手十二井穴刺络放血对一氧化碳中毒昏迷小鼠促醒作用及其机制的初步研究

[目的]观察手十二井穴刺络放血对煤气中毒小鼠的促醒作用,并探讨其部分作用机制。[方法]选用成年雄性昆明小鼠共54只,随机分为正常组、模型组和治疗组,每组18只。模型组和治疗组小鼠分批在罐内静式吸入含一氧化碳(CO)浓度为4 300 ppm的空气60~70 min,正常组小鼠不给予CO气体,置于空罐中,时长同模型组。小鼠从罐中取出后,治疗组进行手十二井血刺络放血。观察染毒后即刻、1 h和4 h小鼠意识状态和静脉血中碳氧血红蛋白浓度变化。[结果]治疗组与模型组相比,小鼠昏迷时间明显缩短;染毒后1 h和4 h,治疗组小鼠静脉血中碳氧血红蛋白浓度明显低于模型组。[结论]手十二井穴刺络放血对急性CO中毒小鼠具有促醒作用,可以缩短昏迷时间,其机制可能与手十二井穴刺络放血可以降低小鼠血液中碳氧血红蛋白含量有关。     

手十二井穴刺络放血对脑缺血大鼠缺血区组织Na~＋、K~＋影响的动态观察

手十二井穴刺络放血对脑缺血大鼠缺血区组织Ｎａ＋、Ｋ＋影响的动态观察马岩王番天津中医学院针灸专业研究生（３００１９３）郭义张艳军徐汤萍天津中医学院针灸系鲍家铸天津中医学院一附院针灸科关键词针刺疗法井穴脑缺血我们以前临床观察到用手十二井穴刺络放血法急救...     

经皮125I植入联合化疗在中晚期非小细胞肺癌治疗中的应用及对CD3+、CD4+、CD8+、CD4+/CD8+的影响

目的 探讨经皮放射性碘125粒子（¹²⁵I）植入联合化疗在中晚期非小细胞肺癌（NSCLC）治疗中的应用及对CD3⁺、CD4⁺、CD8⁺、CD4⁺/CD8⁺的影响。方法 选取2017年1月-2019年1月咸阳市中心医院收治的120例中晚期NSCLC患者,根据治疗方案分为研究组78例（经皮¹²⁵I植入联合化疗）和对照组42例（同步放化疗）。统计两组基线资料,并记录粒子植入情况及并发症情况,治疗6个月后评估两组临床疗效。比较两组外周血T淋巴细胞亚群CD3⁺、CD4⁺、CD8⁺占比及CD4⁺/CD8⁺治疗前后的变化。统计治疗期间不良反应发生情况。结果 两组性别、年龄、病灶部位、肿瘤直径、病理类型、临床分期及治疗前卡氏评分比较,差异无统计学意义（P >0.05）。研究组91.03%（71/78）患者植入粒子的分布符合术前模拟剂量分布;术后气胸30.77%（24/78）,肺内渗血28.21%（22/78）,发热19.23%（15/78）,粒子移位2.56%（2/78）,围术期均无死亡病例。两组临床疗效比较,差异有统计学意义（P <0.05）,研究组有效率高于对照组。两组治疗后外周血CD3⁺、CD4⁺、CD4⁺/CD8⁺及治疗前后的差值比较,差异有统计学意义（P <0.05）,研究组高于对照组;两组治疗后外周血CD8⁺及治疗前后的差值比较,差异无统计学意义（P >0.05）。两组不良反应（胃肠道反应、粒细胞减少及放射性食管炎发生率）比较,差异无统计学意义（P >0.05）;两组放射性肺炎发生率比较,差异有统计学意义（P <0.05）,研究组低于对照组。结论 经皮¹²⁵I植入联合化疗可有效治疗中晚期NSCLC,可明显改善患者免疫功能,减少不良反应。     

十二井穴放血对不同程度颅脑创伤大鼠脑水肿及线粒体生物合成的影响

目的 探讨十二井穴放血对颅脑创伤（TBI）大鼠脑水肿及线粒体生物合成的影响。方法 将56 只 SD 大鼠随机等分为7 组,即轻度TBI 组、轻度TBI 加井穴放血组、中度TBI 组、中度TBI 加井穴放血组、重度 TBI 组、重度TBI 加井穴放血组和对照组,每组8 只。应用电子控制性脑皮质撞击仪,轻度、中度、重度TBI 组 的打击深度分别为1、3 和4 mm。对照组仅开骨窗后缝合皮肤,不进行打击。井穴放血通过1 ml 注射器针头于 大鼠双侧前肢趾端的十二井穴点刺出血完成,出血量为每穴10 μl,每12 h 进行1 次放血。手术后72 h,进行神 经功能损伤评分（mNSS）,随后取10 mg 损伤周围脑组织,qRT-PCR 检测过氧化物酶体增殖物激活受体γ 共激活因子1α（PGC-1α）、线粒体转录因子A（TFAM）基因的表达和线粒体DNA（mtDNA）拷贝数,剩 余脑组织进行脑含水量测量。结果 TBI 后大鼠的mNSS 评分均高于对照组,且随着TBI 严重程度的增加,评分 依次增高（P <0.05）,且轻、中度TBI 组大鼠在应用井穴放血疗法后mNSS 评分与相应的单纯损伤组比较降低 （P <0.05）;TBI 模型大鼠的PGC-1α 和TFAM 基因表达水平以及mtDNA 拷贝数均高于对照组（P <0.05）; 轻度TBI 组大鼠在应用井穴放血疗法后,mtDNA 拷贝数高于相应的未应用放血疗法的大鼠（P <0.05）,中度 TBI 组大鼠在应用放血疗法后PGC -1α 基因表达水平和mtDNA 拷贝数升高（P <0.05）,轻、重度TBI 组大鼠在应 用井穴放血疗法后,虽然PGC -1α 和TFAM 基因表达水平均有升高趋势,但差异无统计学意义（P >0.05）; TBI 后各组大鼠脑组织含水量与对照组比较均增高,且中度TBI 组大鼠在应用井穴放血疗法后脑组织含水量与 相应的单纯损伤组大鼠比较降低（P <0.05）。结论 井穴放血可能通过激活PGC 及下游通路,促进mtDNA 的生 物合成,从而增强损伤脑组织的能量供应,进而改善脑水肿程度,发挥脑保护作用。     

穴位埋线对慢性葡萄膜炎患者T淋巴细胞亚群的影响

目的 观察穴位埋线联合中西医药物治疗对反复发作的慢性葡萄膜炎患者CD3⁺,CD4⁺,CD8⁺细胞及CD4⁺/CD8⁺的影响。方法 将20例38眼慢性葡萄膜炎患者随机分为2组：治疗组10例,采用埋线联合中西医结合药物治疗;对照组10例,采用单纯中西医结合药物治疗。治疗后采用流式细胞术检测各组CD3⁺,CD4⁺,CD8⁺细胞及CD4⁺/CD8⁺的变化。结果 2组对治疗前后总TcellCD3⁺的影响有显著性意义（P<0.01）,2组间比较,差异无统计学意义（P>0.05）;2组对治疗前后ThcellCD4⁺的影响有显著性意义（P<0.01）,治疗组优于对照组（P<0.01）;治疗组对治疗前后TscellCD8⁺的影响有显著性意义（P<0.01）,优于对照组（P<0.01）;2组对治疗前后CD4⁺/ CD8⁺的影响有显著性意义（P<0.05~0.01）。结论 穴位埋线能改善慢性葡萄膜炎患者T淋巴细胞亚群,提高其细胞免疫功能。     

中风初起的急救措施——手十二井穴刺络放血影响脑血流的临床与实验研究

手十二井穴刺络放血法为中风初起行之有效的治疗措施,历代医家多在论述.民间应用甚为广泛.为了确证其疗效并阐释其部位作用机理,我们进行了以下几方面的研究.     

柴胡合剂治疗儿童传染性单核细胞增多症(痰热互结证)40例疗效观察及免疫调节的研究

[目的] 观察柴胡合剂对儿童传染性单核细胞增多症（IM）的临床疗效及免疫调节作用。[方法] 将2014年1月-2016年12月本院收治的80例患儿按随机数字表法随机分为治疗组40例,对照组40例。对照组予静脉滴注更昔洛韦5 mg/kg,每12 h注射1次抗病毒治疗;治疗组在对照组基础上加用柴胡合剂口服,比较两组的临床疗效。[结果] 治疗组体温恢复正常、咽峡炎缓解、淋巴结和肝脾缩小、异型淋巴细胞恢复正常,时间缩短（P<0.01）,肝功能好转（P<0.05）,同时两组治疗后T细胞亚群分析均显示CD3⁺及CD8⁺水平降低、CD4⁺及CD4⁺/CD8⁺均较治疗前升高,治疗组效果明显（P<0.05）,对EBV病毒（EBV）-DNA复制干预与对照组比较无统计学差异（P>0.05）。[结论] 柴胡合剂能有效缓解传染性单核细胞增多症的临床症状及发挥免疫调节作用,对EBV-DNA复制干预无效。     

手十二井穴刺络放血法对脑缺血大鼠局部兴奋性氨基酸的动态观察

采用凝结大脑中动脉的大鼠脑缺血模型 ,观察手十二井穴刺络放血法对大鼠脑缺血组织局部兴奋性氨基酸 (EAA)浓度的动态变化。结果显示 :缺血后 0～ 30min ,EAA浓度上升 ,6 0～ 90min两组EAA浓度下降 ,与 0～ 30min比较 ,刺络组下降幅度较凝结组大 ,90min后 ,脑缺血组织胞外EAA浓度已接近正常水平。提示手十二井穴刺络放血法可降低脑缺血后升高的EAA浓度 ,说明手十二井穴刺络放血可阻止神经毒性 ,起到保护脑损害的作用。     

"手十二井穴"刺络放血对大鼠局灶性脑缺血后SOD活性和MDA含量的影响

目的观察"手十二井穴"刺络放血对大鼠局灶性脑缺血后超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量的影响.方法大鼠随机分为假手术组、缺血组、"手十二井穴"刺络放血组.采用线栓法建立大鼠大脑中动脉栓塞(MCAO)模型,缺血30min、1h、2h、4h后处死动物取脑,分别测定SOD活性和MDA含量.结果与缺血组相比,"手十二井穴"刺络放血组MDA含量明显降低,SOD活性明显升高(P＜0.01).结论"手十二井穴"刺络放血对实验性脑缺血损伤有保护作用,其机制可能与其提高SOD活性、清除自由基、减轻脂质过氧化反应有关.     

高压氧联合井穴放血对脑卒中患者预后的影响

目的 探讨井穴放血联合高压氧治疗对出血性脑卒中患者预后及端粒长度的影响。方法 将120 例 研究对象随机分为井穴放血组、联合组（井穴放血+ 高压氧）及对照组，每组40 例。其中，井穴放血组经血 肿清除术后，在常规内科治疗基础上给予井穴放血治疗；联合组在井穴放血治疗方案基础上同时给予高压氧 治疗；对照组进行常规内科治疗。比较3 组患者入院当日与治疗后36 d 美国国立卫生研究院卒中量表（NHISS）、 Fusl-Meyer 运动功能评定量表评分（FMA）、格拉斯哥昏迷量表评分（GCS）、认知功能评分（MMSE）、日 常生活能力评分（ADL）及临床疗效；实时荧光定量聚合酶链反应检测患者入院当日及治疗后36 d 时外周血 白细胞端粒长度变化。结果 3 组患者入院当日NHISS、FMA、GCS、MMSE 及ADL 评分比较，差异无统 计学意义（P >0.05）。3 组患者治疗后36 d 治疗总有效率比较，差异有统计学意义（P <0.05）。3 组患者治疗 前后NHISS、FMA、GCS、MMSE 及ADL 评分差值比较，差异有统计学意义（P <0.05），联合组FMA、GCS 及MMSE 高于井穴放血组（P <0.05）。3 组患者治疗前后端粒长度差值比较，差异有统计学意义（P <0.05），井 穴放血组和联合组端粒长度长于对照组（P <0.05）。结论 井穴放血疗法联合高压氧治疗能改善出血性脑卒 中患者的预后，促进受损端粒的修复。     

Bloodletting Puncture at Hand Twelve Jing-Well Points Relieves Brain Edema after Severe Traumatic Brain Injury in Rats via Inhibiting MAPK Signaling Pathway

Objective:To investigate whether blood-brain barrier(BBB)served a key role in the edema-relief effect of bloodletting puncture at hand twelve Jing-well points(HTWP)in traumatic brain injury(TBI)and the potential molecular signaling pathways.Methods:Adult male Sprague-Dawley rats were assigned to the shamoperated(sham),TBI,and bloodletting puncture(bloodletting)groups(n=24 per group)using a randomized number table.The TBI model rats were induced by cortical contusion and then bloodletting puncture were performed at HTWP twice a day for 2 days.The neurological function and cerebral edema were evaluated by modified neurological severity score(mNSS),cerebral water content,magnetic resonance imaging and hematoxylin and eosin staining.Cerebral blood flow was measured by laser speckles.The protein levels of aquaporin 4(AQP4),matrix metalloproteinases 9(MMP9)and mitogen-activated protein kinase pathway(MAPK)signaling were detected by immunofluorescence staining and Western blot.Results:Compared with TBI group,bloodletting puncture improved neurological function at 24 and 48 h,alleviated cerebral edema at 48 h,and reduced the permeability of BBB induced by TBI(all P<0.05).The AQP4 and MMP9 which would disrupt the integrity of BBB were downregulated by bloodletting puncture(P<0.05 or P<0.01).In addition,the extracellular signal-regulated kinase(ERK)and p38 signaling pathways were inhibited by bloodletting puncture(P<0.05).Conclusions:Bloodletting puncture at HTWP might play a significant role in protecting BBB through regulating the expressions of MMP9 and AQP4 as well as corresponding regulatory upstream ERK and p38 signaling pathways.Therefore,bloodletting puncture at HTWP may be a promising therapeutic strategy for TBI-induced cerebral edema.     

Research progress in traumatic brain penumbra

Objective Following traumatic brain injury （TBI）,brain tissue that surrounding the regional primary lesion is known as traumatic penumbra; this region may undergo secondary injury and is considered to have the potential to recover.This review aimed to reveal the existence and significance of traumatic penumbra by analyzing all relevant studies concerning basic pathologic changes and brain imaging after TBI.Data sources We collected all relevant studies about TBI and traumatic penumbra in Medline （1995 to June 2013） and ISI （1997 to March 2013）,evaluated their quality and relevance,then extracted and synthesized the information.Study selection We included all relevant studies concerning TBI and traumatic penumbra （there was no limitation of research design and article language） and excluded the duplicated articles.Results The crucial pathological changes after TBI include cerebral blood flow change,cerebral edema,blood-brain barrier damage,cell apoptosis and necrosis.Besides,traditional imaging method cannot characterize the consequences of CBF reduction at an early stage and provides limited insights into the underlying pathophysiology.While advanced imaging technique,such as diffusion tensor imaging （DTI） and positron emission tomography （PET）,may provide better characterization of such pathophysiology.Conclusions The future of traumatic brain lesions depends to a large extent on the evolution of the penumbra.Therefore,understanding the formation and pathophysiologic process of the traumatic penumbra and its imaging research progress is of great significant for early clinical determination and timely brain rescue.     

不同程度颅脑损伤后炎症因子的表达及其临床意义

目的  探讨颅脑创伤（TBI）后炎症因子[肿瘤坏死因子（TNF-α）、白介素-6（IL-6）及C-反应蛋白（CRP）]与颅脑损伤程度、继发性颅脑损伤（SCI）的关系。方法  选取98例TBI患者,根据急性闭合性TBI的分型标准分为轻型、中型及重型TBI,分别为轻型组（29例）、中型组（41例）及重型组（28例）,42例健康志愿者作为对照组;分别于TBI后1、3、5、7及12 d取外周静脉血,采用免疫组织化学法（SP）检测患者的TNF-α、IL-6及CRP表达水平,计算脑出血量及脑水肿体积。结果  TBI后1、3、5、7及12 d血清TNF-α、IL-6及CRP表达水平均先升高,再下降;但TBI后各个时间点的血清TNF-α、IL-6及CRP表达水平均高于对照组（P <0.05）;TBI后1、3及5 d脑出血量逐渐增多、脑水肿体积逐渐增大,TBI后7及12 d脑出血量逐渐减少、脑水肿体积逐渐减小;重型组各个时间点的血清TNF-α、IL-6及CRP表达水平均高于轻型组及中型组（P < 0.05）;中型组各个时间点的血清TNF-α、IL-6及CRP表达水平均高于轻型组（P <0.05）;TBI后TNF-α、IL-6及CRP表达水平与TBI程度、脑出血量及脑水肿体积呈正相关（P <0.05）。结论  TBI程度、脑出血量及脑水肿体积与血清TNF-α、IL-6及CRP表达水平呈单峰性升降密切相关,可作为TBI病情评估、疗效及预后的检测指标,为TBI采取免疫抑制治疗提供依据。

     

Relationship between AQP4 expression and structural damage to the blood-brain barrier at early stages of traumatic brain injury in rats

Background Although some studies have reported that aquaporin-4 （AQP4） plays an important role in the brain edema after traumatic brain injury （TBI）, little is known about the AQP4 expression in the early stage of TBI, or about the correlation between the structural damage to the blood-brain barrier （BBB） and angioedema. The aim of this project was to investigate the relationship between AQP4 expression and damage to the BBB at early stages of TBI. Methods One hundred and twenty healthy adult Wistar rats were randomly divided into two groups： sham operation group （SO） and TBI group. The TBI group was divided into five sub-groups according to the different time intervals： 1, 3, 6, 12, and 24 hours. The brains of the animals were taken out at different time points after TBI to measure brain water content. The cerebral edema and BBB changes in structure were examined with an optical microscopy （OM） and transmission electron microscopy （TEM）, and the IgG content and AQP4 protein expression in traumatic brain tissue were determined by means of immunohistochemistry and Western blotting. The data were analyzed with SPSS 13.0 statistical software. Results In the SO group, tissue was negative for IgG, and there were no abnormalities in brain water content or AQP4 expression. In the TBI group, brain water content significantly increased at 6 hours and peaked at 24 hours following injury. IgG expression significantly increased from 1 to 6 hours following injury, and remained at a high level at 24 hours. Pathological observation revealed BBB damage at 1 hour following injury. Angioedema appeared at 1 hour, was gradually aggravated, and became obvious at 6 hours. Intracellular edema occurred at 3 hours, with the presence of large glial cell bodies and mitochondrial swelling. These phenomena were aggravated with time and became obvious at 12 hours. In addition, microglial proliferation was visible at 24 hours. AQP4 protein expression were reduced at 1 hour, lowest at 6 hours, and began to increase at 12 hours, showing a V-shaped curve. Conclusions The angioedema characterized by BBB damage was the primary type of early traumatic brain edema. It was followed by mixed cerebral edema that consisted of angioedema and cellular edema and was aggravated with time. AQP4 expression was down-regulated during the angioedema attack, but AQP4 expression was upregulated during intracellular edema.     

p38信号通路对大鼠脑创伤后MMP-9的表达及脑水肿形成的影响

目的观察并探讨阻断p38通路激活对大鼠脑创伤后基质金属蛋白酶-9(MMP-9)的表达变化及脑水肿形成的影响及意义。方法健康成年雄性SD大鼠130只,随机分为正常组10只,对照组40只:假手术处理;脑创伤组40只:制作改进式Feeney’s脑创伤模型;p38抑制组40只:脑创伤前15 min股静脉注射p38抑制剂(SB203580,400μg/kg)。分别在脑创伤后2 h、2 d时断头取脑,采用RT-PCR法和Western blotting法检测脑组织P38磷酸化水平及MMP-9 mRNA及蛋白表达水平,Evans Blue法测定血脑屏障通透性变化;干湿比重法测定脑组织含水量。结果(1)与对照组相比,脑创伤组磷酸化p38的水平在伤后2 h明显上升;MMP-9 mRNA和蛋白在脑创伤后2 h未见明显差异(P>0.05),但2 d时表达均显著增高(P<0.01)。与脑创伤组相比,p38抑制组伤后2 h时p38磷酸化水平明显降低(P<0.01),MMP-9 mRNA和蛋白在创伤后2 d时的高表达也均有明显下降(P<0.05);(2)与对照组比较,脑创伤组血脑屏障通透性在创伤后2 h明显增加(P<0.05),2 d时出现继续升高(P<0.01);脑含水量在创伤后2 h无明显变化(P>0.05),在2 d时显著增加(P<0.01)。与脑创伤组相比,p38抑制组血脑屏障通透性及脑含水量在创伤后均有明显降低(P<0.05)。结论阻断p38通路激活可下调大鼠脑创伤后MMP-9高表达,减轻血脑屏障破坏及创伤性脑水肿,提示p38信号通路可通过调节MMP-9的表达变化在创伤性脑水肿中发挥重要作用。     

Neuroprotective effect of AG490 in experimental traumatic brain injury of rats

Background Traumatic brain injury (TBI) is a major cause of death and disability in children and young adults worldwide. Therefore, we investigated the role of AG490 in regulating brain oedema, expression of CD40 and neurological function after TBI.

Methods Sprague Dawley rats (n=240) were randomly divided into a sham operation group, TBI+saline group and TBI+AG490 (JAK/STAT inhibitor) group. Members of each group were euthanized at 6, 12, 24 or 72 hours after injury. Neurological severity score (NSS) was used to evaluate the severity of neurological damage. Brain water was quantitated by wet/dry weight method. The expression of CD40 was assessed by flow cytometry.

Results In both the TBI+saline group and the TBI+AG490 group, the brain water content was elevated after TBI, reached a peak at 24-hour and remained high for the rest of the period investigated; the expression of CD40 reached a peak 24 hours after TBI; the NSS was elevated after TBI and then decreased after 6 hours. Elevations in the level of CD40, degree of brain edema and NSS after TBI were significantly reduced in TBI+AG490 group.

Conclusion Inhibition of the JAK/STAT signalling pathway reduces brain oedema, decreases the expression of CD40 and exerts neuroprotective effects after TBI.

     

孕酮对脑损伤后环氧化酶-2表达和脑水肿的影响

①目的观察孕酮对大鼠脑损伤后环氧化酶-2表达和脑水肿的影响。②方法雄性SD大鼠随机分为假手术组、脑损伤组、安慰剂组和孕酮治疗组。按照改良的Feeney自由落体损伤装置制作大鼠脑损伤模型。各组于伤后1、24、72小时取材。用免疫组织化学法观察大鼠皮质COX-2的表达水平变化,并测量脑组织含水量。③结果脑损伤组和安慰剂组大鼠皮质COX-2阳性细胞数和脑啦肿较假手术组显著增加;孕酮治疗组与脑损伤组和安慰剂组比较,大鼠皮质COX-2阳性细胞数和脑水肿明显减少,差异有统计学意义（P〈0．05）。④结论孕酮可能通过下调COX-2的表达,降低脑内炎症反应,进而降低脑水肿,发挥脑损伤保护作用。     

猫闭合性创伤性脑水肿扩散加权成像的实验研究

目的建立猫急性闭合性脑创伤（TBI）模型,并应用扩散加权成像（DWI）探讨伤后脑水肿类型及演变规律。方法共选取22只猫,以最大角加速度（6．43±0．15）×10^5rad／s2制成TBI模型。其中10只用于常规MRI及DWI扫描,连续观察伤前及伤后3、6、24、48、72h6个时相点,另于上述相同6个时相点,分别选取6只猫用于HE及嗜银染色、6只猫用于透射电镜观察。结果常规MRI显示蛛网膜下腔出血1例、硬膜外或硬膜下出血2例、脑挫裂伤2例、脑室内出血1例、同时显示蛛网膜下腔出血和脑挫裂伤2例、同时显示硬膜下出血和脑实质内点状出血2例。10只猫致伤前后各时点ADC值显示细胞毒性及血管源性两种类型脑水肿,其中7只（70％）猫以细胞毒性脑水肿改变为主,24h达峰值;3只（30％）猫早期以血管源性脑水肿改变为主,6h达峰值,而后期以细胞毒性脑水肿为主。HE、嗜银染色及透射电镜显示血管通透性增加、细胞肿胀,轴索肿胀、断裂、轴索球形成。结论猫急性闭合性创伤性脑水肿包括细胞毒性及血管源性两类,以细胞毒性水肿为主。扩散加权成像是观测脑水肿的一种可靠方法。     

Effects of bloodletting puncture at Jing-Well points in distal ends of finger and toe on survival rate and brain edema in cerebral ischemic rats

OBJECTIVE:To observe the effects of bloodletting puncture at Jing-Well points in the distal ends of the finger and toe on survival rate,survival time,and brain edema in rats with cerebral ischemia.METHODS:Fifty-four male Sprague-Dawley rats were randomly divided into five groups:normal,sham operation,model,bloodletting puncture at Jing-Well points in distal ends of finger and toe,and puncture without bloodletting at these points.Middle cerebral artery occlusion models were established according to Longa’s method.The brains were taken 48 h after the model was established.Brain water content,brain density,brain coefficient,survival rate,and survival time in each group were measured.RESULTS:After bloodletting puncture,the survival time of the rats was prolonged,their brain water content and brain coefficient were reduced,and brain density was increased.CONCLUSION:Bloodletting puncture at Jing-Well points in the distal ends of the finger and toe can improve function in ischemic brain edema.     

21-氨基类固醇类药物U-74389G对创伤性脑水肿的影响

目的：探讨21-氨基类固醇类药物U-74389G对脑外伤后脑水肿和离子含量的影响。方法：分别采用干/湿质量法测定伤后脑含水量,原子吸收光谱分析法测定脑组织内离子含量。结果：伤侧脑组织含水量外伤组较对照组显著增加,但治疗组含水量比外伤组又显著降低。Na+、Ca2+含量外伤组较对照组明显增加,但治疗组比外伤组显著降低;K+、Mg2+含量外伤组较对照组明显降低,但治疗组较外伤组有不同程度的升高。结论：U-74389G能有效地减轻脑外伤后脑水肿