脑牵拉引起脑神经元凋亡的实验研究

目的探讨脑牵拉压（BRP）的测量方法及脑牵拉压引起神经元细胞凋亡的规律和机制.方法利用电阻应变计制作脑牵拉力的测量装置,对其定标.选用新西兰大白兔30只,分为30、40、50 g组,牵拉完毕后,用流式细胞仪检测各组脑牵拉压区神经细胞凋亡的百分率和细胞线粒体的活性变化.结果30 g的BRP牵拉30 min引起较低的细胞凋亡率,几乎不影响细胞线粒体的膜电位;40 g的BRP牵拉30 min引起较高的细胞凋亡率.细胞线粒体的膜电位明显降低;50 g的BRP牵拉15 min引起更高的细胞凋亡率,细胞线粒体的膜电位显著降低.结论该装置可作为脑牵拉压的测量工具,脑牵拉可引起神经元细胞凋亡以及细胞线粒体膜电位降低.实验性脑牵拉时,最好将BRP控制在40 g以下.     

小脑牵拉:意义和后果

在后颅凹手术中,小脑常被牵拉持续相当一段时间,而脑的牵拉是否引起小脑和脑干的损伤,尚无实验性的研究.本文研究了坐位狗的小脑半球牵拉压力的作用.将19只狗分为对照组(4只)和实验组(15只),实验组又分为10mmHg的拉勾压5只(A组),20mmHg的拉勾压4只(B组)、30mmHg的拉勾压6只(C组).     

脑牵拉应用的研究进展

神经外科术中良好的暴露,脑牵拉是不可避免的。脑牵拉则可带来不同程度的脑水肿、脑挫伤、脑梗塞、脑出血。约10%的颅底肿瘤和5%的颅内动脉瘤和其它颅内肿瘤术中脑牵拉可引起脑牵拉伤(brainretractioninjury,BRI)。显然BRI的发生率有很大变化,它与手术的难易、可利用的条件(如术中监控)、手术技巧以及定义脑牵拉伤的标准有关[1]。1脑牵拉的特性及分类BRI的发生与脑压板的形状、数量以及牵拉压的大小及牵拉时间有关。虽然可通过测定局部的脑血流量(rCBF)来判定缺血的程度,但目前为止我们仍没有有效的办法来直接定量牵拉中的脑损伤。文献…     

低温液体静脉灌注对兔局灶性脑缺血的保护作用

目的探讨低温液体(4℃)静脉灌注对家兔局灶性脑缺血的保护作用.方法30只家兔制成大脑中动脉梗死模型后,随机分成3组:对照组(I组)、体表降温组(Ⅱ组)和低温液体(4℃)静脉灌注组(Ⅲ组),脑温(Tc)降至(34.5±0.5)℃,维持24 h,并检测颅内压(ICP)、脑灌注压(CPP)和中心静脉压(CVP)等指标.结果两低温组脑温降至35℃用时分别为(48.0±7.1)min(Ⅱ组)和(52.3±8.9)min(Ⅲ组),两组间无显著性差异(P＞0.05);亚低温期,Ⅲ组ICP从(12.5±2.2)mmHg降至(11.0±2.2)mmHg(12 h)和(10.5±2.0)mmHg(24 h),CPP从(75.9±6.2)mmHg上升至(86.3±7.3)mmHg(2 h)、(81.9±3.9)mmHg(12 h)和(80.9±5.1)mmHg(24 h),与对照组比较,两低温组ICP降低,CPP升高(P＜0.05),同时Ⅲ组CPP显著高于Ⅱ组(P＜0.05).结论低温液体(4℃)静脉灌注能降低脑温和颅内压,并提高脑灌注压,对缺血性脑损伤有明显的保护作用,是一种安全有效的治疗方法.     

脑灌注压对创伤性脑水肿的影响

目的通过观察不同灌注压(CPP)水平对实验性脑创伤早期脑水肿的影响作用来选择适宜的CPP水平,为临床脑创伤治疗提供参考。方法实验用兔30只,随机分为对照组(无颅脑损伤),高CPP组(90～110mmHg),中CPP组(70～80mmHg),低CPP组(60～70mmHg),和极低CPP组(35～45mmHg)5组,每组6只。对照组不予损伤,其余各组均给予(1100±100)N的撞击力致减速性脑损伤(重伤水平)。伤后80min静脉给予升压药或降压药物调控血压使CPP达到设计要求。伤后6h测脑含水量。结果所有颅脑损伤动物均出现了明显的脑损伤生理反应和病理改变,颅内压(ICP)均明显增高(P<0.001)。脑含水量为:对照组,78.18%±0.32%;高CPP组,81.35%±1.02%;中CPP组,80.27%±0.48%;低CPP组80.31%±0.70%;极低CPP组,81.19%±0.74%。与对照组比较损伤组脑含水量均增加(P<0.001)。高CPP和极低CPP两组脑含水量分别较中、低CPP组增高(P<0.05)。结论兔脑创伤后维持CPP在60～80mmHg之间的中低水平,脑水肿轻;CPP降至50mmHg以下和升至90mmHg以上均加重脑水肿。     

颅内手术操作过程中脑自持牵开器压力

脑自持牵开器在颅内手术中的运用日益普遍并成为显微神经外科手术达到良好暴露不可缺少的工具。但运用时在脑表面可产生一定的压力,这种脑自持牵开器压力(BRP)可传递到邻近脑组织,从而减少局部脑灌注压(rCPP)。作者在23例颅内肿瘤和动脉瘤病人的手术过程中,将两压力感受器分置于脑牵开器的前端和中部,测出术中BRP与rCPP的变化。术中测得BRP大部分波动在10-40mmHg,所绘BRP曲线示:开始4分钟急剧下降,以后逐渐下降或保持在恒定水平。在同一牵开器的前端压力比中间要高,运用甘露醇、硝普钠对BRP无影响。有6例BRP超过40mmHg及诱导低血压降到了40mmHg使rCPP低于10mmHg长达6     

重型颅脑损伤后继发脑损伤的研究进展

近几年,继发性脑损伤在重型颅脑损伤病人伤后病程中的作用越来越受到重视,开展了广泛的研究。目前认为:脑灌注压不足、颅内高压、脑氧代谢率降低、脑血流量下降以及失控性炎症反应等是严重创伤后发生继发性脑损伤的重要机制。相互之间平衡关系的调节是预防和治疗继发性脑损伤的关键。颅脑损伤后继发性脑损伤病理生理的研究,对预防颅脑损伤病人的继发性脑损伤和提高疗效具有重要意义。     

不同剂量甘露醇治疗急性大脑半球大面积梗死的TCD评价

目的利用TCD监测颅内动脉的血流动力学变化,探讨甘露醇对急性大脑半球大面积梗死患者脑血流量和脑灌注压的影响。方法选取经颅脑CT和MRI确诊为大脑半球大面积梗死的40例患者为观察对象,随机分为A、B组,每组20例,A组患者在入院后15 min内快速静滴20%的甘露醇125 mL,B组患者在入院后15 min内快速静滴20%的甘露醇250 mL。利用TCD进行相关指标评价。结果 A组患者治疗30 min后Vm较治疗前明显升高,PI较治疗前下降;B组患者在治疗30 min后Vm较治疗前升高,PI较治疗明显下降,差异有统计学意义(P0.05);A组Vm升高幅度明显大于B组,PI下降幅度明显低于B组(P0.05)。结论 125 mL甘露醇静滴对急性大脑半球大面积梗死患者脑血流量的改善效果优于250 mL甘露醇。     

实验性颅脑损伤后兴奋性氨基酸及脑血流量的变化

目的:观察大鼠颅脑损伤后脑组织兴奋性氨基酸和局部血流量(ｒｅｇｉｏｎａｌ ｃｅｒｅｂｒａｌ ｂｌｏｏｄ ｆｌｏｗ,ｒｉＢＦ)的变化规律。方法:用流体冲击装置制作中度大鼠颅脑损伤模型,氨基酸微量分析系统检测脑组织谷氨酸(ｇｌｕａｍａｔｅ,Ｇｌｕ)和天冬氨酸(ａｓｐａｒｔａｔｅ,Ａｓｐ)含量,氢清除法检测脑局部血流量。结果:脑损伤后ｒＣＢＦ明显下降,脑组织Ｇｌｕ、Ａｓｐ的含量在伤后明显增加。结论:脑组织氨基酸的变化与脑血流量有一定的关系,脑损伤后血流量的降低可能是引起氨基酸大量释放的主要因素。     

VEGF-165基因对创伤性脑损伤脑血流动力学影响的实验研究

目的 研究外源性血管内皮细胞生长因子(VEGF)基因治疗大鼠创伤性脑损伤(TBI)后脑灌注的变化,了解其血流动力学改变.方法 创伤性脑损伤大鼠模型建立后随机分为3组:治疗组,质粒对照组,外伤组.通过RT-PCR检测脑伤后1h、6h、24h、3d、7d、14 d VEGF mRNA在损伤局部的表达改变;应用CT灌注像(CTP)研究不同时间脑血流量(CBF)、脑血容量(CBV)等参数在VEGF-165基因治疗前后的动态变化.结果 VEGF-165基因治疗创伤性脑损伤大鼠后经RT-PCR扩增的VEGF mRNA绝对积分光密度值水平显著高于外伤组和质粒对照组(P＜0.05).CTP参数和伪彩图均显示基因治疗组脑灌注在伤后24h CBF、CBV有增高趋势,伤后3d、7d脑灌注明显高于TBI 组(P＜0.05),虽然伤后14 d CBF、CBV开始降低,但和TBI组比较仍然较高.结论 本研究结果显示大鼠创伤性脑损伤后外源性VEGF基因能够提高脑损伤组织的脑灌注,改善脑损伤部位微循环,为损伤组织的恢复提供基础.     

Influence of moderate and profound hyperventilation on cerebral blood flow, oxygenation and metabolism

OBJECTIVE: The aim of the present study was to examine the impact of moderate and profound hyperventilation on regional cerebral blood flow (rCBF), oxygenation and metabolism. MATERIALS AND METHODS: Twelve anesthetized pigs were subjected to moderate (mHV) and profound (pHV) hyperventilation (target arterial pO(2): 30 and 20 mmHg, respectively) for 30 min each, after baseline normoventilation (BL) for 1 h. Local cerebral extracellular fluid (ECF) concentrations of glucose, lactate, pyruvate and glutamate as well as brain tissue oxygenation (p(ti)O(2)) were monitored using microdialysis and a Licox oxygen sensor, respectively. In nine pigs, regional cerebral blood flow (rCBF) was also continuously measured via a thermal diffusion system. RESULTS: Both moderate and profound hyperventilation resulted in a significant decrease in rCBF (BL: 37.9+/-4.3 ml/100 g/min; mHV: 29.4+/-3.6 ml/100 g/min; pHV: 23.6+/-4.7 ml/100 g/min; p<0.05) and p(ti)O(2) (BL: 22.7+/-4.1 mmHg; mHV: 18.9+/-4.9 mmHg; pHV: 13.0+/-2.2 mmHg; p<0.05). A p(ti)O(2) decrease below the critical threshold of 10 mmHg was induced in three animals by moderate hyperventilation and in five animals by profound hyperventilation. Furthermore, significant increases in lactate (BL: 1.06+/-0.18 mmol/l; mHV: 1.36+/-0.20 mmol/l; pHV: 1.67+/-0.17 mmol/l; p<0.005), pyruvate (BL: 46.4+/-7.8 micromol/l; mHV: 58.0+/-10.3 micromol/l; pHV: 66.1+/-12.7 micromol/l; p<0.05), and lactate/glucose ratio were observed during hyperventilation. (Data are presented as mean+/-S.E.M.) CONCLUSIONS: Both moderate and profound hyperventilation may result in insufficient regional oxygen supply and anaerobic metabolism, even in the uninjured brain. Therefore, the use of hyperventilation cannot be considered as a safe procedure and should either be avoided or used with extreme caution.     

Brain retraction injury

This paper reviews the literature of the brain retraction injury during the last century. The review focused on the instrument characteristic as well as the physiopathological and histopathological damage of the brain induced by brain retraction. It was found that lesions were induced by cerebral ischemia. We conclude that a better monitoring system needs to be developed to avoid brain injury.     

Retraction brain ischaemia: cerebral blood flow, evoked potentials, hypotension and hyperventilation in a new animal model.

Undue intraoperative brain retraction can cause significant neurosurgical morbidity. By combining brain retractor blade pressure measurement with monitoring of brain electrical activity, one can determine the limits of safe brain retraction and then test systematically various therapeutic interventions. Cortical evoked potential (EP) mapping and laser-Doppler cerebral blood flow (CBF) measurement were undertaken during brain retraction in the miniature swine (Sus scrofa). Forelimb somatosensory EP recording during subtemporal retraction simulated the pterional and subtemporal approaches, respectively. Retraction pressure of 30 mmHg usually resulted in a 50% decrement in EP amplitude after 10 to 20 minutes in normotensive, normocapnic adult animals. Recovery of EP occurred within 5 to 10 minutes of retraction release. The effects of animal age, induced hypotension (nitroprusside, MAP approximately 40), and induced hypocapnia (hyperventilation, PaCO2 approximately 28) on EP preservation during retraction were then investigated, with data reported here from 23 animals (8 to 35 kg). By Spearman rank correlation coefficients, early loss of EP was associated with the following: lower MAP (p approximately 0.0001), lower CBF (p approximately 0.0005), lower PaCO2 (p less than 0.001), and older age (p approximately 0.01). These results indicate (1) retractors should be relaxed every 10-15 minutes whenever possible (for at least 5 minutes), and (2) hypotension, in particular, but also hypocapnia (hyperventilation) should not be used indiscriminately. Details of this new model of retraction ischaemia are presented.     

Brain retraction injury

Abstract

This paper reviews the literature of the brain retraction injury during the last century. The review focused on the instrument characteristic as well as the physiopathological and histopathological damage of the brain induced by brain retraction. It was found that lesions were induced by cerebral ischemia. We conclude that a better monitoring system needs to be developed to avoid brain injury.     

Microcirculatory changes in the development of the cerebrovascular adaptation]

Recently, long-term cerebrovascular adaptations after unilateral carotid ligation that increase the tolerance of the brain to subsequent episode of ischemia was reported(J Cereb Blood Flow Metab, 1998). However, the pathophysiological mechanisms underlying the phenomenon was unknown. We examined regional cerebral blood flow(rCBF) before, during and after subsequent ischemia in the development of the adaptation. Male Wistar rats(n = 18) were used. Unilateral(right) carotid artery ligation was performed 3 hours(group A: n = 8), 3 days(group B: n = 10) before forebrain ischemia. With bilateral carotid arteries occlusion, mean arterial blood pressure(MABP) was reduced by hypobaric hypotension down to 50 mmHg and maintained constant for 30 min. After hypotension, the experiment continued for 90 min. Local CBF were registered at 25(5 x 5) identical locations by laser Doppler scanning in the cortex during the experiment in bilateral hemispheres(at control phase, after the left carotid artery ligation, during ischemia and after hypotension). The physiological variable such as blood pressure and gas analysis were within normal range in all groups. There were no differences of rCBF between the right and left hemispheres in group A during the experiment. In group A, rCBF of both hemispheres significantly decreased after the ligation of the left carotid artery, during the induced ischemia (P < 0.05), and recovered to the value of before ischemia. Whereas, in group B rCBF of the left side(non-occluded side) decreased after the ligation of the left carotid artery, during the induced ischemia(P < 0.05), and recovered to the value of before ischemia, but rCBF of the right side(occluded side) decreased only during the induced ischemia(P < 0.05) and rCBF of the right side was significantly higher than the left brain after ligation of the carotid artery, during ischemia and after hypotension(P < 0.05). On the basis of these data, we concluded that cerebrovascular adaptations can be acquired by 3 days after unilateral carotid artery occlusion and the tolerance phenomenon is certainly attributed to microcirculatory improvement.     

Opioids and the prostanoid system in the control of cerebral blood flow in hypotensive piglets

The interaction between opioid and prostanoid mechanisms in the control of cerebral hemodynamics was investigated in the conscious hypotensive piglet. Radiomicrospheres were used to determine regional cerebral blood flow (rCBF) in piglets pretreated with the opioid receptor antagonist, naloxone, or its vehicle, saline, during normotension, hypotension, and after the administration of indomethacin, a cyclooxygenase inhibitor, during hypotension. Hemorrhage (30 ml/kg) decreased systemic arterial pressure from 68 +/- 12 to 40 +/- 10 mm Hg but did not decrease blood flow to any brain region. Indomethacin treatment (5 mg/kg) of hypotensive piglets decreased blood flow to all brain regions within 20 min; this decrease in CBF resulted from increases in cerebral vascular resistance of 65 and 281% at 20 and 40 min after treatment, respectively. In hypotensive piglets, cerebral oxygen consumption was reduced from 2.62 +/- 0.71 to 0.53 +/- 0.27 ml 100 g-1 min-1 and to 0.11 +/- 0.04 ml 100 g-1 min-1 at 20 and 40 min following indomethacin, respectively. Treatment with naloxone (1 mg/kg) had no effect on rCBF, calculated cerebral vascular resistance, or cerebral oxygen consumption of normotensive or hypotensive piglets. However, decreases in CBF and oxygen consumption and increases in cerebral vascular resistance upon treatment of hypotensive piglets with indomethacin were attenuated in animals pretreated with naloxone. These data indicate that the removal of prostanoid modulation of an opioid-mediated constrictor influence on the cerebral circulation is a potential mechanism for the increase in cerebral vascular resistance that follows indomethacin treatment of hypotensive piglets.     

Alterations in regional cerebral blood flow following brain injury in the rat

To elucidate the temporal changes in regional cerebral blood flow (rCBF) after experimental traumatic brain injury, serial rCBF measurements were made during a 24-h period following fluid-percussion (F-P) traumatic brain injury in the rat. Brain injury of 2.2 atm was induced over the left parietal cortex and serial measurements of rCBF were performed using the radiolabeled microsphere method. rCBF values were obtained prior to injury and at 15 and 30 min and 1, 2, 4, and 24 h postinjury. At 15 min postinjury, there was a profound, wide-spread reduction in rCBF in all brain regions studied (p less than 0.05). At 30 min and 1 h postinjury, all brain regions except pons-medulla and cerebellum showed significantly reduced rCBF compared to the preinjury values (p less than 0.05). By 2 h postinjury, however, a significant focal reduction of rCBF was observed only in the cerebral tissue surrounding the trauma site (p less than 0.05); rCBF in the remaining brain regions had recovered to the preinjury levels. By 4 h postinjury, rCBF had returned to normal in all brain regions studied. This recovery of rCBF was still evident at 24 h postinjury. The present study demonstrates that, following the experimental traumatic brain injury in the rat, (a) an initial global suppression of rCBF occurs up to 1 h postinjury; (b) at the trauma site, a more persistent focal reduction of rCBF occurs; and (c) these alterations in rCBF after trauma dissolve by 4 h postinjury.(ABSTRACT TRUNCATED AT 250 WORDS)     

Intracranial Pressure and Experimental Model of Diffuse Brain Injury in Rats

Objective

In this study, we present a simple closed head injury model as a two-stage experiment. The height of the weight drop enables gradation of head trauma severity.

Methods

The head injury device consists of three parts and there are three adjustable parameters-weight (100-600 g), height of fall (5-100 cm) and elasticity of the springs. Thirty male Wistar rats underwent monitoring of intracranial pressure with and without induction of the head injury.

Results

The weight drop from 45 to 100 cm led to immediate seizure activity and early death of the experimental animals. Severe head injury was induced from 40 cm weight drop. There was 50% mortality and all surviving rats had behavioral deterioration. Intracranial pressure was 9.3 ± 3.76 mmHg. Moderate head injury was induced from 35 cm, mortality decreased to 20-40%, only half of the animals showed behavioral pathology and intracranial pressure was 7.6 ± 3.54 mmHg. Weight drop from 30 cm caused mild head injury without mortality and neurological deterioration. Intracranial pressure was slightly higher compared to sham group- 5.5 ± 0.74 mmHg and 2.9 ± 0.81 mmHg respectively.

Conclusion

This model is an eligible tool to create graded brain injury with stepwise intracranial pressure elevation.     

Brain perfusion SPECT in patients with corticobasal degeneration: analysis using statistical parametric mapping.

We sought to determine the characteristics of brain perfusion in patients with corticobasal degeneration (CBD) using single photon emission computed tomography (SPECT) and statistical parametric mapping (SPM). Thirteen patients with CBD and 10 age-matched healthy volunteers were examined using brain perfusion SPECT and (99m)Tc-ethyl cysteinate dimer (ECD). Regional cerebral blood flow (rCBF) measurements were performed noninvasively using a graphic analysis method. Both the absolute rCBF data (raw data) and the adjusted rCBF data (global CBF normalized to 50 ml/100 g/min) were used in the SPM analysis. A significant decrease in the absolute rCBF was observed in extended areas of the brain in CBD patients compared to the control group. These areas included the frontal, parietal, and temporal cortices; basal ganglia; thalamus; and pontocerebellar regions. Our results suggest that the extent of the reduced rCBF region in CBD patients is more widespread than previously reported.