急性心肌缺血时红细胞变形性的变化及其机理

本实验观察了犬急性心肌缺血时体循环血与缺血区局部静脉血中红细胞变形性（ＲＣＤ）的变化。结果表明，阻断冠脉血流后高切变率下全血粘度（ηｂｈ）和红细胞刚性指数（ＥＲＩ）明显增高，而缺血区局部血液中此二者的变化明显大于体循环静脉血。事先切断内脏大神经，可使阻断冠脉后体循环血（而不是局部静脉血）的ηｂｈ和ＥＲＩ变化基本消失。缺血区局部血液ｐｈ和ｐＯ２明显降低，ｐＣＯ２明显增高，红细胞内ＡＴＰ含量减少和钙含     

Neuroprotection with felbamate: a 7- and 28-day study in transient forebrain ischemia in gerbils

The use of glutamate antagonists and GABA agonists may protect neurons from the effects of transient ischemia. Felbamate is a new antiepileptic drug with glutamate antagonist and GABA agonist properties, We tested the efficacy of felbamate in a gerbil model of transient forebrain ischemia. Damage assessment was done with silver staining at 7 and 28 days after 5 min of bilateral carotid occlusion, Cerebral cortex, hippocampus (CA1 and CA4), thalamus and striatum were evaluated on a 4-point scoring system, The animals sacrificed at 28 days were also tested in a water-maze task to assess recovery of function, The initial dose of felbamate (300 mg/kg) was given 30 min before the ischemic insult in one set of animals and 30 min after the insult in another set of animals. There were 8 animals tested per group (total: 48 animals). There was significant neuronal protection with the use of felbamate, both before and after ischemia in all regions of the brain. Protection was seen in animals sacrificed at 7 and 28 days, Protection was moderate when felbamate was used before ischemia. It was highly significant when felbamate was given 30 min after the insult. Behavioral studies however did not show any difference in the felbamate treated animals versus the saline treated controls. The structural protection with felbamate was very significant when used in the post-ischemic period. This window for protection merits further evaluation in relation to the clinical setting of stroke.     

凋亡敏感基因在短暂性缺氧再复氧复注血清后的大鼠星形胶质细胞中的表达及其意义

目的研究一种新发现的抗氧化蛋白质--凋亡敏感基因(SAG)在短暂性缺氧再复氧复注血清诱导的细胞坏死和凋亡中的作用.方法用短暂性缺氧再复氧复注血清来诱导原代培养的大鼠大脑皮质星形胶质细胞损伤,用免疫细胞化学方法检测凋亡敏感基因的表达,并作图像分析;用流式细胞仪检测胶质细胞在短暂缺氧再复氧复注血清后不同时间点的凋亡率.结果凋亡敏感基因在缺氧15 min再复氧复注血清5 h后表达最高,在复氧复注血清16 h后恢复至对照组水平;细胞凋亡率在缺氧15 min再复氧复注血清1h时达到最高,而在再复氧复注血清5 h后降至对照组水平.结论凋亡敏感基因具有抗凋亡的作用,可减轻星形胶质细胞的缺血再灌注损伤.     

地塞米松对缺血再灌注鼠视网膜电图的影响

目的观察地塞米松对大鼠视网膜缺血再灌注损伤 (retinalischemiareperfusion ,RIR)视网膜电图 (ERG)的影响。方法应用前房灌注液体升高眼内压的方法 ,建立RIR模型 ,并随机分为防治组和对照组 ,防治组大鼠地塞米松用药从缺血前 6天开始 ,剂量为 1mg/kg ,溶于 1ml生理盐水中腹腔注射 ,给药持续 8天 ,对照组用同体积的生理盐水代替。两组缺血 60分钟后分别再灌注 3 0分钟、2 4小时、72小时 ,进行视网膜电图。结果防治组ERG标化b波振幅显著高于对照组 (P <0 .0 1 )。结论地塞米松对RIR有一定防治作用     

负压对缺血肢体血流动力学影响的实验研究

目的：观察负压对肢体动脉闭塞犬患肢血流动力学的影响。方法：犬15只，随机分治疗组10只和对照组5只。两组均采用切断犬后肢股动脉分支、动脉腔内置入螺旋状金属丝的方法，制作肢体缺血模型。在模型制作后2wk，治疗组行患肢负压治疗10d，对照组不做负压治疗。两组均于模型前、模型后2wk及治疗结束后，用彩色多普勒观察患肢股动脉血流动力学指标：收缩期最大流速(Vmax)、平均流速(Vmean)、阻力指数(R1)、搏动指数(P1)的变化。结果：治疗组在治疗后患肢股动脉Vmax、Vmean显著增加(P＜0．001)，RI、PI显著降低(P＜0.01)；对照组各指标无明显变化(P＞0．05)。结论：负压对缺血肢体血流动力学表现为流速增加，阻力下降。     

黄连素对缺血再灌注心肌细胞损伤的保护作用

目的　研究黄连素对新生大鼠心肌细胞缺血再灌注损伤的保护作用。方法　取体外培养的新生大鼠心肌细胞于缺氧 2 4h复氧 1h造成缺血再灌注 ( I/ R)模型 ,观察细胞损伤情况 ;并将黄连素以 1.5× 10 - 6 m ol/ L、1.5× 10 - 5m ol/ L、1.5× 10 - 4 mol/ L 三种浓度分别加入培养基中 ,预处理 2 4h后 ,再置于上述缺氧复氧环境中培养 ,检测以上不同条件下细胞上清液中的乳酸脱氢酶 ( L DH)、丙二醛 ( MDA)、超氧化物歧化酶 ( SOD)含量 ,并检测各组细胞的凋亡率。结果　与正常对照组相比 ,缺血及再灌组细胞上清液中 L DH、MDA含量明显升高 ( P<0 .0 1) ,SOD活力则显著降低 ( P<0 .0 1) ,缺血组和再灌组凋亡率均升高明显 ( P<0 .0 1)。而用黄连素预处理后缺血及再灌组的 L DH、MDA显著低于用药前 ( P<0 .0 1) ,SOD则高于单纯缺血和再灌组 ( P<0 .0 1) ,上述作用在本实验黄连素浓度为 1.5× 10 - 6 m ol/ L～ 1.5× 10 - 4 mol/ L 范围内 ,随浓度升高而更加明显。特别是用黄连素 1.5× 10 - 5mol/ L 浓度预处理后 ,缺血组和再灌组的细胞凋亡率分别是 14.4%和 2 0 % ,分别与用药前 ( 17.4%和 41% )比较有显著性差异 ( P<0 .0 1)。结论　黄连素对缺血再灌心肌细胞有保护作用 ,其作用与浓度有一定依赖关系     

Compartment syndrome. Exclusively the result of increased pressure in the muscular compartment?

Summary The compartment syndrome (cs) is characterized by an increased tissue pressure in a limited space. Pathophysiologically, it is a multifactorial disease that is potentially induced by an initial trauma and develops according to the existence of cofactors. Cofactors are, for instance, the circulation of the patient and the initial treatment of the impending cs. In particular, the microcirculation is altered with endothelial destruction, development of a capillary leak, protein loss from intravasal space and the development of an interstitial and intracellular third space. An impaired drainage of the lymphatic and venous system causes a venous infarction. An arterial infarction results if the tissue pressure exceeds the arteriolar pressure. An accompanying ischemia reperfusion mechanism increases the trauma load. In disadvantageous cases, the patients are in danger of developing a multi-organ deficiency syndrome (MODS) by an uncontrolled inflammatory reaction, by intravasal volume loss and by a myonephropathic systemic reaction. Clinically, the patients suffer a disproportionate amount of pain, followed by neurological signs. Especially in noncompliant patients, tissue pressure measurement is useful. Resuscitation of the circulation as well as splitting of casts is important. In case of a manifest cs, dermatofasciotomy has to be performed as an emergency operation. Even if cs is diagnosed early and fasciotomy is carried out early, the development of sequellae cannot be avoided in every single case.      

Opiate receptor subtype binding in gerbil hippocampus is altered by forebrain ischemia

A role for endogenous opioids in trauma-induced brain injury has been supported by pharmacological studies. The present series of experiments were initiated to extend these observations by measuring opiate receptor subtype binding in gerbil hippocampus following 7 days recovery from a 10 min ischemic insult. Quantitative in vitro autoradiography was utilized to measure mu [( 3H]DAGO), kappa [( 3H]bremazocine + 10 microM morphiceptin + 100 nM DSLET), delta [( 3H]DSLET + 10 microM morphiceptin) and lambda [( 3H]naloxone + 300 nM diprenorphine) binding. While ischemic tissue samples at the level of the dorsal hippocampus showed complete loss of CA1 pyramidal cells, we observed no significant alterations in mu or delta binding suggesting a non-pyramidal cell localization of these receptors. Kappa binding decreased significantly to 88% of control in the CA1 and CA3 regions while lambda binding in the stratum lucidum (CA3) increased to 165% of control. Our results show that opiate receptor subtypes are differentially affected by an ischemic insult.     

茶氨酸对脑缺血再灌注损伤保护作用的实验研究

目的观察茶氨酸对脑缺血再灌注损伤的保护作用,为临床脑缺血再灌注损伤的预防和治疗提供实验依据。方法将24只健康家兔随机分为四组：假手术组、脑缺血组、茶氨酸予处理组和茶氨酸治疗组。麻醉后分离血管,采用基底动脉、双侧颈总动脉结扎法制备急性全脑缺血再灌注动物模型。假手术组仅分离动脉不结扎,予处理组在缺血前应用茶氨酸,治疗组在缺血后应用茶氨酸,缺血组不作特殊药物处理。各组分别在规定时间点即缺血前、再灌注后30min、1h、2h采血测定神经特异性烯醇化酶(NSE)含量,取脑组织活检观察超微结构,处死动物测定脑含水量。结果茶氨酸予处理组和治疗组以上各项指标均较脑缺血组有显著的改善,提示茶氨酸具有神经保护作用。实验还显示茶氨酸予处理组在再灌注30min时NSE含量与假手术组比较无差异,提示用茶氨酸予处理后可能使缺血后脑损害的发生延迟,为进一步的治疗争取了宝贵时间。结论茶氨酸对脑缺血再灌注损伤有保护作用,值得进一步研究。     

丹参及血管内皮生长因子对动物肢体缺血模型侧支循环建立的作用

目的 :建立兔左后肢无主干及分支动脉供血的缺血模型 ,并观察丹参及血管内皮生长因子 ( VEGF)对兔后肢缺血模型侧支循环建立的作用。方法 :通过手术方法在兔后肢大腿段建立一个无主干及分支动脉供血的严重缺血模型。动物随机分为 5组 :未治疗组、丹参组、VEGF组、丹参加VEGF组及生理盐水对照治疗组。在解剖及生理水平上观察各组动物缺血肢体缺血及侧支循环建立情况。结果 :术后第 1天未治疗组动物左 /右小腿血压比为 0 ;动脉造影显示左侧只有髂外动脉中段以上显影、以下主干及分支均未显影。对侧后肢主干及分支动脉显影良好 ,即左侧毛细血管密度( 4 9.8± 1 7.6)个 /mm2 ,右侧为 ( 385 .7± 36.7)个 /mm2 ,P<0 .0 0 1 ;毛细血管数 /肌束数比值 :左侧( 0 .2 1± 0 .0 7) ,右侧 ( 0 .98± 0 .0 5 ) ,P<0 .0 0 1。治疗结束时 ,丹参加 VEGF组动物小腿血压比最高( 0 .74± 0 .1 7) ,它显著高于对照组、丹参组和 VEGF组 ;毛细血管密度与毛细血管数 /肌束数比值亦以丹参加 VEGF组为最高 ;动脉造影显示 ,丹参加 VEGF组中缺血组织处具有治疗意义的粗大的侧支循环形成。结论 :丹参与 VEGF联合应用具有强大的促进缺血模型侧支循环建立的作用