心脏骤停后全脑缺血犬内皮素和脑型肌酸激酶同功酶的变化

目的　脑复苏为心脏骤停后复苏成功与否的关键 ,本文对心脏骤停后全脑缺血犬损害的实验研究 ,旨在为临床心肺脑复苏工作提供一定的实验资料。方法　 16条成年健康杂种犬 ,随机分为两组 ,以同法诱颤后复苏 ,A组诱颤后 5分钟而B组诱颤后 10分钟开始复苏 ,复苏成功后 ,立即取血、脑脊液标本进行内皮素和脑型肌酸激酶同功酶 (CK BB)检查。结果　A组内皮素 (ET)和脑型肌酸激酶同功酶明显低于B组。结论　心脏骤停后脑复苏成功与否与时间密切相关 ,时间短则脑细胞坏死改变较轻     

犬心脏骤停后脑缺血的病理变化

目的：本文旨在观察心肺脑复苏过程中脑缺血的病理变化。方法：16条成年健康杂种犬，随机分为两组，以同法诱颤后复苏，A组诱颤后5分钟而B组诱颤后10分钟开始复苏，复苏成功后，立即取血、脑脊液标本进行脑型肌酸激酶同功酶（CK－BB）检查，72小时后取脑组织标本进行光、电镜检查。结果：A组脑型肌酸激酶同功酶明显低于B组，且其病理改变也明显轻微。结论：心脏骤停后脑复苏成功与否与时间密切相关，时间短则脑病理改变较轻。     

碱性成纤维细胞生长因子对兔全脑缺血再灌注后血清炎症因子的影响

心脏骤停复苏后产生全身脏器的缺血再灌注损伤，脑组织尤其容易遭受这种损伤，其中炎症反应起重要的介导作用。近年来发现碱性成纤维细胞生长因子(basic fibroblast growth factor，bFGF)对各种原因造成的脑损伤具有保护作用，笔者于2002年4月至2003年2月通过制作兔心脏骤停后脑缺血再灌注损伤的模型，观察bFGF对血清肿瘤坏死     

碟脉灵治疗基底节动脉型偏头痛伴眩晕60例疗效观察

目的 观察碟脉灵治疗基底动脉型偏头痛伴眩晕的临床疗效。方法 60例患者随机分为治疗组32例，对照组28例。对照组给予复方丹参注射液，治疗组给予碟脉灵注射夜。14d为一疗程，治疗期间加用西比灵。结果 两组病例均能很好的改善症状，降低血液粘稠度，TCD检查显示有一定好转。治疗组疗效优于对照组，两组疗效有显著性差异（P〈0．05）。治疗过程中未发现不良反应。结论 碟脉灵治疗基底动脉型偏头痛伴眩晕有肯定疗效，值得推广。     

聚合牛血红蛋白对缺血再灌注脑组织氧自由基和SOD的影响

目的探讨聚合牛血红蛋白（ＰＢＨｂ）在缺血再灌注后脑损伤的治疗作用。方法采用大鼠全脑缺血再灌注损伤模型，观察缺血前后应用ＰＢＨｂ对脑组织氧自由基和超氧化物歧化酶（ＳＯＤ）含量的影响。结果与缺血再灌注组相比，脑保护及复苏ＰＢＨｂ组均能有效减少氧自由基产生，其中脑复苏ＰＢＨｂ组比白蛋白对照组作用更强。同时，ＳＯＤ含量相应降低，尤以脑复苏ＰＢＨｂ组显著。结论ＰＢＨｂ能有效地抑制氧自由基产生而表现出良好的脑保护及复苏作用，这种作用不是通过增强ＳＯＤ活力产生的。     

微透析技术和丹参注射液对Wistar鼠脑缺血时海马细胞外液兴奋性氨基酸释放的影响

本文对微透析技术进行了方法学探讨，并应用该技术观察丹参注射液对脑缺血时Ｗｉｓｔａｒ鼠海马细胞外液氨基酸释放的影响。结果显示：脑缺血时丹参治疗组比缺血组及生理盐水组的海马细胞外液谷氨酸和天门冬氨酸明显减低（Ｐ＜０．０１），结合病理检查结果提示丹参注射液能减低脑缺血时海马细胞外液氨基酸的释放，并具有脑保护作用。微透析技术的应用为药物的研究提供新的方法。     

心脏骤停致脑分水岭梗塞1例报告

心脏骤停致脑分水岭梗塞１例报告刘玉琴，彭翔，戈然患者，男，４０岁，于入院前８日无何明显诱因自觉心慌、心难受昏倒在地，旋即由家人送当地医院，诊断＂心脏骤停＂，当时血压测不出，即刻抢救，２分钟后恢复心跳，６小时后苏醒，不认家人，反应及理解力均差，语言欠清...     

不同方式亚低温对兔心肺复苏后脑保护作用的比较

目的 评估和比较体外血液冷却和体表降温形成亚低温对兔心肺复苏后的脑保护作用。方法 20只兔随机分为两组，电击室颤致心搏骤停5min再复苏，一组采用体表亚低温，另一组采用体外血液冷却法形成亚低温，24小时后评定OPC(overall periormance category，总体情况分类)和NDS(neurological deficit score，神经功能缺损评分)。第72小时处死，取脑病检，评定HDS(histopathologic damage score，组织病理学损害评分)。结果 体外血液冷却法形成亚低温的速度明显快于体表亚低温组，HDS优于体表降温亚低温组，OPC、NDS两组间无统计学差异。结论 心肺复苏后越早形成亚低温脑保护作用越好，体外血液冷却法比体表降温能更早形成亚低温，具有更好的脑保护作用。     

盐源山蛭注射液治疗实验性脑内血肿的研究

目的 探索纯化盐源山蛭注射液脑内血肿吸收作用及其可能机制。方法 采用定量胶原酶注入大鼠尾状核建立脑出血模型,观察山蛭注射液对大鼠脑血肿容积、神经功能缺失评分、血肿周围脑组织水含量及组织病理变化的影响。脑水含量采用称重法,用微血管灌注法观察脑局部微血管。结果 盐源山蛭注射液能使治疗后6天、10天的大鼠脑内血肿较对照组明显缩小（P＜0．05）;脑水肿减轻,神经功能缺损体征,加快脑出血后的病理组织修复。结论 盐源山蛭注射液对大鼠脑出血后脑内肿有治疗作用。     

聚合牛血红蛋白对缺血再灌注脑组织兴奋性氨基酸递质和钙代谢的影响

采用大鼠全脑缺血再灌注损伤模型,观察缺血前后应用聚合牛血红蛋白（PBHb）对脑组织兴奋性氨基酸（EAA）递质和钙代谢的影响。结果显示：与缺血再灌组和白蛋白对照组相比,脑保护PBHb组能明显减少谷氨酸（Glu）释放,而脑复苏PBHb组此作用不显著。脑保护及复苏PBHb组均能有效地抑制钙超载的发生。上述结果提示PBHb能通过减少EAA释放等途径来阻断钙超载发生,在脑保护及复苏中发挥良好作用。     

Sudden cardiac arrest in a patient with epilepsy induced by chronic inflammation on the cerebral surface

The present study analyzed a patient with epilepsy due to chronic inflammation on the cerebral surface underwent sudden cardiac arrest. Paradoxical brain discharge, which occurred prior to ep-ileptic seizures, induced a sudden cardiac arrest. However, when the focal brain pressure was re-lieved, cardiac arrest disappeared. A 27-year-old male patient underwent pre-surgical vid-eo-electroencephalogram monitoring for 160 hours. During monitoring, secondary tonic-clonic sei-zures occurred five times. A burst of paradoxical brain discharges occurred at 2-19 seconds (mean 8 seconds) prior to epileptic seizures. After 2-3 seconds, sudden cardiac arrest occurred and lasted for 12-22 seconds (average 16 seconds). The heart rate subsequently returned to a normal rate. Results revealed arachnoid pachymenia and adhesions, as well as mucus on the focal cerebral surface, combined with poor circulation and increased pressure. Intracranial electrodes were placed using surgical methods. Following removal of the arachnoid adhesions and mucus on the local ce-rebral surface, paradoxical brain discharge and epileptic seizures occurred three times, but sudden cardiac arrest was not recorded during 150-hour monitoring. Post-surgical histological examination indicated meningitis. Experimental findings suggested that paradoxical brain discharge led to car-diac arrest instead of epileptic seizures; the insult was associated with chronic inflammation on the cerebral surface, which subsequently led to hypertension and poor blood circulation in focal cerebral areas.     

Cerebral Edema After Cardiopulmonary Resuscitation: A Therapeutic Target Following Cardiac Arrest?

We sought to review the role that cerebral edema plays in neurologic outcome following cardiac arrest, to understand whether cerebral edema might be an appropriate therapeutic target for neuroprotection in patients who survive cardiopulmonary resuscitation. Articles indexed in PubMed and written in English. Following cardiac arrest, cerebral edema is a cardinal feature of brain injury and is a powerful prognosticator of neurologic outcome. Like other conditions characterized by cerebral ischemia/reperfusion, neuroprotection after cardiac arrest has proven to be difficult to achieve. Neuroprotection after cardiac arrest generally has focused on protecting neurons, not the microvascular endothelium or blood–brain barrier. Limited preclinical data suggest that strategies to reduce cerebral edema may improve neurologic outcome. Ongoing research will be necessary to determine whether targeting cerebral edema will improve patient outcomes after cardiac arrest.     

A case of cardiac arrest encephalopathy in athetotic cerebral palsy]

A 25-year-old woman with cerebral palsy of spastic quadriplegia and athetosis showed typical cardiac arrest encephalopathy on neuropathology. The etiology of cerebral palsy was perinatal origin including prematurity, asphyxia and hyperbilirubinemia. Ventricular premature beats had developed since about 20 years of age. Muscle tone also increased with aging and symptoms of vago-vagal reflex were occasionally observed after eating. At 25 years, cardiac arrest occurred and cardiopulmonary resucitation was done immediately. She remained unconscious with absent corneal reflex and irregular respiration. EEG or auditory brain stem response showed flat activity. She died of respiratory failure 53 days after the episode of cardiac arrest. Neuropathology showed bilaterally symmetrical necrosis in the superior colliculi, gracilis nuclei, cuneate nuclei and spinotrigeminal nuclei accompanied with severe necrosis in the cerebrum and cerebellum. These findings in this adult case of total asphyxia were compatible with those observed in total plus partial asphyxia in the neonates. This discrepancy may be due to difference in cerebral maturity. Children or young adults with athetotic type cerebral palsy have a high risk of sudden death. Sudden cardiac arrest seems to play an important role in sudden death of these patients.     

Protective effects of combined superoxide dismutase and deferoxamine on recovery of cerebral blood flow and function after cardiac arrest in dogs

Oxygen free radicals generated during reoxygenation after cardiac arrest may impair recovery of cerebral blood flow and function. In a randomized study in vivo, we tested the following anti-free radical combination therapy administered at the beginning of cardiopulmonary resuscitation after apnea-induced cardiac arrest of 7 minutes: 1) ventilation with 100% nitrogen for 30 seconds to allow the delivery of therapy before oxygen, 2) 10 mg/kg i.a. superoxide dismutase followed by 10 mg/kg i.v. over 1 hour to scavenge the superoxide anion radical, and 3) 20 mg/kg i.v. deferoxamine over 1 hour to prevent membrane lipid peroxidation. We evaluated the effects of this combined treatment on the recovery of cardiovascular variables, cerebral blood flow and oxygen consumption, and somatosensory evoked potentials in 20 dogs 6 hours after resuscitation. Compared with standard treatment (n = 10), the combined treatment (n = 10) did not affect cardiovascular variables, significantly mitigated cerebral blood flow changes after cardiac arrest, and enhanced recovery of somatosensory evoked potentials. We conclude that oxygen free radicals play a role in the pathogenesis of the arrest-related derangements of cerebral blood flow and function that are effectively reduced by this combined treatment; we recommend evaluation of its components in outcome studies.     

Prognostic value of myoclonus status in comatose survivors of cardiac arrest

Generalized myoclonus status is common in comatose patients after cardiac resuscitation, but its prognostic value is uncertain. We studied the clinical, radiologic, and pathologic findings in 107 consecutive patients who remained comatose after cardiac resuscitation. Myoclonus status was present in 40 patients (37%). Features more prevalent in patients with myoclonus status were burst suppression on electroencephalograms, cerebral edema or cerebral infarcts on computed tomography scans, and acute ischemic neuronal change in all cortical laminae. All patients with myoclonus status died. Of 67 patients without myoclonus, 20 awakened. We conclude that myoclonus status in postanoxic coma should be considered an agonal phenomenon that indicates devastating neocortical damage. Its presence in comatose patients after cardiac arrest must strongly influence the decision to withdraw life support.     

Cerebral blood flow in humans following resuscitation from cardiac arrest

Cerebral blood flow was measured by xenon-133 washout in 13 patients 6-46 hours after being resuscitated from cardiac arrest. Patients regaining consciousness had relatively normal cerebral blood flow before regaining consciousness, but all patients who died without regaining consciousness had increased cerebral blood flow that appeared within 24 hours after resuscitation (except in one patient in whom the first measurement was delayed until 28 hours after resuscitation, by which time cerebral blood flow was increased). The cause of the delayed-onset increase in cerebral blood flow is not known, but the increase may have adverse effects on brain function and may indicate the onset of irreversible brain damage.     

CHANGES IN CISTERNAL FLUID POTASSIUM CONCENTRATION FOLLOWING CARDIAC ARREST

The purpose of this study was to measure the changes in potassium concentration in human cisternal Cerebrospinal fluid following successful resuscitation after cardiac arrest. We also wished to examine whether or not changes in potassium concentration in the cisternal cerebrospinal fluid could be correlated to the ability to regain normal cerebral function. 41 patients were studied, of whom 20 regained consciousness and 21 did not. In those who did not regain consciousness there mas a significant increase in the potassium concentration found in samples obtained between 40 and 50 min, and between 50 and 60 min after cardiac arrest. The potassium Concentration decreased to normal values during the following hours. Lumbar spinal fluid did not reflect the changes in cisternal fluid. The results suggest that the potassium concentration of cisternal cerebrospinal fluid, obtained soon after cardiac arrest, might give an indication of the degree of cerebral damage caused by cardiac arrest.     

Deferoxamine improves early postresuscitation reperfusion after prolonged cardiac arrest in rats.

The no-reflow phenomenon and delayed hypoperfusion after transient cardiac arrest (CA) impede postischemic recovery. Activation of lipid peroxidation (LPO) after ischemia and reperfusion is considered one of the mechanisms responsible for such abnormalities. The present study investigates the influence of iron-dependent LPO inhibitor deferoxamine (DFO) on the cerebral perfusion after prolonged CA and resuscitation. Fourteen male Sprague-Dawley rats were subjected to 17 minutes of CA, induced by esmolol (an ultrashort-acting beta-blocker) and apnea, followed by resuscitation by retrograde intraaortic infusion of oxygenated donor blood mixed with a resuscitation cocktail inside a vertical-bore 9.4-T magnetic resonance imaging (MRI) magnet. Animals were randomized double-blindly into two groups to receive DFO or saline, respectively. Cerebral perfusion was measured by MRI continuously using the arterial spin-labeling method before, during, and after CA. All animals were successfully resuscitated in 1.36 +/- 0.04 minutes with well-controlled arrest time (17.99 +/- 0.03 minutes) in both groups. Deferoxamine significantly increased cerebral perfusion in hippocampus, thalamus, hypothalamus, and amygdala, but not in cortex, during the first 20 minutes of reperfusion. In the DFO-treated group, the neurologic deficit score was significantly better (400 +/- 30 vs. 250 +/- 47, out of 500 as the best, P < 0.05) and weight loss was significantly less (33 +/- 6 vs. 71 +/- 19 g, P < 0.05) 5 d after arrest. The finding supports the notion that early reperfusion immediately after resuscitation is important for long-term outcome and that LPO may be involved in microvascular disorders during the reperfusion, particularly in the brain after prolonged cardiac arrest and resuscitation.