Effects of vasodilatation and acidosis on the blood-brain barrier

Hypercapnia protects the blood-brain barrier against disruption during acute hypertension. Our goal was to determine whether protection of the blood-brain barrier by hypercapnia may be related to an affect of acidosis on the barrier, vasodilatation produced during hypercapnia, or attenuation of increases in cerebral venous pressure by hypercapnia. Pial vessels were examined in rats by means of fluorescent microscopy. We examined disruption of the blood-brain barrier in response to acute hypertension during hypercapnia (vasodilatation with acidosis), during topical adenosine (vasodilatation without acidosis), and during passive increases in cerebral venous pressure produced by venous occlusion during hypercapnia. Acute hypertension in normocapnic rats increased venular pressure and disrupted the blood-brain barrier and often produced bleeding from cerebral venules. Hypercapnia alone increased venular pressure, and acute hypertension produced only a modest further increase in venular pressure, with minimal disruption of the blood-brain barrier. Venous occlusion in hypercapnic rats increased venular pressure and disrupted the blood-brain barrier. We conclude that vasodilatation and acidosis produced by hypercapnia do not protect the blood-brain barrier from disruption during acute hypertension. Protection by hypercapnia during acute hypertension appears to be related to attenuation of increases in cerebral venous pressure.     

不同时期高血压性脑出血病人脱水治疗后颅内血肿的变化

目的观察甘露醇对早期高血压性脑出血病人血肿大小以及血流动力学参数的影响,并探讨甘露醇的用药指证.方法 40例高血压性脑出血病人随机分为甘露醇治疗组和非甘露醇治疗组,使用头颅CT测量血肿大小以及经颅多普勒(transcranial doppler, TCD)测定大脑中动脉平均血流速度 (blood flow mean velocity, Vm)及脉动指数 (Pulse Indexes, PI),对实验前后参数的变化进行统计学分析.结果治疗前高血压性脑出血病人头颅CT测量血肿量以及使用TCD测定Vm及PI值两组无统计学意义(P>0.05);治疗后CT显示实验组血肿量增加,而对照组有所减小,两者比较有统计学意义(P<0.05);Vm值、PI值两组比较有统计学意义(P<0.05).结论对早期发病的颅内压增高症状不明显的少量高血压脑出血病人慎用甘露醇脱水治疗,以免血肿扩大,加重病情, TCD血流动力学参数对脱水治疗有指导意义.     

中小量高血压脑出血早期应用半量甘露醇与针刺治疗的疗效观察

目的探讨半量甘露醇与针刺对中小量高血压脑出血早期血肿扩大、临床疗效的影响及如何正确使用甘露醇。方法选取高血压幕上非丘脑出血、颅压增高不突出、发病6h内、血肿量〈50mL的病人60例，将24h内应用20％甘露醇250mL者作为常规A组（30例），150mL者为半常规B组（30例），B组10d后再分为C组、D组各15例，C组为半常规朱针刺组，D组为半常规针刺组。48h～72h复查脑CT。血肿增大33％为血肿早期扩大。分析早期应用甘露醇对血肿扩大的影响；对C组、D组治疗20d后进行神经功能缺损评分及临床疗效对照比较。结果常规A组发生血肿扩大11例，B组3例，A组与B组血肿扩大比较有统计学意义。神经功能评分及临床疗效比较，A组与B组无统计学意义；C组与D组有统计学意义。结论中小量脑出血病人发病24h内不适当应用甘露醇可增加早期血肿发生率，使病情加重；半量甘露醇配合针刺治疗中小量高血压脑出血临床疗效显著。     

Role of veins and cerebral venous pressure in disruption of the blood-brain barrier

The goal of this study was to determine whether increases in cerebral venous pressure contribute to, and may account for, disruption of the blood-brain barrier during acute hypertension and hyperosmolar stimuli. We studied the relation between pial venous pressure and disruption of the blood-brain barrier during acute arterial hypertension, superior venae cavae occlusion, and superfusion with hyperosmolar arabinose. Sprague-Dawley rats were studied using intravital fluorescent microscopy and fluorescein-labelled dextran (mol. wt. = 70,000). Disruption of the blood-brain barrier was characterized by the appearance of microvascular leaky sites and quantitated by the clearance of fluorescein dextran. We measured pressure (servo null) in pial arterioles and venules 40-60 micron in diameter. Acute hypertension, occlusion of the superior venae cavae, and hyperosmolar arabinose produced leaky sites primarily in venules. Acute hypertension increased arteriolar pressure and also venular pressure, from 7 +/- 1 (mean +/- SE) to 28 +/- 2 mm Hg. Clearance of fluorescein dextran increased from 0.03 +/- 0.01 to 2.90 +/- 0.40 ml/sec X 10(-6). Occlusion of the superior venae cavae increased pial venous pressure from 7 +/- 1 to 30 +/- 3 mm Hg, and clearance of fluorescein dextran, from 0.02 +/- 0.01 to 3.10 +/- 0.59 ml/sec X 10(-6). In contrast to acute hypertension, there was a decrease in arterial and pial arteriolar pressure during occlusion of the superior venae cavae. Thus, similar increases in venous pressure during acute hypertension and superior venae cavae occlusion, despite directionally opposite changes in arterial and arteriolar pressure, produced similar disruption of the blood-brain barrier.(ABSTRACT TRUNCATED AT 250 WORDS)     

Nitric oxide deficiency contributes to large cerebral infarct size

The purpose of this study was to examine the role played by a deficit in nitric oxide (NO) in contributing to the large cerebral infarcts seen in hypertension. Cerebral infarction was produced in rats by occlusion of the middle cerebral artery (MCA). Studies were performed in Sprague-Dawley (SD) rats subjected to NO synthase blockade (N(G)-nitro-L-arginine [L-NNA], 20 mg x kg(-1) x d(-1) in drinking water) and in spontaneously hypertensive stroke-prone rats (SHRSP). NO released in the brain in response to MCA occlusion was monitored with a porphyrinic microsensor in Wistar-Kyoto rats. The increment in NO released with MCA occlusion was 1.31+/-0.05 micromol/L in L-NNA-treated rats, 1.25+/-0.04 micromol/L in SHRSP, 2. 24+/-0.07 micromol/L in control SD rats, and 2.25+/-0.06 micromol/L in Wistar-Kyoto rats (P<0.0001 for control versus the other groups). Infarct sizes in the L-NNA-treated and control SD rats were 8.50+/-0. 8% and 5.22+/-0.7% of the brain weights, respectively (P<0.05). The basilar arterial wall was significantly thicker in L-NNA-treated rats compared with their controls. We conclude that both the deficit in NO and the greater wall thickness contribute to the larger infarct size resulting from MCA occlusion in SHRSP and in L-NNA-treated rats compared with their respective controls.     

485例脑白质改变的影像学与血管性因素的相关性研究

目的探讨脑白质MRI高信号表现特征及相关病理机制。方法对485例连续住院患者行头颅MRI检查,并将其脑室周围高信号严重程度分级,对不同级别脑白质损害与患者年龄、性别以及相关疾病间联系进行统计学分析。结果脑白质高信号严重程度随年龄增长而加重,性别对脑白质信号没有明显影响。脑室周围脑白质高信号与脑梗死、糖尿病、高血压、心房颤动呈正相关,深部脑白质高信号与脑梗死和高血压呈正相关,差异有统计学意义。短暂性脑缺血发作、脑出血及高脂血症与脑白质高信号没有显著联系。结论脑白质高信号与脑梗死、高血压、糖尿病有密切联系,脑白质改变与脑出血不相关。脑脊液回流障碍、大血管病变以及低灌注状态可能参与脑白质高信号的形成。     

Middle cerebral artery occlusion in the hypertensive and normotensive rat: a study of histopathology and behaviour

Brain infarct size and behaviour were studied in spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY) 3 weeks after occlusion of the right middle cerebral artery in order to compare the effects of vascular occlusions on the normotensive and hypertensive cerebral vasculature. The brain tissue reduction, assessed by measuring the cross-sectional area of remaining tissue and weight of the cerebral hemispheres, was greater in SHR than in WKY (P less than 0.01). Deficits in sensorimotor integration were highly correlated to the degree of brain damage (r = 0.91). Amphetamine induced no rotation asymmetry in normal rats, whereas lesioned rats rotated more ipsilaterally to the lesion (P less than 0.05). Rotation asymmetry did not correlate with total infarct size. The more severe outcome after middle cerebral artery occlusion in SHR as opposed to WKY, can probably be explained by reduced collateral capacity secondary to the altered vascular design in hypertension.     

甘露醇对高血压性脑出血早期血肿扩大的影响

为了探讨甘露醇对高血压性脑出血早期血肿扩大的影响 ,将 71例急症就诊的高血压性脑出血患者随机分为甘露醇治疗组 (A组 )和速尿治疗组 (B组 ) ,并行颅脑 CT复查观察治疗后 2 4小时两组血肿扩大情况。结果显示 ,血肿扩大发生率为 A组 33.3% ,B组 17.1%。提示应用大剂量甘露醇脱水治疗可能是高血压性脑出血早期引起血肿扩大的原因之一 ,建议发病 2 4小时内应用速尿降低颅内压 ,病情危重者可联用甘露醇与速尿。     

Effect of a new hyperosmotic agent, NIK-242 injection, on brain water content, metabolites and cerebral blood flow in cerebral ischemia in the spontaneously hypertensive rat.

We examined the effects of a new hyperosmotic agent (NIK-242inj.) on brain edema, energy metabolites and regional cerebral blood flow (r-CBF) during acute cerebral ischemia. Cerebral ischemia was induced by bilateral common carotid artery ligation (BLCL) using spontaneously hypertensive rats (SHR). The experimental animals were divided into 4 groups, A:20% NIK-242inj., B:20% mannitol, C:10% glycerol in 5% fructose, D:normal saline. All the animals were administered the agent or saline intravenously beginning at 1h after BLCL and continuing for 2h for a total dose of 6.8 ml/kg body weight. Brain water content and metabolites (ATP, lactate, pyruvate) were determined 3h after BLCL. Regional cerebral blood flow (r-CBF) in thalamus was also measured by the hydrogen clearance technique. The brain water content in the NIK-242inj. group was significantly lower than that of saline group. The concentration of brain ATP in the NIK-242inj. group remained higher than those of saline group. Accumulation of lactate in the NIK-242inj. group was less than in the mannitol and saline groups. The lactate/pyruvate ratio of the NIK-242 inj. group was significantly lower than that of the saline and mannitol groups. At 3h after BLCL, the reduction of r-CBF in the NIK-242inj. group was smaller than that of saline group. The present study suggests that NIK-242inj. as well as glycerol could ameliorate brain edema, disruption of brain energy metabolism and reduction of r-CBF in acutely induced cerebral ischemia.     

Influence of hypertonic mannitol on regional myocardial blood flow and ventricular performance in awake, intact dogs with prolonged coronary artery occlusion.

The influence of hypertonic mannitol on regional myocardial blood flow and ventricular performance in awake, intact, unsedated dogs with myocardial infarction resulting from chronic occlusion of the proximal left anterior descending coronary artery was studied. tmannitol given to increase serum osmolality 20 mOsm increased regional myocardial blood flow to that portion of the left ventricle supplied by the occluded left anterior descending coronary artery by 22 +/- 2.8% (1.06 +/- 0.19 to 1.36 +/- 0.23 ml/min with g-1) without changing the inner:outer wall flow ratio. Mannitol also significantly increased regional myocardial blood flow to other areas of the left ventricle and the ventricular septum. Mean aortic pressure, maximal LV dP/dt, LV dP/dt/P, and cardiac output also increased significantly after mannitol. Thus hypertonic mannitol increases regional myocardial blood flow and ventricular performance in the awake, unsedated dog with prolonged occlusion of the proximal left anterior descending coronary artery. The increase in regional myocardial blood flow after mannitol under these circumstances probably is at least in part secondary to the increase in blood pressure and contractility. The increases in regional myocardial blood flow after mannitol in this study are less impressive than those that have been previously reported in the setting of either no myocardial ischaemia or acute myocardial ischaemia; this is probably due to the vasodilatation that chronic myocardial ischaemia itself produces in the canine heart.     

Elevated vascular angiotensin converting enzyme in chronic two-kidney, one clip hypertension in the dog

The possible role of the vascular angiotensin converting enzyme (ACE) in the development of two-kidney, one clip (2-K, 1C) hypertensive dogs was studied in different blood vessels. Vascular ACE activity per mg protein differed in a variety of blood vessels; the activity appeared to vary inversely with the outer diameter of arteries. The systemic blood pressure in mongrel dogs increased after partial occlusion of the left renal artery, and the hypertension lasted for 8 months. Plasma renin activity (PRA) was raised only for the first 4 weeks after the operation and then returned to the original level in the chronic stage of hypertension. Plasma ACE activity did not alter during the experimental period. In contrast, ACE activities in the jejunal, pulmonary and renal arteries, aorta, lung and cerebral cortex, significantly increased in the chronic hypertensive stage (8 months after occlusion). The production of angiotensin II (ANG II) from ANG I was significantly greater in isolated arteries from 8-month hypertensive dogs than in those from normotensive dogs when assessed by the contractile responses to ANG I and ANG II. These results indicate that acceleration by increased vascular ACE activity of the production of ANG II in the vascular wall may contribute to the maintenance of hypertension in the chronic stage of 2-K, 1C hypertensive dogs having normal PRA and plasma ACE activity.     

大脑中动脉闭塞患者软脑膜侧支循环的影响因素

目的：探讨卒中危险因素对大脑中动脉闭塞患者软脑膜侧支循环形成的影响。方法从南京卒中注册系统中提取自2006年6月至2011年12月期间影像学证实为大脑中动脉闭塞的急性脑梗死患者,收集基线临床资料,通过脑血管造影评估软脑膜侧支循环。结果共纳入137例患者,男性100例,平均年龄(55．26±11．71)岁,65例(47．4%)患者侧支循环良好。单变量分析显示,侧支循环不良组年龄[(57．9±9．5)岁对(52．3±13．2)岁;t =2．866,P =0．005]和高血压的患者构成比(70．8%对52．3%;χ2=4．978,P =0．026)显著高于侧支循环良好组。多变量 logistic 回归分析显示,年龄是影响急性大脑中动脉闭塞患者软脑膜侧支循环形成的独立危险因素(优势比0．965,95%可信区间0．934~0．997;P =0．034)。结论年龄是影响大脑中动脉闭塞患者软脑膜侧支循环形成的独立危险因素。     

Effects of phenytoin on regional cerebral blood flow, electroencephalogram, and electrolyte contents in cerebral blood and cerebral cortex following total cerebral ischemia in dogs

To study the protective effect of phenytoin on postischemic brain damage, total cerebral ischemia was produced for 8-12 min (aortic occlusion balloon catheter method) in 36 adult mongrel dogs. The regional cerebral blood flow (rCBF), sodium:potassium ratio in the cerebral cortex, electroencephalogram (EEG), and plasma electrolytes in the superior sagittal sinus blood were examined before ischemia and during the acute stage up to 120 min after recirculation in the control and phenytoin-treated groups. Measurement of rCBF (microsphere method) indicated easing of postischemic hypoperfusion of the cerebral cortex. The time from total cerebral ischemia to EEG electrical silence was significantly prolonged, and recovery of the electrical activity after recirculation was hastened. The increase in plasma potassium concentration in the superior sagittal sinus tended to be suppressed immediately after recirculation, and the sodium:potassium ratio in the cerebral cortex was lowered. Phenytoin increased the rCBF in the cerebral cortex, hastened the recovery of electrical activity, and stabilized the water and electrolyte balance in the cerebral cortex, suggesting some protecting effect on total cerebral ischemia.     

Assessment of drug intervention on the ischemic myocardium: serial imaging and measurement with computerized tomography.

Computerized tomography was evaluated as a technique for imaging and measuring the effect of an intervention on acutely ischemic myocardium. Because cell edema occurs with acute myocardial ischemia and decreases the X-ray attenuation coefficients (tissue density) of myocardium, computerized tomographic images were used to quantitate the effect of hyperosmotic mannitol on ischemia-induced edema. Canine hearts were arrested and scanned after (1) temporary occlusion of the proximal circumflex artery followed by reflow of blood, or (2) continued occlusion of the distal left anterior descending coronary artery. X-ray attenuation values (Hounsfield units) were linearly related to tissue wet/dry weight ratios (r = 0.87, P less than 0.001). After 2 hours of occlusion of the left anterior descending coronary artery the hearts that received mannitol manifested a significant reduction (P less than 0.05) in the volume of left ventricular wall involved with edema. Although the area of edema measured with computerized tomography tended to be smaller in the hearts treated with mannitol than in untreated hearts subjected to a 6 hour occlusion of the left anterior descending coronary artery, the size of the lesion was variable and did not differ significantly from that in untreated hearts. With either short periods of circumflex arterial occlusion followed by blood reflow or with 2 or 6 hours of prolonged occlusion of the left anterior descending coronary artery, the difference in mean attenuation coefficients between the ischemic and nonischemic areas of myocardium in mannitol-treated and untreated hearts was significantly less. These results indicate that computerized tomography in the arrested heart can detect and quantitate the lesion of early acute myocardial ischemia and can quantitate the effect of drug intervention.     

Hypertension and the brain. The National High Blood Pressure Education Program.

Neurogenic mechanisms are important in the maintenance of most forms of hypertension, yet the brain is highly vulnerable to the deleterious effects of elevated blood pressure. Hypertensive encephalopathy results from a sudden, sustained rise in blood pressure sufficient to exceed the upper limit of cerebral blood flow autoregulation. The cerebral circulation adapts to chronic less severe hypertension but at the expense of changes that predispose to stroke due to arterial occlusion or rupture. Stroke is a generic term for a clinical syndrome that includes focal infarction or hemorrhage in the brain, or subarachnoid hemorrhage. Atherothromboembolism and thrombotic occlusion of lipohyalinotic small-diameter end arteries are the principal causes of cerebral infarction. Microaneurysm rupture is the usual cause of hypertension-associated intracerebral hemorrhage. Rupture of aneurysms on the circle of Willis is the most common cause of nontraumatic subarachnoid hemorrhage. Stroke is a major cause of morbidity and mortality, particularly among persons aged 65 years or older. Treatment of diastolic hypertension reduces the incidence of stroke by about 40%. Treatment of isolated systolic hypertension in persons aged 60 years and older reduces the incidence of stroke by more than one third. Blood pressure management in the setting of acute stroke and the role of antihypertensive therapy in the prevention of multi-infarct dementia require further study.     

脑血流监测对大鼠脑缺血模型制备的评价作用

目的 探讨脑血流监测对线栓法制备大鼠大脑中动脉阻塞(MCAO)局灶性脑缺血模型的评价作用。方法 分别将线栓插入30只SPF级Wistar Han大鼠颈内动脉颅内段(16.0±0.5)、(18.0±0.5)和(20.0±0.5)mm,制备3种局灶性脑缺血模型(各10只),然后将所有实验大鼠依据颅底有无血凝块及2,3,5氯化三苯基四氮(TTC)染色后大脑中动脉供血区有无梗死灶分为不全阻塞组、完全阻塞组及过深阻塞组,对阻塞颈内动脉颅内段前后及拔出线栓再灌注后每只大鼠大脑中动脉供血区脑皮质的血流量以激光多普勒法进行监测记录并进行统计学分析。大脑中动脉供血区脑皮质的血流量以相对流量单位PU值表示;阻塞后及再灌注后的脑皮质血流量变化以与阻塞前脑皮质血流量的百分比表示。结果 模型制作过程中,1只大鼠死亡;不全阻塞组9只,完全阻塞组15只,过深阻塞组5只。不全阻塞组8只大鼠线栓插入深度在(16.0±0.5)mm,不能完全阻止大脑前动脉向大脑中动脉的血流,缺血6 h后大鼠Longa评分0~1分;颅底动脉环周围无血凝块,经TTC染色后无梗死灶。完全阻塞组9只大鼠线栓插入深度在(18.0±0.5)mm,大脑前动脉的血流被完全阻断,缺血6 h后大鼠Longa评分2~3分;颅底动脉环周围无血凝块而TTC染色提示存在大脑中动脉供血区的梗死灶。过深阻塞组5只大鼠线栓插入深度在(20.0±0.5)mm,可完全阻断大脑前动脉血流,缺血6 h后大鼠Longa评分3~4分;解剖可见颅底血凝块,TTC染色后可见中动脉供血区梗死灶。插入线栓后,不全阻塞组、完全阻塞组和过深阻塞组大鼠脑皮质血流量均较阻塞前下降(分别为94±17比256±36、43±9比286±44、44±6比294±46,均P0.05),组间差异有统计学意义(F=56.57,P0.01),完全阻塞组和过深阻塞组血流量明显低于不全阻塞组(均P0.05),完全阻塞组与过深阻塞组间差异无统计学意义(P0.05);3组阻塞后与阻塞前脑皮质血流量的百分比分别为(36.93±0.06)%、(15.09±0.02)%、(15.52±0.04)%,组间差异有统计学意义(F=39.14,P0.01)。再灌注后,不全阻塞组、完全阻塞组和过深阻塞组脑皮质血流量(分别为213±31、147±17、96±14)均较阻塞后有明显回升(均P0.05),组间差异有统计学意义(F=50.05,P0.01),过深阻塞组脑皮质血流量明显低于完全阻塞组(P0.05);3组再灌注后与阻塞前脑皮质血流量水平百分比分别为(83.10±0.02)%、(51.83±0.05)%、(33.49±0.09)%,差异有统计学意义(F=93.23,P0.01)。结论 以激光多普勒对脑血流进行监测,可作为判断线栓法制备大鼠MCAO脑缺血模型成功与否的一种实时、便捷、微创、客观可靠的评价手段。     

Controlled trial of dexamethasone and mannitol for the cerebral oedema of fulminant hepatic failure.

A controlled trial of 44 patients was undertaken to evaluate the use of dexamethasone (32 mg stat, 8 mg qds) in preventing, and intravenous mannitol (1 g/kg) in reversing the cerebral oedema of fulminant hepatic failure. Diagnosis of cerebral oedema was based on intracranial pressure recordings or the presence of defined clinical signs. Cerebral oedema developed in 34 patients with similar frequency in those treated with and without dexamethasone (16 of 21 and 18 of 23 respectively). In those 34 patients episodes of cerebral oedema resolved significantly more frequently in the 17 patients who received mannitol than in the 17 patients who did not (44 of 53 and 16 of 17 respectively, p less than 0.001). Dexamethasone did not affect survival but among patients who developed cerebral oedema those who received mannitol had a significantly better survival than those who did not receive it (47.1% and 5.9% respectively, p 0.008, Fisher's one-tail test).     

脑出血继续出血与甘露醇应用时间的关系

目的探讨甘露醇对脑出血继续出血的影响及正确使用甘露醇的方法。方法选择150例脑出血、入院在1h以内,经CT检查,出血量在40ml以内的患者,无脑疝迹象,分为即刻应用甘露醇组(75例)和24h后应用甘露醇组(75例);7d复查脑CT,血肿增大超过33%为脑出血继续出血,分析不同时间应用甘露醇对脑出血继续出血的影响。结果即刻使用甘露醇组发生血肿扩大39例,24h后用甘露醇组发生血肿扩大13例,两组比较差异有非常显著性意义(P<0·01);两组患者疗效间差异有非常显著性意义(P<0·01);两组患者死亡率间差异有非常显著性意义(P<0·01)。结论高血压性脑出血患者发病24h内不适当应用甘露醇可增加脑出血继续出血的发生率,使病情加重。对于脑压增高没有危及生命的患者,尤其发病24h内的高血压性脑出血患者,不宜盲目使用甘露醇,以免使血肿扩大,加重病情。     

猫局灶脑缺血模型的改进并建立功能检查模型

目的　对猫持续性局灶性脑缺血模型加以改进 ,使其制作简便 ,模型标准、稳定 ,并建立功能检查模型。方法　猫麻醉后 ,经眶后暴露大脑中动脉 ,在其发出外侧纹状体动脉的外侧部电凝闭塞 ,以医用耳脑胶及明胶海绵粘合硬膜和骨窗。在术前及术后以1 8FDG(1 8F fluorodeoxyglucose)作示踪剂 ,进行PET(positronemissiontomography)检查 ,经计算机处理 ,得出各脑区的标准吸收值 (thestandardizeduptakevalue ,SUV)及脑结构图像。术后第 7天处死动物 ,行TTC染色 ,确定梗死部位及计算体积。结果　手术后在猫大脑中动脉 (MCA)皮层分布区均产生梗死灶 ,7d后的梗死体积为 (19 3± 0 70 ) % ,动物无死亡及并发症的发生 ;猫脑PET图像大体结构清晰 ,MCA闭塞后 1h即可见该侧MCA皮层区放射性浓聚影明显减低 ,且与最后梗死区相一致。结论　该模型制作方便 ,重复性及稳定性好 ,适合于脑血管疾病的功能性研究     

Thiopental infusion in the treatment of intracranial hypertension complicating fulminant hepatic failure

Intracranial hypertension complicating fulminant hepatic failure has a mortality in excess of 90% in the presence of renal failure if not rapidly responsive to mannitol and ultrafiltration. Based on data which suggest that barbiturates can be of value in controlling the intracranial hypertension of head injury, intravenous thiopental was assessed in 13 patients with fulminant hepatic failure. All had developed acute renal failure complicated by intracranial hypertension unresponsive to other modes of therapy and were likely by all published criteria to have little chance of survival. The dosage of thiopental was adjusted incrementally until intracranial pressure, measured by extradural transducers, fell to within normal limits or adverse hemodynamic changes occurred. The intracranial pressure was reduced, in each case, by 185 to 500 mg (median: 250 mg) thiopental given over 15 min, and in eight cases continuing infusion achieved stable normal intracranial pressure and cerebral perfusion pressure. Five of the patients made a complete recovery and there were only three deaths from intracranial hypertension. Side effects were few and included minor hypotension controlled by dose reduction. The response of otherwise intractable intracranial hypertension and the 38% survival rate was remarkable for a group of patients with such a poor prognosis.