Pretreatment with Tongxinluo protects porcine myocardium from ischaemia/reperfusion injury through a nitric oxide related mechanism

Background The traditional Chinese medicine Tongxinluo can protect myocardium against ischaemia/reperfusion injury, but the mechanism of its action is not well documented. We examined the involvement of nitric oxide in the protective role of Tongxinluo. Methods Miniswine were randomized to four groups of seven: sham, control, Tongxinluo and Tongxinluo coadministration with a nitric oxide synthase inhibitor Nω-nitro-L-arginine (L-NNA, 10 mg/kg i.v.). Three hours after administration of Tongxinluo, the animals were anaesthetised and the left anterior descending coronary artery ligated and maintained in situ for 90 minutes followed by 3 hours of reperfusion before death. Area of no reflow and necrosis and risk region were determined pathologically by planimetry. The degree of neutrophil accumulation in myocardium was obtained by measuring myeloperoxidase activity and histological analysis. Myocardial endothelial nitric oxide synthase activity and vascular endothelial cadherin content were measured by colorimetric method and immunoblotting analysis respectively.Results Tongxinluo significantly increased the local blood flow and limited the infarct and size of no reflow. Tongxinluo also attenuated myeloperoxidase activity and neutrophil accumulation in histological sections and maintained the level of vascular endothelial cadherin and endothelial nitric oxide synthase activity in the reflow region when compared with control group. The protection of Tongxinluo was counteracted by coadministration with L-NNA. Conclusions Tongxinluo may limit myocardial ischaemia and protect the heart against reperfusion injury. Tongxinluo regulates synthesis of nitric oxide by altering activity of endothelial nitric oxide synthase.     

Release of chemoattractants and neutrophil activation in acute myocardial infarction immediately after successful recanalization of the infarct-related vessel by angioplasty

The study investigated inflamatory responses in evolving myocardialinfarction. Fifteen patients with acute myocardial infarction,who had undergone balloon recanalization of the infarct-relatedcoronary artery within 4 h after onset of symptoms, were examined.Blood samples were obtained through the guiding catheter andfrom the pulmonary artery before and immediately after successfulrecanalization. After recanalization, plas from the pulmonaryartery was 47% (quartiles: l9%, 78; P =0·001) more chemotacticto neutrophils from normal donors than before recanalization.Furthermore, significant changes in neutrophil function werefound in the pulmonary artery. Compared to the values beforerecanalization, the nitroblue tetrazolium score rose by 31%(quartiles: 4%, 37% P=0·003), FMLP-stimulated superoxideanion production by 10% (quartiles: 0%, 39% P=0·020),and chemotaxis by 46% (quartiles: 0%, 81%, P=0·011),while neutrophil filterability decreased by 28% (quartiles:15%, 47%; P=0·010). No significant changes in neutrophilparameters were found in the arterial blood The study indicatesthat chemoattractants are released in the early reperfusionperiod of evolving myocardial infarction. These chemoattractantsmay act as inflammatory mediators causing neutrophil activation.     

The role of postischemic recirculation in the development of ischemic neuronal injury following complete cerebral ischemia

Summary The neuronal response to complete cerebral ischemia (CCI) of 5–15 min duration was evaluated at the light and electron microscopic level subsequent to postischemic recirculation periods of up to 60 min. Following postischemic reperfusion, the homogeneous neuronal changes characteristic of permanent CCI were modified into a heterogeneous pattern of selectively vulnerable neuronal responses. Four basic types of neuronal injury were represented within this heterogeneous neuronal population. The Type I neuronal response was most numerous and consisted of chromatin clumping, nucleolar condensation and a breakdown of polysomes. This response may represent a reversal of some of the neuronal changes observed after permanent CCI. In addition to the above changes, Type II neurons contained swollen mitochondria and Golgi saccules which appeared as microvacuoles under the light microscope. Type III neurons displayed varying degrees of neuronal shrinkage and numerous swollen mitochondria. Type IV neurons were markedly shrunken and electron-dense with few identifiable subcellular structures. The distribution of Type I neurons was random but the other neuronal responses occurred in selectively vulnerable brain regions. The number of Type II, III, and IV neurons increased with extended insult durations but were unaffected by the length of recirculation. Ten minutes of CCI represented the threshold for a significant increase in the number of severely altered neurons. These findings suggest that considerable neuronal injury may be present after 10–15 min of CCI, and the lack of a recirculation period following CCI appears to afford the brain parenchyma an extensive degree of structural protection.Supported by PHS Grant NS-12587     

环维黄杨星D对实验性脑缺血的保护作用

目的：探讨环维黄杨星D(Cycloirobuxiure D，CVB-D)对大鼠局灶性脑缺血再灌注损伤及PC12细胞缺氧性损伤的保护作用。方法：采用线栓法制成局灶性脑缺血再灌注大鼠模型和连二亚硫酸钠(Na2S2O4)引起的PC12细胞缺氧损伤模型，探讨CVB-D对模型大鼠神经行为、脑梗塞范围、脑含水量、脑指数的影响，以及其对PC12细胞缺氧样损伤的保护作用。结果：CVB-D能降低模型大鼠神经行为学评分、脑梗塞率、脑指数、脑含水量，抑制Na2S2O4造成的PC12细胞缺氧样损伤，降低LDH的漏出，增加细胞存活率。结论：CVB-D对实验性脑缺血有保护作用。     

益肾补气活血法对脑缺血及再灌注大鼠脑水肿、自由基的影响

[目的]从缺血再灌注损伤的主要病理过程出发,研究了益肾补气活血法对脑缺血再灌注损伤的保护作用。[方法]用日龄62d的Wistar大鼠采用Warner方法做成脑缺血再灌注模型,平行观察假手术、盐水对照、益肾补气活血法对照3个组脑组织自由基和脑含水量的变化。[结果]益肾补气活血法中药组脑组织自由基和脑含水量明显低于盐水组。[结论]益肾补气活血法在一定程度上可以抑制自由基的产生及连锁反应的发生,促进神经细胞结构及功能的恢复,延缓神经细胞的坏死,具有治疗的多向性及疗效的准确性。     

Piracetam in acute stroke: a systematic review

We studied whether the administration of piracetam in acute, presumed ischemic stroke affects case fatality and functional outcome. The Cochrane Stroke Group strategy was used to evaluate all randomized controlled trials of patients with presumed ischemic stroke examined within 48 h; death and (when available) functional outcome were used as end points. Three studies were included; the most recent one contributed more than 97% of the data. There were 501 patients treated with piracetam and 501 controls. Piracetam was associated with a nonsignificant 31% increase in the odds of death (95% CI –5% to 81%). This result was due almost completely to the effect of the larger trial, which, however, reported that the difference in case fatality rate between piracetam and control disappeared after correcting for the imbalance in stroke severity between the two groups. Data on functional outcome were available only for the largest study, and no difference was reported. Data obtained from the manufacturer suggested a nonsignificant trend (–10%) towards reduction in dependency with piracetam (CI –33% to 20%); the proportions of patients dead or dependent in the two groups were the same. Relevant adverse effects were not reported. The evidence from this review does not support routine administration of piracetam in patients with acute ischemic stroke; however, since a possible beneficial effect cannot completely be ruled out, further controlled trials are warranted. Received: 31 August 1999/Received in revised form: 3 November 1999/Accepted: 25 November 1999     

严重肺挫伤及休克缺血再灌注早期呼吸功能变化

目的研究兔严重肺挫伤及休克缺血再灌注早期呼吸功能变化。方法25只实验兔随机分为严重肺挫伤组(SLC,n=10)、严重肺挫伤休克缺血再灌注组(SLC+IR,n=10)和对照组(MC,n=5),建立动物模型,在挫伤前及挫伤后1、2、3、4小时各时点监测心率、血压、呼吸频率、潮气量、气道压力、呼吸流率曲线、呼气末CO2浓度、动脉血气分析及动静脉混和血气分析,根据公式计算出每分钟通气量、肺泡通气量、肺内分流、肺泡-动脉血氧分压差、肺顺应性、气道阻力及生理死腔与潮气量之比,用以评价肺通气功能、换气功能及呼吸力学的变化。结果肺挫伤及休克再灌注后1h实验兔呼吸频率变浅变快,出现明显的肺内肺分流(p<0.05);肺挫伤及休克再灌注后2h实验兔生理死腔/潮气量明显增加,休克再灌注组肺泡-动脉血氧分压差亦增大明显(p<0.05);肺挫伤及休克再灌注后3～4h实验兔肺泡通气量降低、动脉血压分压下降(p<0.05),肺顺应性降低,肺阻力增大(p<0.01)。结论严重肺挫伤及休克再灌注后1～2h已有通气功能损害,3～4h通气功能、换气功能及呼吸力学损害更明显,并且严重肺挫伤合并休克呼吸功能损害比单纯肺挫伤损害出现早且严重。     

醒脑静注射液对脑缺血再灌注氧化损伤的实验研究

[目的]研究中药醒脑静注射液对沙土鼠急性脑缺血再灌注损伤的作用。[方法]采用沙土鼠双侧颈总动脉夹闭制作沙土鼠急性全脑缺血模型,观察干预性腹腔注射西药尼莫地平和中药醒脑静注射液对缺血再灌注急性期沙土鼠脑组织中MDA含量和SOD活力的影响。[结果]西药尼莫地平和醒脑静注射液均能显著提高脑缺血再灌注后SOD活力和降低MDA含量,醒脑静注射液疗效和西药尼莫地平无显著差异,而醒脑静大中小剂量组之间有较显著的差异,疗效随剂量的增加而增大。[结论]醒脑静注射液作为抗自由基损伤的中药和西药尼莫地平有相当的疗效。     

乌司他丁对原位肝移植术肺损伤的保护作用

目的:观察原位肝移植术(OLT)中肺损伤的程度,探讨乌司他丁(UTI)对OLT中肺损伤的保护作用.方法:40例择期行OLT手术患者随机分为UTI组和对照组各20例,UTI组(n=20)切皮后将UTI 100万单位加入100mL生理氯化钠溶液,持续静脉输注,之后每隔4 h重复使用.对照组(n=20)以等容量生理氯化钠溶液代替.于麻醉后切皮前、无肝前期120 min、无肝期30 min、新肝期10 min、新肝期60 min和术毕对肺顺应性、吸气阻力、呼气阻力、峰值压力和平台压力进行观察.结果:在新肝期10 min、新肝期60 min和术毕时,对照组的肺顺应性显著下降,吸气阻力、呼气阻力、峰值压力和平台压力显著升高(P<0.05).UTI组的吸气阻力、呼气阻力、峰值压力和平台压力值均明显低于对照组(P<0.05),而肺顺应性值明显高于对照组(P<0.05).结论:0LT过程造成肺损伤,UTI在OLT中对肺损伤有保护作用.     

针刺为主治疗缺血性视乳头病变临床观察

目的:观察针刺与西药治疗缺血性视乳头病变的疗效差异.方法:31例患者以针刺治疗为主,辅以穴位注射.对于发病2周之内者,局部配合球后注射.记录治疗前后视力、视野的变化.结果:治疗前后视力、视野比较,差异均有极显著性意义(P<0.001).结论:该疗法是改善缺血性视乳头病变患者视功能的有效方法.