A multiparametric index of platelet in vitro aggregation in cerebrovascular disease

148 patients with various forms of cerebrovascular disease (CVD) were studied by means of a multiparametric analysis ofin vitro platelet aggregation, based on the following six parameters: ADP and epinephrine primary and secondary aggregation thresholds and percent maximum aggregation induced by optimal concentrations of ADP and epinephrine. These patients were assigned to four study groups, according to clinical diagnosis supported by CT scan, of transient ischemic attack and reversible neurological deficit (TIA-RIND), or completed stroke, in the presence or absence respectively of antiplatelet medical treatment at the time of the study. A statistically significant increase of thein vitro platelet aggregation was found in 44.4% of the untreated TIA-RIND patients and in 33.9% of the untreated stroke patients. However this last group showed a higher percentage of very marked hyperaggregation. Differences between the two treated study groups and controls were not signicant. No difference was found in collagen-and ristocetin-induced aggregation between the patient groups and the controls.

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Sommario 148 pazienti con varie forme di malattia cerebrovascolare, sono stati studiati con analisi multiparametriche dell'aggregazione piastrinica in vitro sulla base dei seguenti sei parametri: le soglie di aggregazione primaria e secondaria e l'aggregazione massima percentuale indotta da ADP ed Epinefrina. Questi pazienti sono stati suddivisi in 4 gruppi di studio in accordo con la diagnosi clinica confortata dai dati della TAC e cioè: TIA, RIND, o rammollimento in presenza o in assenza rispettivamente di un trattamento antiaggregante nel momento dello studio. è stato trovato un aumento statisticamente significativo dell'aggregazione in vitro delle piastrine nel 44.4% dei casi TIA, RIND non trattati e nel 33,9% dei casi di rammollimento non trattati. Quest'ultimo gruppo, però, ha dimostrato una più alta percentuale di iperaggregazione molto marcata. Le differenze tra i 2 gruppi di studio trattati con antiaggreganti e i controlli non erano significative. Inoltre nessuna differenza è stata riscontrata tra i gruppi e i controlli nell'aggregazione indotta da collageno e ristocetina.

     

新生儿缺氧缺血性脑病的MRI表现

目的:探讨新生儿缺氧缺血性脑病(HIE)的MRI表现。材料和方法:对87例临床确诊为HIE的患儿行MRI扫描,并对其MRI表现进行分析。结果:87例HIE患儿中,74例(85.1%)可见皮层、皮层下及深部白质T1WI迂曲条状、点状高信号;69例(79.3%)显示基底节、丘脑T1WI异常高信号及内囊后肢高信号消失;62例(71.3%)出现弥漫性脑水肿;58例(66.7%)可见颅内出血,包括蛛网膜下腔出血、硬膜下出血、脑室内出血及脑实质出血;19例(21.8%)可见侧脑室周围白质软化;7例(8.0%)可见脑梗死。结论:MRI在HIE正确诊断和早期治疗中具有重要临床价值。     

急性胰腺炎恢复期并Wernicke脑病一例

患者男，34岁。大量饮酒后出现剑突下疼痛，伴恶心、发热，体温最高达38．5℃，发病3天入住当地医院治疗，诊断为“急性胰腺炎”。经禁食、胃肠减压、抑制胰酶分泌、抑酸、抗感染治疗，3天后疼痛明显减轻，血淀粉酶恢复正常、尿淀粉酶仍高于正常值。维持原治疗，治疗16天后，自觉上述症状消失后拔除胃管，但化验检查发现尿淀粉酶高（1294u／L），1天后再次留置胃管行胃肠减压，治疗33天后拔除胃管。出现头晕、恶心呕吐，呕吐物为胃内容物，予以“吗丁啉、思密达、多酶片”等药物对症治疗，效差。治疗38天后出现复视、视物不清、耳鸣，为进一步诊治，以“尿淀粉酶升高42天，呃逆1天，复视、乓鸣5天”为主诉入住我院。     

急性低氧运动对血液流变性和红细胞形态的影响及电解质饮料的干预效果

目的:探讨急性低氧运动对血液流变性和红细胞形态的影响以及补充电解质饮料的干预效果。方法:受试者为8名健康成年男性,均进行两次实验。第1次为急性低氧运动加补充电解质饮料(运动前和运动中)实验,第2次为急性低氧运动不补充任何液体实验,两次实验间隔1周。受试者以70%最大摄氧量(VO2max)强度在低氧环境(O2浓度为15.5%,环境温度为20℃,湿度为55%)下进行1小时的功率自行车运动。分别测定受试者运动前、后的血液流变学指标并观察其红细胞形态的变化。结果:不补液情况下,受试者运动后的血液粘度、红细胞压积及红细胞刚性指数显著增加(P<0.01)。红细胞形态由双凹圆盘形变为一面凸、一面凹的草帽形。运动前和运动中补充电解质饮料,受试者运动后的各项血液流变学指标与运动前相比变化均不显著(P>0.05),且运动后红细胞形态未见明显变化。结论:运动前和运动中补充电解质饮料可缓解急性低氧运动对机体血液流变性产生的不良影响。     

Concomitant mitral valve repair and left ventricular reconstruction in a patient with chronic ischemic mitral regurgitation and inferior left ventricular aneurysm

The surgical approach to ischemic mitral regurgitation with concomitant inferior left ventricular aneurysm remains uncertain in terms of the indication for operation and the short-and long-term outcomes. We performed concomitant mitral valve repair, left ventricular reconstruction, and aortic valve replacement on a 71-year-old male with severe ischemic mitral regurgitation, inferior left ventricular aneurysm, and degenerative aortic regurgitation. Postoperative status was in New York Heart Association functional class I without mitral regurgitation 8 months after operation. We discuss, and review the procedures reported in the literature.     

脑梗死急性期降压治疗对预后的影响

目的 研究脑梗死急性期降压及在不同时间进行降压治疗对患者近期预后的影响.方法 据发病后是否降压及进行降压的时间,将198例急性脑梗死患者分为6组,观察各组患者神经功能缺损程度及心脑血管事件的再发生率和病死率.结果 在发病后进行降压治疗的患者中其心脑血管事件再发率和病死率明显低于未降压组（P＜0.01） 3d后降压组患者神经功能恢复的程度明显好于未降压组（P＜0.01）.结论 降压治疗可以降低患者心脑血管事件的发生率和病死率3d后进行降压治疗的患者神经功能恢复明显要好.     

大鼠脑缺血再灌注后水孔蛋白-4的免疫组化表达与脑水肿关系的研究

目的　研究大鼠脑缺血再灌注后脑组织中水孔蛋白 - 4 (AQP- 4 )的表达与脑水肿的关系。方法　采用大鼠大脑中动脉栓塞 (MCAO)模型 ,经免疫组化法测定 AQP- 4表达阳性细胞数 ,干、湿重法测定脑水含量 ,脑水肿以脑水含量评价。结果　脑缺血再灌注后 12 h,脑缺血坏死周边区 AQP- 4表达阳性细胞及脑水含量增加 ,于 4 8～ 12 0 h 达到高峰 ,16 8h后仍处于较高水平 ,两者之间呈正相关 (r=0 .95 8,P<0 .0 1)。结论　脑缺血再灌注后AQP- 4参与脑水肿的发生 ,为脑缺血再灌注损伤的重要因素之一。     

间歇性低氧训练对男子赛艇运动员大负荷训练期间生理机能的影响

目的:探讨在大负荷训练期间进行间歇性低氧训练对男子赛艇运动员生理机能的影响。方法:12名男子赛艇运动员分成低氧组和对照组,低氧组在赛前大负荷训练期间进行为期4周、每周5天、每天1小时的间歇性低氧训练,其余日常训练两组相同。实验期间每周测试运动员的睡眠质量、耐缺氧能力以及血红蛋白、血尿素、肌酸激酶等指标。结果:4周间歇性低氧训练后,低氧组运动员血红蛋白含量显著高于对照组,血尿素水平和肌酸激酶活性显著低于对照组;低氧组在耐缺氧实验中血氧饱和度显著高于对照组,心率显著低于对照组;低氧组睡眠质量指标得分显著低于对照组。结论:间歇性低氧训练可以提高男子赛艇运动员大负荷训练期间的耐缺氧能力,改善睡眠质量,间接促进机体在承受大负荷训练负荷时的恢复能力。     

1,6-二磷酸果糖治疗新生儿缺氧缺血性脑病合并心肌损害疗效观察

目的探讨1,6-二磷酸果糖(FDP)治疗新生儿缺氧缺血性脑病(HIE)合并心肌损伤的疗效.方法随机分成治疗组和对照组,均给予常规治疗,治疗组加用FDP 0.25～0.4g/(kg·次),1 次d静滴,10 d为一疗程,治疗前后均进行心肌酶测定.结果治疗组临床症状改善及心肌酶恢复效果均优于对照组,两组差异有显著性(P＜0.05).结论 FDP对HIE时的脑损伤及心肌损伤均有良好效果.     

Developmental spectrum of the excitotoxic cascade induced by ibotenate: a model of hypoxic insults in fetuses and neonates

Ibotenate, a glutamatergic agonist, was used to study the spectrum of excitoxic disturbances at different ages of cerebral development. Cultures of whole mouse embryo were submitted to ibotenate at E8 for 20 h: during the phase of early premigratory differentiation; ibotenate did not induce any detectable histological lesion. During migration of supragranular neurons, newborn hamsters intracerebrally injected at P0 with ibotenate display neuronal migration disorders graded from nodular heterotopias to extensive laminar heterotopias mimicking some aspects of lissencephalic and double-cortex syndromes. After completion of neuronal layer V, P0 mice injected with ibotenate exhibit laminar neuronal depopulation of layer V-VIa mimicking human micro-gyria. At P5 in mouse, after completion of neuronal migration of the cortical plate, ibotenate induces neuronal loss in all cortical layers and the formation of porencephalic cysts. This study emphasizes the dramatic role played by glutamate in brain development, in the occurrence of neuronal migration disorders in the cortex. and in grey and white matter damage.