静脉滴注尼莫地平治疗急性缺血性脑梗死

发病72h内的急性缺血性脑梗死60例,分为2组。尼莫地平组30例(男性21例,女性9例;年龄59±s10a)。wk1.2给支持疗法(脱水剂,维生素C等)和尼莫地平2mg/d于5％葡萄糖液500ml内静脉滴注。wk3.4改用扩容、改善微循环,细胞活性药。wkl-4口服尼莫地平60mg.qn。对照组30例(男性23例,女性7例;年龄58±9a)。不给尼莫地平,其余同上。4wk后,前组神经功能缺损积分值较后组下降显著(P相似文献   

银杏叶提取物对兔心肌缺血再灌注损伤时中性粒细胞活化的影响

目的 观察兔心肌缺血再灌注前后ＰＭＮ（中性粒细胞）的活性变化过程。了解银杏叶提取物保护心肌是否与影响中性粒细胞活化作用有关。方法 取３０只日本大耳白兔随机均分为３组,假手术对照组、缺血再灌注组和实验用药组。用药方法：用自制的银杏叶提取物注射剂（总黄酮含量５ｍｇ／ｍｌ）５ｍｌ静滴给药。分别于冠脉结扎前和结扎缺血１ｈ后采血用布式显微镜观察白细胞活化状态的变化。检测白细胞表面粘附分子ＣＤ１１／ＣＤ１８表     

Role of reactive oxygen in phospholipase A2 activation by ischemia/reperfusion of the rat kidney

Purpose. To investigate the role of phospholipase A₂ (PLA₂) in reperfusion injury of the kidney in an in vivo animal model, renal mitochondrial PLA₂ activity was measured under three different conditions. Methods. Male Wistar rats (n = 72) anesthetized with pentobarbital underwent renal ischemia surgically for 45 min and were reperfused for the indicated time (renal ischemia/reperfusion). Treatments included reperfusion for various predetermined periods (phase 1), exposure to hyperbaric oxygen (phase 2), and administration of reactive oxygen species (ROS) scavenger (phase 3). Thereafter, each kidney was harvested, and mitochondrial PLA₂ activity was measured by a radioisotope technique. Results. Ischemia/reperfusion resulted in time-related PLA₂ activation in the renal mitochondria up to 48 h of reperfusion after renal ischemia. Renal mitochondrial PLA₂ activity was further augmented by hyperbaric oxygen exposure prior to reperfusion, whereas administration of the ROS scavengers suppressed mitochondrial PLA₂ activity. Conclusion. These data suggest that ROS may play an important role in the in vivo activation of PLA₂ associated with renal ischemia/reperfusion. Received for publication on July 6, 1998; accepted on November 30, 1998     

Effect of intracerebral norepinephrine depletion on outcome from severe forebrain ischemia in the rat

Manipulations of plasma catecholamine concentrations influence outcome from ischemic brain insults. It has been suggested that these effects are mediated by influences on brain catecholamine concentrations. This study examined whether major changes in brain norepinephrine concentrations can alter outcome from severe forebrain ischemia. Sprague-Dawley rats were administered 50 mg/kg i. p. N-(chloroethyl)-N-ethyl-2-bromobenzylamine (DSP-4) or were left untreated (control). One week later, these rats were subjected to either 7 or 8 min of normothermic forebrain ischemia (bilateral carotid occlusion and MABP=30 mmHg) and allowed to recover for 4 days. Histologic damage was then evaluated. In other control and DSP-4-treated animals, hippocampal microdialysate norepinephrine concentrations were measured before, during and after 8 min of forebrain ischemia. Norepinephrine concentrations were also determined in brain homogenates from non-ischemic DSP-treated and control rats. A 95% depletion of norepinephrine was observed in brain homogenates from non-ischemic DSP-4-treated rats compared with control. During ischemia, microdialysate norepinephrine concentrations increased in control but not in DSP-4-treated rats (P=0.002). For plasma, intra-ischemic epinephrine concentrations increased 8-10-fold and returned to baseline values post-ischemia with no differences between groups. Plasma norepinephrine values remained unchanged in both groups. Histologic damage resulting from either 7 or 8 min of ischemia in hippocampal structures, caudoputamen, and neocortex was similar between DSP-4-treated and control groups. This study could not identify any effect of major changes in brain norepinephrine concentrations on ischemic brain damage. These data indicate that peripheral catecholamine effects on near-complete forebrain ischemic outcome are unlikely to be mediated by effects on central catecholamine concentrations.     

氯沙坦对在体实验性大鼠心肌缺血再灌注诱导的心肌细胞凋亡及基因表达影响的研究

目的　研究氯沙坦对大鼠在体心肌缺血再灌注后细胞凋亡的影响及bcl 2和bax基因表达。方法　采用末端标记、原位杂交、免疫组织化学 3种方法分别检测细胞凋亡、基因表达产物的mRNA和蛋白质 ,通过图像分析系统测量阳性染色区域的平均吸光度对原位杂交和免疫组织化学检测物质进行量化处理。结果　细胞凋亡数目手术对照组为 (38± 9)个 /HP ,假手术组为 (0～ 1 )个 /HP ,药物治疗组为 (9± 4)个 /HP ,各组间差异有非常显著性 (P <0 0 0 1 ) ;原位杂交bcl 2手术对照组为 0 0 75± 0 0 2 0 ,假手术组为 0 0 60± 0 0 1 0 ,治疗组为 0 0 76±0 0 1 4 ,免疫组织化学bcl 2手术对照组为 0 1 37± 0 0 1 4 ,假手术组为 0 0 85± 0 0 1 9,治疗组为 0 1 2 5± 0 0 2 1 ,对照组、治疗组的升高与假手术组之间差异有显著性 (P <0 0 5) ,治疗组和对照组之间差异无显著性 (P >0 1 ) ;免疫组织化学bax手术对照组为 0 0 97± 0 0 2 2、假手术组为 0 0 62± 0 0 1 4、治疗组为 0 0 62± 0 0 1 4 ,对照组的升高与治疗组、假手术组间差异有非常显著性 (P <0 0 0 1 ) ,治疗组和假手术组之间差异无显著性 (P >0 9) ;bcl 2 /bax比值手术对照组为 1 41 3 ,假手术组为 1 376 ,治疗组为 2 0 1 6。结论　氯?     

股骨头缺血性坏死的介入治疗

目的 探讨介入治疗股骨头缺血性坏死的临床效果。方法 对13例16髋股骨头缺血性坏死．经患髋的旋股内、外动脉或闭孔动脉灌注溶栓药物及血管扩张药物等。结果 随访3～6个月．髋关节疼痛消失6髋，减轻8髋；功能恢复5髋，功能改善8髋。结论 介入治疗股骨头缺血性坏死，能改善股骨头血液循环，能有效地改善临床症状和髋关节的活动功能，其创伤小且安全可靠。     

常温下肝脏缺血/再灌注损伤及其机制的实验研究

目的　研究常温下肝脏缺血 /再灌注损伤及其机制。方法　 2 4只兔随机均分为缺血组和对照组。组织气体分析仪持续测定兔肝组织氧压 (HepatictissueoxygeonpressurePtiO2 ) ;光镜及电镜观察肝脏组织病理改变 ;全自动生化仪测定血清丙氨酸氨基转氨酶 (ALT)。结果　缺血组兔肝脏在缺血后肝PtiO2 值开始下降、30min降至 2 0 1± 2 8,再灌注后的肝PtiO2 值开始恢复 ,再灌注 6 0min肝PtiO2 未恢复正常 (P <0 0 5 )。肝细胞出现变性、坏死 ,血清ALT值显著升高 ,在肝脏再灌注 6 0min时最为严重。结论　常温下用Pringle氏法阻断入肝血流可导致肝脏缺血/再灌注后肝细胞功能障碍和病理损害。其作用机制与缺血期肝细胞缺氧、再灌注期肝脏微循环障碍和肝细胞线粒体的损伤有关。     

电针预处理对兔脊髓缺血再灌注损伤细胞内Ca~(2 )变化的影响

目的 :探讨重复电针预处理诱导缺血耐受对脊髓缺血再灌注损伤保护作用的机制。方法 :76只雄性新西兰大白兔随机分成 4组 :对照组 (C组 ) ,戊巴比妥钠组 (SP组 ) ,假手术组 (S组 ) ,电针预处理组 (EA组 )。最后一次预处理后 2 4h ,阻闭肾下腹主动脉 ,制作兔脊髓缺血模型 ;S组动物手术操作同C组 ,但不阻闭腹主动脉。分别于阻闭后不同时相点测定细胞内Ca2 含量 ,并分别对动物后肢运动功能评分。结果 :EA组脊髓组织细胞内Ca2 含量显著低于C组和SP组各时相值 (P <0 0 1) ,神经功能评分EA组明显高于C组 (P <0 0 1) ,C组和SP组细胞内Ca2 和神经功能评分无显著性差异 (P >0 0 5 )。结论 :电针预处理具有降低脊髓组织细胞内Ca2 含量 ,防止Ca2 超载 ,稳定细胞内环境的能力 ,对腹主动脉阻断所致的脊髓缺血再灌注损伤具有良好的保护作用。     

丹参注射液加强缺血预处理对大鼠心肌的保护作用

以整体麻醉SD大鼠心脏冠状动脉左前降支结扎／松开作为缺血／再灌注动物模型，研究丹参注射液（SM）在加强缺血须处理（IP）的心肌保护中的作用。结果显示，IP能减轻复灌性心律失常的严重程度，缩小心肌梗死范围；SM能缩小心肌梗死范围；SM联合IP与单纯IP比较，心肌梗死范围进一步缩小；SM联合IP与单纯SM比较，心律失常严重程度减弱且心肌梗死面积进一步减小。结果表明，SM能加强IP的心肌保护作用，特别是加强IP的抗心肌梗死作用。