一氧化氮与肺缺血再灌注损伤的研究进展

一氧化氮（nitricoxide，NO）是一种活性很强的自由基，具有广泛的生物学活性。多项研究提示NO在急性肺缺血／再灌注（ischemia／reperfusion，I／R）损伤中具有重要作用。本文重点描述有关一氧化氮在肺I／R损伤中作用的研究进展。     

P38MAPK抑制剂对缺血/再灌注大鼠肾脏功能损伤的保护作用

目的：观察P38MAPK抑制剂对缺血／再灌注大鼠肾脏功能损伤的保护作用。方法：夹闭肾动脉制遣大鼠肾脏缺血／再灌注损伤动物模型，静脉注射P38MAPK抑制剂阻断P38MAPK信号转导通路，测量其对肾功能及细胞因子含量的影响。结果：肾脏和血浆中TNF—α和IL-β含量随缺血／再灌注时间的延长而升高，肾功能损伤也随缺血／再灌注时间的延长而加重。应用P38MAPK抑制剂可显著降低TNF-α和IL-β含量，对缺血／再灌注所致的肾功能损伤具有明显改善作用。结论：P38MAPK抑制剂可通过抑制致炎因子的产生而减轻缺血/再灌注所致的大鼠肾脏功能损伤。     

预防性应用钙拮抗剂对缺血大鼠心肌细胞和红细胞内钙变化的影响

利用大鼠缺血模型观察预防性应用钙桔抗剂尼莫地平对大鼠缺血心肌和红细胞内钙的影响发现，缺血时大鼠心肌细胞、心肌组织和红细胞内均有钙积聚，红细胞膜钙泵活性下降；缺血前30分钟给予尼莫地平可使红细胞内钙恢复至正常水平，红细胞膜钙泵活性升高；心肌细胞和心肌组织内钙虽较缺血鼠降低，但仍高于对照组。提示：（1）缺血时细胞的钙内流可能是全身性的；（2）预防性应用尼莫地平可阻滞或减轻细胞内钙超载，同时还可保护细胞膜膜泵活性。     

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.