell death due to global ischemic injury and that Akt activation and Bad phosphorylation by estradiol mediated these protective effects.     

Effects of dizocilpine pretreatment on parvalbumin immunoreactivity and Fos expression after cerebral ischemia in the hippocampus of the Mongolian gerbil

The mechanisms of ischemic neuronal death have been focused on glutamate receptor activation and subsequent elevation of intracellular Ca2+ concentration. The purpose of this study was to evaluate the effects of dizocilpine, an NMDA receptor antagonist, pretreatment on Fos expression and parvalbumin (PV, calcium binding protein) immunoreactivity in the hippocampus of the mongolian gerbil after global ischemic insults. The number of PV-immunoreactive (PV-ir) neurons in CA1 were significantly decreased from 1 day after cerebral ischemia, while dizocilpine pretreatment completely suppressed the loss of PV-ir neurons in CA1. Dizocilpine pretreatment also protected the structural loss of microtubule-associated protein 2 immunoreactivity in CA1 after ischemic insults. In addition, dizocilpine pretreatment increased Fos expression in both hippocampal CA3 and CA4 after 3 hr ischemic reperfusion as compared to that of the saline pretreated group. Subsequently, the Fos-defined cellular activity of PV-ir neurons was slightly increased by dizocilpine pretreatment in the hippocampal area. This study demonstrated that NMDA receptor mediated calcium influx was associated with the loss of PV-ir neurons in CA1 hippocampal region, and that dizocilpine pretreatment increased Fos expression and the neuronal activity of PV-ir neurons in the non-vulnerable region of hippocampus after cerebral ischemia. Based on this data, we conclude that the protective effect of dizocilpine may be induced by the regulation of calcium overload, or by the upregulation of a neuroregenerative initiator such as Fos protein.     

Activation of Akt/protein kinase B mediates the protective effects of mechanical stretching against myocardial ischemia-reperfusion injury

Akt/protein kinase B is a well-known cell survival factor and activated by many stimuli including mechanical stretching. Therefore, we evaluated the cardioprotective effect of a brief mechanical stretching of rat hearts and determined whether activation of Akt through phosphatidylinositol 3-kinase (PI3K) is involved in stretch-induced cardioprotection (SIC). Stretch preconditioning reduced infarct size and improved post-ischemic cardiac function compared to the control group. Phosphorylation of Akt and its downstream substrate, GSK-3β, was increased by mechanical stretching and completely blocked by wortmannin, a PI3K inhibitor. Treatment with lithium or SB216763 (GSK-3β inhibitors) before ischemia induction mimicked the protective effects of SIC on rat heart. Gadolinium (Gd³⁺), a blocker of stretch-activated ion channels (SACs), inhibited the stretch-induced phosphorylation of Akt and GSK-3β. Furthermore, SIC was abrogated by wortmannin and Gd³⁺. In vivo stretching induced by an aorto-caval shunt increased Akt phosphorylation and reduced myocardial infarction; these effects were diminished by wortmannin and Gd³⁺ pretreatment. Our results showed that mechanical stretching can provide cardioprotection against ischemia-reperfusion injury. Additionally, the activation of Akt, which might be regulated by SACs and the PI3K pathway, plays an important role in SIC.     

Cerebral Computed Tomography Scan Demonstrating Ischemic Stroke in a Filly After Intravenous Antibiotic Administration

Performing a brain computerized tomography scan (CT scan) on a foal requires specific equipment and anesthesia for large animals. However, the information obtained may demonstrate lesions responsible for the neurological deficits. Especially, CT scan findings may help to understand a mechanism of cerebral ischemia. Indeed, categories of cerebral ischemia are divided in three types: territorial infarctions (downstream of the territory of an artery), watershed infarctions (slow-flow at the junction of two arterial territories), and lacunar infarctions (small-vessel occlusions). Hypersensitivity reactions and type I anaphylactic IgE antibody reactions are severe potential adverse effects of sulfonamide administration, which occur in about three percent of cases. In horses, anaphylaxis is often clinically expressed as hypotension and collapse. Cardiovascular collapse may lead to multiorgan slow-flow leading to infarction with multiorgan failure and death. We report the case of a filly that suffered a presumed watershed cerebral infarction after antibiotic injection, indicated on a brain CT scan. This was attributed to a cerebral slow-flow during cardiovascular collapse, at the posterior junction of the right cerebral arteries. No abnormalities were initially identified on the CT scan; however, a review of the imaging by a radiologist specialized in cerebrovascular diseases detected a limited right occipital cortico-subcortical lesion in the visual cortex, interpreted as an ischemic scar in the watershed area related to hemodynamic infarction. This case highlights that detection of brain lesions by CT scan might require specialized knowledge and careful reading for interpretation particularly in the case of limited lesions.     

N-乙酰L-半胱氨酸预处理对大鼠局灶性脑缺血再灌注损伤的保护机制

制备大鼠局灶性脑缺血再灌注实验模型,通过N-乙酰L-半胱氨酸（NAC）预处理对脑缺血再灌注损伤的保护作用,探索脑梗死病理过程及药物治疗途径。NAC预处理21d,利用栓线法建立大鼠大脑中动脉栓塞模型,造模后24h进行神经症状评分,TTC染色,检测血浆MDA、GSH含量,观察大脑皮质细胞凋亡情况及凋亡相关蛋白Bcl-2、Bax的表达。结果显示,通过神经症状评分和TTC染色判定大鼠局灶性脑缺血实验模型建立成功。与对照组相比,NAC预处理组（100mg·kg^-1）大鼠血浆中MDA含量显著降低（P〈0.05）,GSH含量显著升高（P〈0.05）;NAC模型组细胞凋亡率及Bax/Bcl-2比值明显低于对照组。结果表明,NAC通过改善氧化应激状态,调控凋亡蛋白Bcl-2、Bax表达,从而对大鼠脑缺血再灌注损伤具有一定的保护作用。     

Activation of Akt/protein kinase B and extracellular signal-regulated kinase in rats with acute experimental testicular torsion

The Akt/protein kinase B (PKB) and extracellular signal-regulated kinase (ERK) pathways are involved in cell survival. This study examined the temporal profiles and localization of Akt/PKB and ERK1/2 activation in rat testis after ischemia/reperfusion (I/R). Testicular tissue was collected from normal control rats and rats exposed to reperfusion for 6, 24, and 48 hr after ischemic injury; the tissues were analyzed via Western blotting and immunohistochemistry. Western blot analysis showed that the levels of phosphorylated Akt/PKB (pAkt/PKB) and ERK1/2 (pERK1/2) increased significantly during the first 6-24 hr of reperfusion after ischemia. However, both of these activated proteins were decreased slightly at 48 hr after reperfusion. Immunohistochemically, low levels of pAkt/PKB expression were observed in Sertoli cells from the normal control. After I/R, pAkt/PKB expression increased mainly in the adluminal portion of the Sertoli cells, as well as in spermatogenic cells. In addition, pERK1/2 expression was observed in Sertoli and Leydig cells in the normal control. After I/R, pERK1/2 expression increased in some surviving spermatogenic cells (mainly spermatocytes), as well as in the adluminal portion of Sertoli cells. These results suggest that both Akt/PKB and ERK1/2 are involved in the survival of testicular cells during the early phase of testicular I/R. These pathways may represent important targets for increasing cell survival in testicular injury, including testicular torsion.     

大鼠短暂性全脑缺血再灌注后海马神经元动态变化

采用股动脉放血并双侧颈总动脉夹闭制作大鼠全脑缺血再灌注模型,分别于术后6h、1d、3d、5d处死动物,取脑,制作石蜡切片和冰冻切片,通过HE染色、TUNEL检测及Caspase-3活性测定,对大鼠海马各区锥体细胞形态进行动态观察。结果表明:在短暂性全脑缺血中,海马锥体细胞存在着凋亡和坏死两种死亡形式,细胞凋亡在海马各区中的分布是一动态过程,各区对缺血易损伤性的顺序是:CA1及门区>CA2>CA3>齿状回;脑缺血再灌注不同时间,海马锥体细胞中DNA断裂及Caspase-3的表达与细胞凋亡呈现相似的变化趋势,且DNA的断裂早于Caspase-3的表达;与青年组相比,老年组海马神经元出现凋亡时间早且损伤严重。试验证明:在脑缺血再灌注损伤中,海马各区存在着缺血耐受性差异;细胞凋亡是神经元死亡的一种重要形式。     

Nicotinamide prevents the down-regulation of MEK/ERK/p90RSK signaling cascade in brain ischemic injury

Nicotinamide attenuates neuronal cell death related to focal cerebral ischemic injury. This study investigated whether nicotinamide exerts a neuroprotective effect through the activation of Raf- mitogen-activated protein kinase kinase (MEK)-ERK and its downstream targets, including p90 ribosomal S6 kinase (p90RSK) and Bad. Adult male Sprague-Dawley rats were treated with nicotinamide (500 mg/kg) or vehicle 2 hr after the onset of middle cerebral artery occlusion (MCAO). Brains were collected 24 hr after MCAO. In the present study, nicotinamide significantly reduces the volume of infarct regions and decreases the number of positive cells by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining in the cerebral cortex. Nicotinamide prevents injury-induced decrease in Raf-1, MEK1/2, and ERK1/2 phosphorylation. As part of the downstream cascade, nicotinamide inhibits the injury-induced decrease in p90RSK and Bad phosphorylation. Moreover, nicotinamide prevents the injury-induced increase in cleaved caspase-3 levels. These findings suggest that nicotinamide protects neuronal cells against cerebral ischemic injury and that MEK-ERK-p90RSK cascade activation by nicotinamide contributes to these neuroprotective effects.     

大鼠局灶性脑缺血后适应动物模型的建立与评估

试验旨在从方法学的角度比较3种有脑保护效应的大鼠局灶性脑缺血后适应(ischemic postconditioning,IPOC)模型的成功率、稳定性及其保护作用,以期为IPOC机制的研究建立良好的动物模型。将SD大鼠随机分为模型1组(开颅电凝大脑中动脉+双侧颈总动脉夹闭30 min)、模型2组(线栓法大脑中动脉阻塞60 min)、模型3组(线栓法大脑中动脉阻塞100 min),3个组再按假手术组、缺血再灌组及缺血后处理组各分为3个亚组,计9组,每亚组10只,分别在灌注2和24 h后进行神经功能缺损评分;在灌注24 h后取大脑进行2,3,5-3氯4氮唑(TTC)染色确定脑梗死体积百分比,并进行统计学分析;比较3种模型后处理后大鼠脑梗死体积的变异系数。结果显示,3种大鼠模型均呈现了不同程度的神经功能缺损体征,且IPOC均不同程度的降低脑梗死体积,改善了神经功能缺损评分,其中电凝法缺血30 min时建模的成功率最高。电凝法缺血30 min后适应模型脑梗死体积下降42.9%;线栓法缺血60 min后适应模型脑梗死体积下降15.9%;线栓法缺血100 min后适应模型脑梗死体积下降33.4%。电凝法缺血30 min后适应模型脑梗死体积的变异系数最低。开颅电凝法缺血30 min再灌30 s/缺血10 s,反复3次的IPOC模型不仅保护作用强,而且模型成功率高、稳定性好,可作为研究IPOC机制较好的动物模型。     

Dysregulated expression of the key effectors of the mammalian target of rapamycin signalling pathway in cutaneous papillomas of dogs

Cutaneous papillomas (CP) are one of the most common skin neoplasms in dogs. Different murine models have shown that persistent activation of the phosphatidylinositol 3‐kinase/Akt/mammalian target of rapamycin (PI3K/Akt/mTOR) pathway has a central role in the development and progression of CP. The purpose of this study were to evaluate the immunohistochemical expression pattern of two key molecules involved in the PI3K/Akt/mTOR signalling pathway, pAkt^Ser473, and pS6^Ser235/236, on 36 canine specimens of CP using a tissue microarray. The results show that the PI3K/Akt/mTOR signalling pathway is persistently activated in CP of dogs, pointing to this pathway as a potential therapeutic target.     

Comparison of Surgical Methods of Transient Middle Cerebral Artery Occlusion between Rats and Mice

Rodent models of focal cerebral ischemia that do not require craniotomy have been developed by intraluminal suture middle cerebral artery occlusion (MCAo). Mouse MCAo models have been widely used and extended to genetic studies of cell death or recovery mechanisms. Therefore, we compared surgery-related parameters and techniques between such rats and mice. In rodent MCAo models, has to be considered body temperature during the operative period, as well as the need for the use of a standardized tip in terms of the outer diameter of probes. Induction of focal cerebral ischemia was measured by neurological dysfunction parameters. Our methods could induce stable moderate-severity ischemic brain injury models and histological alteration at 24 hr after MCAo surgery. Moreover approximately 80% (rats) and 85% (mice) survival ratios were shown indicating with model engineering success. Finally, we described and compared major parameters between rats and mice, including probe size, thread insert length, operation and occlusion periods, and differences in the procedures.     

基于网络药理学研究丹参-川芎抗脑缺血再灌注损伤作用机制及试验验证

【目的】 通过网络药理学研究丹参-川芎药对治疗缺血性脑卒中的有效性成分及相应基因靶标，探讨其作用机制。【方法】 应用中药系统药理学计数平台（TCMSP）、GeneCards、OMIM数据库，筛选出丹参-川芎药对治疗缺血性脑卒中的潜在靶点并进行GO功能和KEGG通路富集分析。分别设置假手术组、模型组、丹参-川芎低、中、高剂量组，采用预防和治疗给药方式对线栓制备的脑缺血再灌注模型大鼠进行干预，采用Zea-longa评分法对脑缺血再灌注24 h模型大鼠进行神经功能评分，苏木素-伊红（HE）染色法观察脑组织病理学变化进行初步验证。【结果】 本研究共筛选到丹参-川芎药对主要有效活性成分共72个，其中川芎7个，丹参65个，缺血性脑卒中的靶点基因1 972个，有效活性成分与缺血性脑卒中共同作用靶标94个，包括IL6、IL10、TNF、MMP9、VEGFA、CASP3等；GO功能和KEGG通路富集结果提示，丹参-川芎药对治疗缺血性脑卒中与PI3K-Akt、cGMP-PKG、VEGF等多个信号通路有关。动物试验结果表明，丹参-川芎可减轻脑组织病理改变，减轻神经功能缺损，改善脑缺血再灌注损伤。【结论】 丹参-川芎药对可能是通过PI3K/Akt信号通路改善脑缺血再灌注损伤，发挥抗细胞凋亡的作用。     

Ischemic Postconditioning Does Not AttenuateIschemia–Reperfusion Injury of Rabbit Small Intestine

Objective— To determine whether ischemic postconditioning can attenuate intestinal ischemia–reperfusion (I–R) injury and has a beneficial effect on tissue blood flow during reperfusion. Study Design— In vivo experimental study. Animals— New Zealand White rabbits (n=6). Methods— Rabbits were anesthetized with pentobarbital, to avoid the preconditioning effects of volatile anesthetics, and ventilated with room air. Rectal temperature, hemodynamics, and normocapnia were maintained. After celiotomy, 3 jejunal segments were isolated in each rabbit for the following groups: (1) control, (2) I–R, and (3) I–R with postconditioning. I–R was induced by a 45‐minute occlusion of the segment jejunal artery followed by 2‐hour reperfusion. The postconditioning segment had 4 cycles of 30‐second reperfusion and 30‐second reocclusion during the initial 4 minutes of reperfusion. Stable isotope‐labeled microspheres were used to measure intestinal blood flow at baseline, end occlusion, and end reperfusion. At the end of reperfusion, intestine segments were harvested and the rabbits euthanatized. A semiquantitative histopathologic evaluation (0–5) was conducted by a single, blinded observer. Wet‐to‐dry weight ratios were calculated to assess intestinal edema. Results— There was no significant difference in grade of necrosis, tissue wet‐to‐dry weight ratios, or blood flow at any time point between ischemic and postconditioning groups. Conclusions— Ischemic postconditioning was ineffective in this model of intestinal I–R. Clinical Relevance— Further experimental studies will need to be performed before clinical application of postconditioning for intestinal ischemia.     

长爪沙鼠脑底动脉Willis环变异缺失类型与脑缺血模型症状相关性分析

通过观察398只长爪沙鼠右侧颈总动脉结扎脑缺血模型,比较研究其脑底动脉Willis环缺失类型和半脑缺血模型症状的相关性。结果显示,长爪沙鼠脑底动脉Willis环的前、后交通支各有4种类型。在Willis环后交通支缺失的前提下,当行单侧颈总动脉结扎时,一侧脑缺血症状显著程度与前交通支变异类型有关,其中前交通支完整型与其余3种类型的症状有显著性差异(P=0.000)。结果表明,经颈总动脉结扎后半脑缺血模型高发生率和典型症状的基础是Willis环后交通支缺失并伴有前交缺失或细小为前提的。     

编码日本血吸虫Akt蛋白的cDNA克隆及原核表达

本研究利用生物信息学分析日本血吸虫编码Akt蛋白的cDNA并对编码该蛋白的cDNA进行了克隆和原核表达。生物信息学分析表明日本血吸虫存在两个Akt蛋白。利用PCR将其中一个Akt蛋白催化功能域的编码cDNA进行了克隆,并利用原核表达系统对此蛋白片段进行诱导表达并进行了重组蛋白的纯化,将重组蛋白免疫新西兰大白兔制备了多克隆抗体。Western blot分析表明,该抗体能被日本血吸虫Akt重组蛋白特异性识别。本研究为进一步研究该蛋白的功能奠定了基础。     

金属硫蛋白对海马CA1区锥体细胞凋亡的抑制作用

采用股动脉放血并双侧颈总动脉夹闭制作全脑缺血再灌注模型 ,于术后 1d处死动物 ,取脑 ,制作石腊切片 ,通过 HE染色、Tunel检测 ,对海马 CA1 区锥体细胞形态进行了观察。结果表明 :在短暂性全脑缺血中 ,海马锥体细胞存在着凋亡和坏死 2种死亡形式 ;与对照组相比 ,缺血再灌注后 1d,海马 CA1 区损伤较重 ,出现了较多的凋亡细胞 ,而MT- 1可明显抑制锥体细胞的凋亡。本试验证明 :在脑缺血再灌注损伤中 ,细胞凋亡是神经元死亡的一种重要形式 ;MT- 1对脑缺血再灌注有明显神经保护作用     

The neuroprotective effects of lidocaine and methylprednisolone in a rat model of retinal ischemia-reperfusion injury

Retinal ischemia is a common cause of visual impairment for humans and animals. The neuroprotective effects of lidocaine (LDC) and methylprednisolone (MP) upon retinal ischemic injury were investigated in a rat model. Sprague-Dawley rats were divided into 3 groups, the IR control, LDC and MP. A very high intraocular pressure (HIOP) and retinal ischemia were induced. In LDC group, LDC bolus (1.5 mg/kg) was i.v. injected 30 min before ischemia and then a constant rate infusion (CRI) with 2 mg/kg/hr was given until 60 min after reperfusion. In MP group, MP bolus (30 mg/kg) was i.v. administered twice at 2 min before and immediately after ischemia, respectively. The HIOP damage to retina was evaluated by electroretinogram (ERG) and morphometrical histology. The functional analysis of the retina by ERG revealed a 35.2% reduction of a-wave in the IR group, 49.7% reduction in the LDC group but no significant change in the MP group compared to normal controls. An 81.0% reduction of b-wave was observed in the IR group, 80.7% reduction in the LDC group and 17.6% reduction in the MP group. In the morphometrical histology, the retinal inner plexiform layer/outer nuclear layer (IPL/ONL) ratio was reduced to 48.8% in the IR group, 80.1% in the LDC group and 96.2% in MP group. In conclusion, the MP showed significantly good neuroprotective effects on retinal IR injury, and the LDC showed moderate neuroprotective effects demonstrated in retinal structure but not in retinal function.     

干旱预处理对抗旱性不同的2个草地早熟禾品种耐热性能的影响

为探讨干旱预处理诱导草地早熟禾耐热性效应和生理机制及不同品种对干旱预处理的差异响应,对抗旱性不同的2个草地早熟禾品种,“Midnight”(抗)和“Brilliant”(敏感)分别进行充足浇水(对照)和两轮干旱预处理,然后置入35℃/30℃(昼/夜)高温中胁迫25 d。在胁迫的0,5,10,15,20,25 d分别测定草坪外观质量及相应生理反应的动态变化。在胁迫期间,预处理“Brilliant”的草坪质量(TQ)显著(P<0.05)高于未经预处理材料;在胁迫5 d后,经预处理的“Brilliant”渗透势(OP)不断下降,而对照材料基本维持不变,在10和15 d时,预处理Brilliant的相对含水量(RWC)显著(P<0.05)高于对照;在胁迫的10～20 d,经预处理“Brilliant”的超氧化物歧化酶(SOD)和过氧化氢酶(CAT)活性显著(P<0.05)高于未经预处理材料,而电解质渗透率(EL)值则相反;15 d时,经预处理的棕榈酸(16∶0)和硬脂酸(18∶0)含量显著(P<0.05)低于未经预处理材料,而亚麻酸(18∶3)含量正好相反,与之相对应,预处理“Brilliant”的双键系数(DBI)显著(P<0.05)高于对照。“Midnight”两处理的各测定指标变化趋势相近,无明显差异。结果表明,干旱预处理未能进一步提高抗旱性品种“Midnight”的耐热性,而有效提高了干旱敏感品种“Brilliant”的耐热性。“Brilliant”耐热性的获得与干旱预处理诱导其渗透调节能力的提高,激活抗氧化酶(SOD、CAT)活性从而保护膜脂中不饱和脂肪酸(18∶3)免受活性氧伤害而急剧下降密切相关,从而有效阻止叶片失水,稳定膜结构,延缓植株衰老。     

Necrotizing mycotic vasculitis with cerebral infarction caused by Aspergillus niger in a horse with acute typholocolitis.

An 18-year-old Morgan mare was presented to the Veterinary Medical Teaching Hospital, University of Illinois, with a 10-day history of watery diarrhea, depression, and dysphagia. On admission, the animal was severely dehydrated, depressed, and unable to swallow and had no clinical signs of diarrhea. The respiratory and heart rate and body temperature were within normal limits. Following fluid therapy, the mare developed severe watery diarrhea and continued to be depressed, incoordinated, and dysphagic. The animal died on the fourth day after admission and was sent to the Laboratories of Veterinary Diagnostic Medicine for necropsy. Gross postmortem findings were consistent with an acute cerebral infarction in the right cerebral hemisphere, an acute necrotizing typhlocolitis, multifocal petechial and ecchymotic hemorrhages, enlarged and congested pars intermedia of the pituitary gland, and marked bilateral adrenocortical hyperplasia with multifocal areas of necrosis and hemorrhage. Histologic evaluation of the affected brain demonstrated an area of coagulative necrosis of the gray matter, with hemorrhage, vasculitis, and thrombosis. There were many fungal hyphae 3.5-6.0 microm, pale basophilic, septate, and occasionally branching at 45 degrees present in the arterial walls and throughout the necrotic tissue. Immunohistochemical analysis revealed Aspergillus niger as the etiologic agent responsible for the mycotic vasculitis and infarction in the brain. Bacteria culture and immunohistochemical staining of the colon and cecum failed to demonstrate specific pathogens.     

Severe brain damage after punitive training technique with a choke chain collar in a German shepherd dog

The features of severe ischemic brain damage after strangulation by the owner of a 1-year-old German shepherd dog are described. The dog was disciplined by the owner during training by holding the dog off the ground by his choke chain collar. At first, the dog behaved normally, but he became increasingly ataxic and started circling to the left and showed reduced consciousness. The neurological examination revealed severe disorientation, left lateral pleurothotonus, and circling. The neurological findings were consistent with a multifocal brain lesion. A magnetic resonance imaging scan was performed and showed changes in the T2- and diffusion-weighted images, consistent with severe cerebral edema resulting from ischemia. Because of the severity of the clinical features, the dog was later euthanized. To the author's knowledge, this is the first report of a severe brain ischemia after strangulation in a dog.