尼莫地平、别嘌呤醇对完全性脑缺血后脑血流和氧耗影响的实验研究

２４只健康杂种犬随机平分为四组，单纯缺血组，尼莫地平组，别嘌呤醇组和复合治疗组。各治疗组在完全性脑缺血２０分钟后即刻，静注２０ｕｇ／ｋｇ尼莫地平或别嘌呤醇 ２０ｍｇ／ｋｇ，观察再灌注期间脑血流及氧耗的变化。研究结果显示，各治疗组脑血流量在再灌注期间明显增加，５～３０分钟时达最大值。随时间延长，脑血流量逐渐减少。再灌注初期，脑血管阻力明显降低。随后，脑血管阻力逐渐增加。脑组织可供氧量、矢状窦氧分压与脑血流量变化一致，脑组织氧耗变化不显著。本研究表明，尼莫地平。别嘌呤醇可以改善完全性脑缺血后微循环障碍，增加脑血流和可供氧量。两种药物可部分地发挥协同治疗作用。     

尼莫地平和别嘌呤醇对缺血后微循环血液流变学的影响

完全性脑缺血后，常常出现血液流变学变化，直接影响脑组织血流灌注。本研究选择钙拮抗药尼莫地平和自由基清除药别嘌呤醇对完全性脑缺血后脑矢状窦血液流变学变化，为脑复苏治疗提供实验依据。材料与方法２４只健康杂种犬，体重１０～１８ｋｇ，随机分为四组，缺血组（Ⅰ组）、尼莫地平治疗组（Ⅱ组）、别嘌呤醇治疗组（Ⅲ组）以及两种药物复合治疗组（Ⅳ组）。采用闭塞双侧颈总动脉和椎动脉伴体循环控制性降压技术复制的完全性脑缺血模型，缺血时限为２０分钟。尼莫地平及别嘌呤醇静脉注射用量为２０ｇ／ｋｇ和２０ｍｇ／ｋｇ。分别于缺血…     

大鼠肝脏缺血再灌注及低温保存过程中氧自由基变化的实 …

目的 观察大鼠肝脏缺血再灌注及低温保存过程中氧自由基的变化。方法 建立大鼠肝脏假手术、热缺血再灌注和原位肝移植模型,分别测定再灌注１ｈ和移植术后２ｈ下腔静脉血中超氧化物歧化酶（ＳＯＤ）、乳酸脱氢酶（ＬＤＨ）和血清中指质过氧化物（ＬＰＯ）的变化,并进行组织学观察。结果 术前３０ｍｉｎ静脉注射别嘌呤或灌洗液及保存液中加别嘌呤的实验组大鼠,其全血中ＳＯＤ的活力高于条件相同、但不给予别嘌醇的对照组,ＬＰＯ     

肢体缺血再灌注导致脂质过氧化增强和血栓素A2合成增加的研究

骨骼肌缺血再灌注可导致肌肉微血管的实质损伤，观察了肌肉缺血再灌注时脂质过氧化物（ＬＰＯ）和ＴｘＡ２与ＰＧＩ２的代谢状况。缺血组家兔（ｎ＝６）。双后肢缺血２小时。再灌注２小时后，左股薄肌丙二醛（ＭＤＡ）含量，下腔静脉血ＭＤＡ和乳酸浓度均显著高于对照组（ｎ＝６）。再灌注后１０和３０分钟，缺血组血中ＴｘＢ２水平和ＴｘＢ２／６－ｋｅｔｏ－ＰＧＦ１ａ比率明显增高，再灌注后血中ＳＯＤ活性和６－ｋｅｔｏ－ＰＧＦ     

改良的St.Thomas停跳液对未成年兔心肌的保护作用

目的 探讨不同停跳液对未成年兔心肌缺血再灌注损伤的保护作用。方法 应用离体心脏工作模型对１６只未成年兔心脏灌注改良的Ｓｔ．ＴｈｏｍａｓＮｏ１停跳液（Ａ组）及改良的Ｓｔ．ＴｈｏｍａｓＮｏ２停跳液（Ｂ组）,观察经１５℃缺血１２０ｍｉｎ再灌注６０ｍｉｈ后兔心功能恢复情况。结果 离体心脏再灌注后,１５℃血２ｈ条件下,Ｂ组心功能恢复明显好于Ａ组,而心肌含水率,冠脉漏出液的肌酸磷酸激酶及乳酸脱氢酶及心肌细胞超     

体外循环下心肌缺血再灌注后血清心肌酶,SOD活性变化及复方…

２０例先天性室内隔或房间隔缺损患者，ＡＳＡⅡ￣Ⅲ级，麻醉后随机分为两组，组Ｉ为对照组（ｎ＝１０），组Ⅱ为复方丹参治疗组（ｎ＝１０）。组Ⅱ于手术开始前及复温后心脏复跳前分别静脉注射复方丹参２００ｍｇ／ｋｇ。结果表明，组Ｉ缺血（Ｔ２）及再灌注后各期血清乳酸脱氢酶（ＬＤＨ）、肌酸激酶（ＣＫ）与术前（Ｔ０）比较显著增高，而超氧化物岐化酶（ＳＯＤ）明显下降，与组Ⅱ各时期值有显著差异，且术后心功能恢复较组Ⅱ差     

亚低温对慢性脑缺血再灌注大鼠脑氧代谢的影响

目的 评价亚低温对慢性脑缺血再灌注大鼠脑氧代谢的影响.方法 健康清洁级雌性SD大鼠12只,体重170～210 g,随机分为2组(n=6):常温再灌注组(NT组)和低温再灌注组(MH组).采用右侧颈总动脉与右侧颈外静脉端端吻合建立大鼠脑缺血再灌注模型.缺血6周后,恢复血流灌注,同时NT组采用可控性保温垫维持直肠温37℃,MH组喷洒乙醇行全身物理降温,并通过可控性保温垫维持直肠温32℃.直肠温恒定至再灌注3 h时自然复温.于再灌注前即刻(T_1)、再灌注即刻(T_2)和再灌注24 h时(T_3)行激光多普勒血流灌注成像,记录脑血流灌注量;同时采集股动脉和上矢状窦静脉血样,行血气分析,计算动脉-静脉血氧饱和度差、脑氧摄取率和动脉.静脉血乳酸浓度差.结果 与T_1时比较,NT组T_2时对侧、T_3时双侧脑血流灌注量降低,T_3时动脉-静脉血乳酸浓度差降低,MH组T_2和T_3时实验侧和对侧脑血流灌注量降低,T_2时脑氧摄取率降低(P<0.05或0.01);与NT组比较,MH组脑血流灌注量降低,再灌注即刻脑氧摄取率和动脉-静脉血乳酸浓度差降低(P<0.05),动脉.静脉血氧饱和度差差异无统计学意义(P>0.05).结论 亚低温有利于维持慢性脑缺血再灌注大鼠脑组织氧供需平衡.     

纳络酮对乳猪不完全性脑缺血缺氧的影响

１５只乳猪随机分为三组，正常对照组，缺血缺氧模型组和纳络酮治疗组。观察脑组织乳酸，葡萄糖，超氧化物歧化酶（ＳＯＤ），脂质过氧化物（ＬＰＯ）和形态学改变。结果显示：（１）模型组乳酸和ＬＰＯ明显高于对照组，葡萄糖和 ＳＯＤ明显低于对照组；（ ２）治疗组葡萄糖和 ＳＯＤ明显高于模型组，乳酸明显低于模型组，ＬＰＯ未见明显改变；（３）病理学观察发现模型组严重水肿、出血、变性甚至坏死。治疗组水肿和出血较轻，未见坏死性改变。提示，纳络酮对不完全性脑缺血缺氧具有治疗作用，纳络酮对缺血缺氧脑的保护作用可能与自由基清除有关。     

一氧化氮供药减轻大鼠移植肝保存再灌注损伤

目的 研究一氧化氮供体药硝酸甘油（ＮＴＧ）对大鼠移植肝再灌注损伤的影响。方法 用０～４℃含或不含ＮＴＧ１０ｕｇ／ｍｌ的乳酸林格液灌洗及保存肝脏４ｈ后行原位肝移植，观察再灌注１０ｍｉｎ，２ｈ受体鼠血清氨基丙酸转氨酶（ＡＬＴ）、天冬氨酸转氨酶（ＡＳＴ）、乳酸脱氢酶（ＬＤＨ）；再灌注１ｈ，２ｈ的胆汁分泌量；再灌注２ｈ组织环到鸟苷（ｃＧＭＰ）含量；大于１ｄ和７ｄ的大鼠生存率。结果 再灌注１０ｍｉｎ血清ＡＳ     

大鼠上矢状窦闭塞模型脑血流和脑组织血氧饱和度的变化

目的　探讨大鼠上矢状窦闭塞模型脑血流与脑组织血氧饱和度的变化。方法　利用大鼠上矢状窦闭塞模型 ,激光多谱勒扫描法测定脑表 2 5处局部脑血流 (lCBF)和脑组织血氧饱和度 ,以 2 5处lCBF的中位数代表区域脑血流 (rCBF)。荧光血管造影技术检测上矢状窦闭塞情况和血栓扩展情况。大鼠分为以下 3组 :A组 ,对照组 (n =5 ) ;B组 ,上矢状窦结扎组 (n =8) ;C组 ,上矢状窦结扎加上矢状窦内注入血栓形成因子 (n =10 )。结果　C组上矢状窦结扎加上矢状窦内注入血栓形成因子后rCBF与脑组织血氧饱和度明显降低 (P <0 .0 5 ) ,B组上矢状窦结扎后rCBF降低(P <0 .0 5 ) ,15min后又恢复到结扎前水平。B组的平均动脉压较A、C组增高 15 %左右 (P <0 .0 5 )。结论　急性上矢状窦闭塞血栓扩展到脑皮层静脉后rCBF和脑组织血氧饱和度降低 ,脑血管造影及rCBF和脑组织血氧饱和度监测可早期诊断上矢状窦闭塞 ,提升脑灌注压可以延长静脉窦血栓形成的治疗时间窗。     

Effects of hyperglycemia and effects of ketosis on cerebral perfusion, cerebral water distribution, and cerebral metabolism

Diabetic ketoacidosis (DKA) may cause brain injuries in children. The mechanisms responsible are difficult to elucidate because DKA involves multiple metabolic derangements. We aimed to determine the independent effects of hyperglycemia and ketosis on cerebral metabolism, blood flow, and water distribution. We used magnetic resonance spectroscopy to measure ratios of cerebral metabolites (ATP to inorganic phosphate [Pi], phosphocreatine [PCr] to Pi, N-acetyl aspartate [NAA] to creatine [Cr], and lactate to Cr) and diffusion-weighted imaging and perfusion-weighted imaging to assess cerebral water distribution (apparent diffusion coefficient [ADC] values) and cerebral blood flow (CBF) in three groups of juvenile rats (hyperglycemic, ketotic, and normal control). ATP-to-Pi ratio was reduced in both hyperglycemic and ketotic rats in comparison with controls. PCr-to-Pi ratio was reduced in the ketotic group, and there was a trend toward reduction in the hyperglycemic group. No significant differences were observed in NAA-to-Cr or lactate-to-Cr ratio. Cortical ADC was reduced in both groups (indicating brain cell swelling). Cortical CBF was also reduced in both groups. We conclude that both hyperglycemia and ketosis independently cause reductions in cerebral high-energy phosphates, CBF, and cortical ADC values. These effects may play a role in the pathophysiology of DKA-related brain injury.     

Association of cerebral arteriovenous malformation and cerebral aneurysm. Diagnosis and management

Summary Between 1979 and 1989, 7 patients were admitted, with cerebral arteriovenous malformations (AVM) and associated aneurysms (7% of the AVM patients and 2% of the aneurysm patients admitted during the same period). 6 of these patients were admitted because of an intracranial haemorrhage (in 3 of them the AVM, angiographically occult, was discovered at surgery). The last patient was referred for seizures.Preoperatively it was supposed that the haemorrhage was related to the aneurysm in 3 cases, and to the AVM in 3 cases. But surgery allowed one to correct this supposition. Haemorrhage was due to AVM rupture in all 6 cases, and no aneurysm had ruptured. Overall three situations were demonstrated in this series: aneurysm and occult AVM (3 cases); AVM and independent aneurysm in the same area (2 cases); large AVM and aneurysm on a feeding artery (2 cases). All 6 patients admitted for haemorrhage were operated upon, at one operation in 5 of them. Both the malformations were excluded in these six patients. For the patient admitted for seizure, intra-vascular embolization of the AVM was performed, the aneurysm was not treated. The pathogenesis of the association AVM-aneurysm is discussed. In the authors' opinion, haemodynamic relationship should be considered in two cases (large AVM and aneurysm on a feeding vessel). For the other 5 cases, both the AVM and the coexisting aneurysm may be the end-result of a common congenital vascular malformation syndrome.     

HIV and cerebral aneurysms

Patients infected with the human immunodeficiency virus (HIV) or suffering from acquired immunodeficiency syndrome (AIDS) are now surviving for longer periods of time secondary to improvements in medical management. As the classical causes of morbidity and mortality in this patient population have come under better control, new complications are becoming more prevalent. In our clinical practice, there appears to have been a rise in the number of patients with HIV infection and AIDS who have experienced aneurysmal subarachnoid hemorrhage (SAH). In this paper, we review the available literature regarding cerebral aneurysms in patients infected with HIV and/or suffering from AIDS.