调控血脂改善脑梗死患者血管内皮功能的研究

目的　研究降低血脂水平对改善脑梗死患者内皮依赖性血管舒张功能的影响。方法　给 33例脑梗死患者口服普伐他汀 2 0mg,每日 1次 ,连续服 6周 ,观察治疗前后血脂及颈内动脉内皮依赖性血管舒张功能的变化 ,并与对照组比较。结果　治疗 6周后 ,普伐他汀组胆固醇、低密度脂蛋白胆固醇明显降低 (分别降低 2 6 9%和 2 5 8% ) ,与治疗前比较差异有显著性 (均P <0 .0 1) ;对照组血脂各项指标虽有降低 ,但与治疗前比较差异无显著性 (均P >0 .0 5 )。颈动脉内皮依赖性血管舒张功能治疗前后普伐他汀组差异有显著性 ,对照组差异无显著性。结论　普伐他汀对脑梗死患者的血脂水平和血管内皮舒张功能均有明显改善作用。     

绝经后妇女缺血性脑卒中患者性激素变化及其意义

目的 探讨绝经后妇女缺血性脑卒中患者性激素变化规律及其与血脂的关系。方法 测定45例绝经2年以上发病3天内急性动脉硬化性脑梗死患者,35例绝经2年以上健康妇女和35例绝经前行经期健康妇女的血清雌二醇(E_2)、孕酮(P)、促卵泡刺激素(FSH)、促黄体生成素(LH)及血脂谱。结果 脑卒中患者E_2水平,较绝经前妇女下降57％,而绝经后健康妇女下降51％。相关分析表明,E_2与TC、LDL-C呈负相关,与HDL-C、HDL-C_2呈正相关,相关系数分别为- 0.6178、-0.5326、0.4371和0.5649,(P均<0.01)。结论 绝经后动脉硬化性缺血性脑卒中与性激素失调有关,影响绝经后妇女血脂水平的可能是雌二醇对动脉硬化性脑卒中发挥作用。     

强化他汀降脂与传统降脂治疗进展性脑卒中的对比研究

目的对进展性脑卒中患者采用强化他汀治疗与传统降脂治疗行疗效对比研究,探讨强化治疗方案的临床应用价值。方法收集我院2013-09—2014-07收治的120例进展性脑卒中患者,随机分为对照组和观察组各60例。对照组予氟伐他汀钠缓释片40mg/d(常规降脂治疗),观察组予氟伐他汀钠缓释片80mg/d(强化降脂治疗),2周后观察血脂变化与临床疗效,比较2组治疗前后的总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)与高密度脂蛋白胆固醇(HDL-C)水平及NIHSS评分。结果治疗前2组血脂水平无显著性差异,治疗后TC、LDL-C水平均显著降低(P0.05),HDL-C的表达水平则显著升高。与对照组相比,观察组疗效更明显,NIHSS评分降低幅度更大(P0.05)。2组不良反应发生率差异无统计学意义(P0.05)。结论进展性脑卒中患者采用强化他汀方案治疗安全有效,有较高临床应用价值。     

百忧解治疗脑卒中后抑郁及神经功能缺损的疗效观察

目的　观察百忧解治疗脑卒中后抑郁状态的疗效。方法　对 5 6例脑卒中后抑郁状态患者 ,随机分为治疗组 (加用百忧解 )和对照组 (常规治疗 )各 2 8例 ,进行对照观察。治疗前后行汉密尔顿抑郁量表 (HAMD)、日常生活能力 Barthel指数(BI)量表及神经功能缺损评分 (SSS)量表进行评定其疗效。结果　治疗组 HAMD评分治疗后 (4.8± 1.6 )较治疗前 (2 1.4±4 .1)显著下降 (P <0 .0 1) ,对照组治疗后 (15 .1± 2 .3)与治疗前 (2 0 .4± 3.6 )比较无显著差异 (P >0 .0 5 )。治疗组治疗后 SSS评分显著降低 ,BI评分明显提高 ,与对照组比较也有显著差异 (均 P <0 .0 1)。结论　百忧解治疗脑卒中后抑郁状态不仅对抑郁有明显效果 ,且可促进脑卒中后神经功能的恢复     

不同剂量氯氮平与精神分裂症患者血脂、血糖代谢的对照研究

目的　探讨不同剂量氯氮平对精神分裂症患者治疗前后血脂、血糖的影响。方法　87例男性精神分裂症患者分为3组接受氯氮平治疗,低剂量组<150mg/d(30例);中剂量组150 ~300mg/d(29例);高剂量组>300mg/d( 28例)。治疗前及治疗第6周后分别进行葡萄糖耐量试验(OGTT)、血脂检测,并计算体质量指数。结果　治疗第6周后, 3组患者甘油三酯(TG)均升高,差异有统计学意义(F=12 16,P=0 000),其中以低剂量组为著(P<0 05);低剂量组总胆固醇(TC)高于高剂量组(P<0 05);高剂量组高密度脂蛋白胆固醇(HDL)下降和低密度脂蛋白胆固醇(LDL)水平明显升高(P<0 05,P<0 01 )。3组患者血糖于餐后1h升高,差异有统计学意义(F=4 67,P=0 015),其中高剂量组增高明显(P<0 01)。同时,高剂量组OGTT异常的发生率明显高于低剂量组(χ2 =5 087,P=0 024)。3组患者治疗后体质量增加的差异无统计学意义(P>0 05)。未发现体质量增加与血糖、TG、HDL和LDL有明显相关关系(均P>0 05)。结论　氯氮平可导致精神分裂症患者不同程度的血脂水平改变、血糖升高及体质量增加,其程度可能与氯氮平的剂量有关。     

不同剂量氯氮平对精神分裂症患者脂代谢影响的对照研究

目的　探讨不同剂量氯氮平对精神分裂症患者治疗前后血脂水平的影响。方法　 87例男性精神分裂症患者分 3组接受氯氮平治疗 ,低剂量组 :氯氮平 <15 0mg/d ;中剂量组 :氯氮平 15 0～ 3 0 0mg/d ;高剂量组 :氯氮平 >3 0 0mg/d。治疗前和治疗 6周后分别检测血脂、体重 ,并计算体重指数。结果　低剂量组治疗 6周后甘油三酯 (TG)水平升高 (P <0 0 5 ) ,高剂量组治疗 6周后高密度脂蛋白 (HDL)下降和低密度脂蛋白 (LDL)水平明显升高 (P <0 0 5、P <0 0 1) ;高、中剂量组治疗前后体重增加差异具有显著性意义 (P <0 0 1,P <0 0 5 ) ;体重增加与血清TG、HDL和LDL未发现明显相关关系 (P >0 0 5 )。结论　氯氮平治疗可导致血脂水平改变 ,体重随氯氮平剂量的增加而增加。     

阿托伐他汀钙治疗颈动脉粥样硬化疗效观察

目的观察阿托伐他汀钙在颈动脉粥样硬化中的治疗效果。方法92例合并颈动脉粥样硬化以及血脂异常的缺血性脑血管病患者随机分为常规治疗组46例,阿托伐他汀钙治疗组46例(常规治疗基础上加阿托伐他汀钙治疗)分别给予相应的药物治疗12个月;比较2组治疗前后血清C-反应蛋白(CRP)、血脂水平以及颈动脉内-中膜厚度(IMT)、颈动脉斑块面积的变化以及脑血管事件的复发率。结果2组治疗前后血清CRP水平较治疗前显著降低(均P0.05);阿托伐他汀钙组治疗后颈动脉IMT、斑块面积以及血脂水平显著降低(均P0.05);常规治疗组治疗前后颈动脉IMT、斑块面积以及血脂水平差异无统计学意义;2组患者脑血管病复发率差异无统计学意义。结论阿托伐他汀钙干预对于降低CRP水平,延缓和逆转劲动脉粥样硬化优于常规治疗组,并可能预防脑血管病复发。     

低分子肝素治疗进展性脑卒中的疗效观察

目的　探讨低分子肝素对进展性缺血性脑卒中的治疗作用。方法　将起病在 48h内 10 2例脑梗死患者随机分成治疗组及对照组。治疗组在常规治疗的基础上加用低分子肝素钙 5 0 0 0U皮下注射 ,2次 /d ,连续 7d。对照组采用常规治疗。治疗前后检测凝血酶原时间、出凝血时间和血液流变学指标 ,同时对进展性缺血性脑卒中患者的神经功能缺损进行评分。结果　治疗组 11例发生进展性缺血性脑卒中 ,对照组 2 4例发生进展性缺血性脑卒中 ,两组比较有显著性差异 (P <0 0 5 )。其治疗组进展的严重程度比对照组轻 (P <0 0 1) ;近期预后较对照组好 (P <0 0 5 )。结论　低分子肝素治疗能降低进展性缺血性脑卒中发生率 ,减轻其进展程度 ,有利于进展性缺血性脑卒中患者神经功能的恢复     

雌激素对绝经后妇女脑梗死及血脂水平的影响

目的探讨雌激素对绝经后妇女脑梗死及血脂水平的影响。方法 用放射免疫分析法和全自动生化分析仪测定50例绝经后妇女脑梗死患者及24例正常人血清E2、TC、TC、HDLC、LDL-C水平。结果 绝经后老年与非老年组脑梗死患者血清E2和HDLC水平均明显低于对照组,而TC、TC、LDLC水平均明显高于对照组(P<0.05~P<0.01)。上述各指标,以老年组改变为最明显,与非老年组相比有显著性差异(P<0.05)。同时老年组有多灶梗死者也明显多于非老年组(P<0.05)。相关分析,E2与IC、IC、LDLC呈负相关,与HDL-C水平呈正相关。结论 绝经后妇女脑梗死患者血清雌激素水平降低是导致脂代谢紊乱及脑梗死发生的主要危险因素。     

盐酸帕罗西汀治疗老年脑卒中后抑郁症32例观察

目的　观察盐酸帕罗西汀对老年脑卒中后抑郁状态的疗效。方法　对 64例老年脑卒中合并抑郁的患者随机分为治疗组 (加用盐酸帕罗西汀 )和对照组 (常规治疗 )各 3 2例。治疗前后行汉密尔顿抑郁量表 (HAMD)、日常生活能力Barthel指数(BI)量表及神经功能缺损计分 (SSS)量表进行评定 ,对照观察其疗效。结果　治疗组HAMD评分治疗后 ( 9 0 8± 1 5 8)较治疗前 ( 17 5 0± 3 3 7)显著下降。治疗组治疗后SSS评分显著降低 ,BI评分明显提高 ,与对照组比较有显著性差异 (均P <0 0 1)。结论　盐酸帕罗西汀治疗老年脑卒中后抑郁状态疗效显著 ,并有效提高脑卒中后神经功能的恢复     

绝经期女性脑梗死患者雌激素水平与血脂关系研究

目的 研究绝经期女性脑梗死患者血清中雌二醇(E2)、血脂含量变化,探讨雌激素对缺血性脑血管疾病的关系。方法 取78名绝经期女性脑梗死患者和62名对照组患者空腹静脉血,测定血清E2、甘油三酯(TG)、总胆固醇(TC)、高密度脂蛋门胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、载脂蛋白-AI(Apo-AI)及载脂蛋白B100(Apo-B100)。结果脑梗死组E2水平(12.86pg/ml)低于对照组(25.59pg/ml),有显著差异(P<0.01)。脑梗死组TG、TC、LDL-C、Apo-B100显著高于对照组(P分别<0.01、0.01、0.01、0.05),脑梗死组HDL-C显著低于对照组(P<0.01),脑梗死组ApoA-I与对照组相比无显著性差异(P>0.05)。雌激素水平与TG、TC、LDL-C、Apo-B100呈显著负相关(r分别为-0.63、-0.44、-0.57、-0.30,P<0.01),与HDL-C呈显著正相关(r=0.53,P<0.01)。结论 雌激素水平降低可导致血脂谱异常改变,从而促进动脉粥样硬化,低雌激素水平可能是缺血性脑血管病发生的危险因素之一。     

基线血压水平与急性缺血性脑卒中早期降压治疗3个月结局的关系

目的探讨基线血压水平与急性缺血性脑卒中早期降压治疗3 m结局关系。方法收集2009年8月-2013年5月发病48 h内住院且经影像学确诊合并高血压的急性期缺血性脑卒中患者828例,根据入组时收缩压(Systolic Blood Pressure,SBP)水平分为140~160 mmHg组(n=276)、160~180 mmHg组(n=350)、180~200 mmHg组(n=158)、200~220 mmHg组(n=44),随机给予降压治疗或不予降压治疗。降压治疗者24 h内降压10%~20%,收缩压和舒张压在7 d分别低于140 mmHg和90 mmHg,并在2 w内维持在这一水平。不予降压治疗者停止或不给予降压药物,所有患者测量并记录血压水平。比较患者出院后3 m死亡率和良好预后率。结果随访3 m,140~160 mmHg组降压治疗患者死亡率明显高于无降压治疗患者(13.7%vs 5.8%,P<0.05),良好预后率明显低于无降压治疗患者(65.5%vs 77.4%,P<0.05),160~180 mmHg组、180~200 mmHg组、200~220 mmHg组死亡率比较差异无统计学意义(9.2%vs 13.4%,11.8%vs 12.3%13.6%vs 9.1%,P>0.05),良好预后率比较差异亦无统计学意义(71.8%vs 62.6%,69.4%vs 60.3%,54.5%vs 59.1%,P>0.05)。结论急性缺血性脑卒中患者轻度血压升高时(SBP 140~160 mmHg)不宜降压治疗;中高度血压升高时(SBP 160~220 mmHg)降压治疗对3 m结局影响是中性的。     

糖尿病前期对缺血性卒中患者发生卒中后抑郁的影响

目的 探讨糖尿病前期对缺血性卒中患者发生卒中后抑郁(PSD)的影响.方法 选取本院2016年1月～2019年6月间收治200例急性缺血性卒中患者,依据患者血糖水平分为正常血糖组(n=80)与糖尿病前期组(n=120),糖尿病前期组依据自愿接受干预控制原则分为血糖控制亚组(n=68)、无血糖控制亚组(n=52).分别于患...     

雌激素对MPP+诱导的PC12细胞损伤过程中细胞凋亡相关基因的研究

目的　探讨雌激素 (Estrogen ,E)在 1-甲基 - 4 -苯基吡啶离子 (MPP+ )对PC12细胞损伤过程中对神经细胞的作用机制 ,特别是雌激素与细胞凋亡的关系。方法　用半定量逆转录PCR(RT PCR)检测细胞凋亡过程中促进细胞增殖基因Bcl x和促进细胞死亡基因白细胞介素 1β转换酶 (interleukin 1βconverten zyme ,ICE)的有效蛋白mRNA的表达水平 ,比较各组的差异。 结果　雌激素组的Bcl x的有效蛋白mRNA的表达水平显著高于对照组、MPP+ 组及E +MPP+ 组 (P <0 .0 5 ) ;ICE的有效蛋白mRNA的表达水平显著低于对照组、MPP+ 组及E +MPP+ 组 (P <0 .0 5 )。E +MPP+ 组Bcl x的有效蛋白mRNA的表达水平显著高于MPP+ 组 ;ICE的有效蛋白mRNA的表达水平显著低于MPP+ 组 (P <0 .0 5 )。E +MPP+ 组和对照组相比无显著性差异 (P >0 .0 5 )。结论　雌激素对于MPP+ 诱导的ICE增加和Bcl x降低可起一定的拮抗作用 ,从而在一定程度上抑制了凋亡的发生。     

Effects of combined estrogen and progesterone on brain infarction in reproductively senescent female rats.

Recent data from the Women's Health Initiative have highlighted many fundamental issues about the utility and safety of long-term estrogen use in women. Current hormone replacement therapy for postmenopausal women incorporates progestin with estrogen, but it is uncertain if combined therapy provides major cerebrovascular risks or benefits to these women. No experimental animal stroke studies have examined combined hormone administration. The authors tested the hypothesis that combined hormone treatment reduces ischemic injury in middle-aged female rat brain. Reproductively senescent female rats underwent 2-hour middle cerebral artery occlusion (MCAO) followed by 22 hours reperfusion. Estrogen implants were placed subcutaneously at least 7 days before MCAO, and progesterone intraperitoneal injections were given 30 minutes before MCAO, at initiation, and at 6 hours of reperfusion. Rats received no hormone, a 25-microg estrogen implant, a 25-microg estrogen implant plus 5 mg/kg intraperitoneal progesterone, or 5 mg/kg intraperitoneal progesterone. Cortical, caudoputamen, and total infarct volumes were assessed by 2,3,5-triphenyltetrazolium chloride staining and digital image analysis at 22 hours reperfusion. Cortical and total infarct volumes, except in the acute progesterone-treated group, were significantly attenuated in all estrogen-alone and combined hormone-treated groups. There were no significant differences in caudoputamen infarct volumes in all hormone-treated groups as compared with untreated rats. These data have potential clinical implications relative to stroke for postmenopausal women taking combined hormone replacement therapy.     

17beta-estradiol reduces stroke injury in estrogen-deficient female animals.

BACKGROUND AND PURPOSE: The importance of postmenopausal estrogen replacement therapy for stroke in females remains controversial. We previously showed that female rats sustain less infarction in reversible middle cerebral artery occlusion (MCAO) than their ovariectomized counterparts and that vascular mechanisms are partly responsible for improved tissue outcomes. Furthermore, exogenous estrogen strongly protects the male brain, even when administered in a single injection before MCAO injection. The present study examined the hypothesis that replacement of 17beta-estradiol to physiological levels improves stroke outcome in ovariectomized, estrogen-deficient female rats, acting through blood flow-mediated mechanisms. METHODS: Age-matched, adult female Wistar rats were ovariectomized and treated with 0, 25, or 100 microgram of 17beta-estradiol administered through a subcutaneous implant or with a single Premarin (USP) injection (1 mg/kg) given immediately before ischemia was induced (n=10 per group). Each animal subsequently underwent 2 hours of MCAO by the intraluminal filament technique, followed by 22 hours of reperfusion. Ipsilateral parietal cortex perfusion was monitored by laser-Doppler flowmetry throughout ischemia. Cortical and caudate-putamen infarction volumes were determined by 2,3, 5-triphenyltetrazolium chloride staining and digital image analysis. End-ischemic regional cerebral blood flow was measured in ovariectomized females with 0- or 25-microgram implants (n=4 per group) by (14)C-iodoantipyrine quantitative autoradiography. RESULTS: Plasma estradiol levels were 3.0+/-0.6, 20+/-8, and 46+/-10 pg/mL in the 0-, 25-, and 100-microgram groups, respectively. Caudate-putamen infarction (% of ipsilateral caudate-putamen) was reduced by long-term, 25-microgram estrogen treatment (13+/-4% versus 31+/-6% in the 0-microgram group, P<0.05, and 22+/-3% in the 100-microgram group). Similarly, cortical infarction (% of ipsilateral cortex) was reduced only in the 25-microgram group (3+/-2% versus 12+/-3% in the 0-microgram group, P<0.05, and 6+/-3% in the 100-microgram group. End-ischemic striatal or cortical blood flow was not altered by estrogen treatment at the neuroprotective dose. Infarction volume was unchanged by acute treatment before MCAO when estrogen-treated animals were compared with saline vehicle-treated animals. CONCLUSIONS: Long-term estradiol replacement within a low physiological range ameliorates ischemic brain injury in previously ovariectomized female rats. The neuroprotective mechanism is flow-independent, not through preservation of residual ischemic regional cerebral blood flow. Furthermore, the therapeutic range is narrow, because the benefit of estrogen in transient vascular occlusion is diminished at larger doses, which yield high, but still physiologically relevant, plasma 17beta-estradiol levels. Lastly, unlike in the male brain, single-injection estrogen exposure does not salvage ischemic tissue in the female brain. Therefore, although exogenous steroid therapy protects both male and female estrogen-deficient brain, the mechanism may not be identical and depends on long-term hormone augmentation in the female.     

缺血性脑卒中患者雌二醇水平及其临床意义

目的现对急性脑梗死患者的雌二醇水平和脑血管病的相关危险因素进行观察,探讨雌二醇与缺血性脑血管病的关系。方法选取100例绝经后急性脑梗死女性患者和健康对照组40人,检测体内的雌二醇水平,血脂,血糖,凝血四项,血小板聚集率等临床指标及应用NIHSS量表进行神经功能缺损评分,时以上数据进行比较。结果脑梗死组的雌二醇含量显著低于对照组（P〈0．01）。脑梗死组的胆固醇、甘油三酯以及低密度脂蛋白（LDL）显著高于对照组（P〈0．01）。雌二醇与胆固醇、甘油三酯、I。DI。以及NIHSS均呈负相关（P〈0．01）,与高密度脂蛋白（HDI。）呈正相关（P〈0．01）。结论脑梗死患者的雌激素水平降低,雌激素水平降低可致血脂改变,神经功能缺损程度加重。     

Loss of benefit from estrogen replacement therapy in diabetic ovariectomized female rats subjected to transient forebrain ischemia

In nondiabetic animals, estrogen has been shown to provide significant neuroprotection in focal and transient forebrain ischemia models. However, that neuroprotection may be diminished or lost in the diabetic. In this study, we compared the level of brain damage in intact, ovariectomized (OVX) and 17beta-estradiol (E(2))-treated OVX female rats rendered diabetic and chronically ( approximately 4 weeks) hyperglycemic via streptozotocin (STZ). Rats were subjected to 20 min of unilateral transient forebrain ischemia (reduction in cortical CBF to 20% of baseline). Neurologic function was analyzed daily and brain histopathology (in H&E-stained sections) was evaluated at 72 h of reperfusion. Supplemental histopathologic information was obtained from additional TUNEL-stained sections. When comparing neurologic outcome scores in the three groups, E(2)-treated OVX females displayed the highest degree of dysfunction and intact females the least (OVX rats not treated with E(2) were intermediate), with the difference between the intact and E(2)-treated groups being statistically significant. That same order was often observed with the regional histopathologic analyses of H&E-stained tissue. A significantly higher magnitude of neuronal loss in both OVX groups, when compared to intact females, was observed in the CA4 sector of the hippocampus and in the cortex. In addition, cell loss in the dorsal thalamus of the E(2)-treated group was significantly greater than in the intact females. Those results were generally corroborated by TUNEL-analysis, with 67% of the E(2)-treated, 33% of the control OVX, and only 17% of the intact females displaying TUNEL-positive cells in multiple regions. In conclusion, the present findings strongly suggest that the neuroprotective benefits of estrogen replacement therapy may be lost in the diabetic female rat.     

缺血性脑卒中静脉溶栓后早期血压变异与组织再灌及远期预后的关系

目的观察缺血性脑卒中静脉溶栓后早期血压变异对组织再灌的影响,探讨与其神经功能恢复及远期预后关系,为临床缺血性脑卒中静脉溶栓后早期血压管理提供客观依据。方法选择我院2014-06-2016-09收治的缺血性脑卒中患者128例,按24h收缩压变异率顺序,分为血压低变异率组(A组)和血压高变异率组(B组)。评估2组治疗前后组织再灌和美国国立卫生研究院卒中量表(NIHSS)评分,治疗3个月后,应用改良Rankin量表评分(mRS)评估患者远期预后状况和预后不良结果,并进行Logistic回归分析。结果B组治疗后组织再灌率为42.19%(27/64),低于A组的59.38%(38/64),B组治疗后MIHSS评分为(20.49±5.27)分,高于A组,差异有统计学意义(P0.05);B组3个月后mRS评分、mRS评分2分及预后不良结果总发生率分别为(2.85±0.80)分、53.12%(34/64)和35.94%(25/64),高于A组的(2.13±0.93)分、39.06%(25/64)和14.06%(9/64),差异有统计学意义(P0.05)。结论缺血性脑卒中静脉溶栓后早期血压较大波动幅度为患者组织再灌和远期临床预后不佳的独立风险因素。患者脑组织再灌率低,神经功能恢复较差,远期预后不良。     

Effects of estrogen replacement therapy on the myelin sheath ultrastructure of myelinated fibers in the white matter of middle‐aged ovariectomized rats

The effects of estrogen replacement therapy (ORT) on white matter and the myelin sheath ultrastructure in the white matter of middle‐aged ovariectomized (OVX) rats were investigated in this study. Middle‐aged rats were ovariectomized and divided into a placebo replacement (OVX + O) group and an estrogen replacement (OVX + E) group. Then, the Morris water maze, electron microscope techniques, and stereological methods were used to investigate the effects of ORT on spatial learning capacity, white matter volume and the myelin sheath ultrastructure in the white matter. We found that the spatial learning capacity of the OVX + E rats was significantly improved compared with that of the OVX + O rats. When compared with that of OVX + O rats, the total volume of the myelin sheaths in the white matter of the OVX + E rats was significantly increased by 27%, and the difference between the outer perimeter and inner perimeter of the myelin sheaths of the white matter in the OVX + E rats increased significantly by 12.6%. The myelinated fibers with mean diameters of 1.2–1.4 μm were significantly longer (46.1%) in the OVX + E rats; the difference between the mean diameter of myelinated fibers and the mean diameter of axons (0–0.4 μm) was significantly increased by 21.6% in the OVX + E rats. These results suggested that ORT had positive protective effects on the spatial learning ability and on the myelin sheath ultrastructure in the white matter of middle‐aged OVX rats.