超选择动脉溶栓及血管成形术治疗急性脑梗死的临床研究

目的：探讨超选择经动脉尿激酶（UK）溶栓及血管成形术（PTA）治疗急性脑梗死的临床疗效。方法：随机取56例急性脑梗死病人为研究组，行超选择动脉溶栓及PTA治疗，取脑梗死病人为对照组，行UK静脉溶栓治疗，复查血管再通率，比较两组临床疗效及并发症。结果：颈内动脉（ICA），大脑中动脉（MCA），椎基底动脉闭塞血管再通率分别为50％，95％，和100％，PTA组6例中，ICA2例，椎基底动脉4例，均有血管再通，治疗后研究组神经功能缺损（NFD）评分，语言功能障碍恢复，3个月后临床神经功能均好于对照组，研究组并发症的数量和严重程度均明显低于对照组。结论：尿激酶超选择动脉溶栓及血管成形术是治疗急性脑梗死安全有效的方法，血管内精巧细致的超滑导丝和球囊扩张等机械性作用显弥补了单纯溶栓药物治疗的不足。     

超选择性动脉溶栓治疗急性脑梗死12例临床报告

目的：观察尿激酶超选择性动脉内溶栓治疗急性脑梗死的方法、用药剂量、临床疗效及安全性。方法：12例急性脑梗死超早期进行脑血管造影后，超选择性地把微导管插至梗死灶近端，注入尿激酶接触溶栓并在治疗前和治疗后分别查头颅CT，对病人进行神经功能评分。结果：12例患者中5例溶栓治疗术中复流再通，3例部分恢复血供（仍存部分狭窄）。溶栓后2周神经功能评分达100分5例，神经功能评分≥84分5例，64分1例，死亡1例。结论：超选择性动脉内溶栓治疗急性脑梗死，可使梗死血管复流再通，神经功能迅速恢复，是急性脑梗死最有效的治疗方法。     

急性脑梗死超早期应用尿激酶动脉溶栓治疗四例

目的评价急性脑梗死超早期应用尿激酶动脉溶栓的疗效及安全性。方法应用尿激酶动脉溶栓治疗4例急性脑梗死患者,分析溶栓时间窗、尿激酶剂量、责任供血动脉再通情况与转归的关系等。结果例2大脑中动脉溶栓后症状完全缓解;例4颈内动脉溶栓后颈内动脉完全再通,但有皮层支梗死;例1、3大脑中动脉溶栓后部分再通。本文4例患者溶栓后2周神经功能缺损评分明显降低。结论急性脑梗死超早期应用尿激酶动脉溶栓治疗能明显提高责任供血动脉再通率,改善患者预后。动脉溶栓对大、中动脉急性闭塞性脑梗死患者疗效显著,对穿支动脉急性闭塞脑梗死患者疗效欠佳,有待进一步随机、双盲、大样本证实。     

超选择性动脉溶栓治疗急性脑梗死的临床研究

目的 探讨尿激酶超选择性动脉溶栓治疗急性脑梗死的安全性和有效性。方法 前瞻性收集急性脑梗死病人217例,先行全脑血管造影明确责任血管部位,然后用导引导管或微导管按1万U/min的速度向责任血管泵入尿激酶,每注射10万U即重复血管造影,如果造影显示堵塞血管已经再通则停止溶栓治疗,在治疗2 h、 24 h、7 d、14 d按我国第四届脑血管病学术会议通过的脑卒中患者临床神经功能缺损程度评分标准评定疗效。结果 溶栓后,血管再通率为65.90%（143/217）,溶栓2 h、24 h、7 d和14 d的有效率分别为70.05%、70.97%、76.96%和79.26%。结论 对于急性脑梗死患者,超早期溶栓能恢复血流灌注,阻断脑梗死病理过程,避免脑细胞坏死,明显提高治愈率,降低致残率。     

超早期超选择性动脉溶栓治疗急性脑梗死的临床疗效

目的探讨超早期超选择性动脉溶栓治疗急性脑梗死临床效果,以期提高临床诊治水平。方法选取2010-01—2015-01 82例急性脑梗死患者为研究对象,分成2组,均经超早期选择性动脉溶栓治疗,观察组41例,超早期(6h)治疗,对照组41例,在6~24h治疗,观察治疗后在相关指标变化。结果对照组显效率34.15%,总有效率78.05%,血管再通率51.22%,出血转化率29.27%;观察组显效率51.22%,总有效率90.24%,血管再通率82.93%,出血转化率9.76%,2组比较差异有统计学意义(P0.05)。2组治疗后较治疗前在血液流变学高切、低切和Fib、ADL均有改善,治疗前后比较差异均有统计学意义(P均0.05),治疗后2组间以上指标差异有统计学意义(P均0.05)。2组治疗前NIHSS评分比较差异无统计学意义(P0.05),治疗后2h、24h、1周、2周较治疗前有改善,治疗后2h、24h、1周、2周比较差异均有统计学意义(P均0.05)。结论超早期超选择性动脉溶栓治疗急性脑梗死临床效果显著,能提高血管再通,降低出血转化。     

尿激酶治疗急性脑梗死动脉内溶栓28例分析

目的观察及评价选择性动脉内溶栓治疗急性脑梗死的临床疗效和安全性。方法 28例急性脑梗死患者(前循环发病6 h内11例,后循环发病12 h内17例)行动脉内选择性尿激酶溶栓治疗。结果发现闭塞24例85.7%,溶栓后完全再通15例62.5%,部分再通7例29.2%,未再通2例8.3%,总体血管再通率91.7%,颅内出血2例8.3%,死亡1例4.2%。4例后循环梗死患者未发现明显闭塞,在小剂量使用尿激酶后临床症状明显好转。结论选择性动脉内溶栓能提高闭塞血管再通率,明显改善预后,是治疗急性脑梗死的一种有效和较安全的方法。     

急性脑梗死血管内个体化溶栓治疗

目的探讨动脉溶栓治疗急性脑梗死的疗效及其安全性。方法选择急性发病且在12h内的脑梗死病人68例,采用不同方式机械性动脉溶栓,通过脑血管造影判断其血管开通情况并对其治疗疗效进行评估。结果 68例急性脑梗死患者中血管完全再通率58.8%(40/68),部分再通率为35.3%(24/68),未开通4例,占5.9%;临床治愈42例(61.8%),显著好转16例(23.5%),有效6例(8.8%),无效4例(5.8%);本组无死亡病例。结论经动脉溶栓是治疗急性脑梗死的一种安全有效的方法;建立急救绿色通道和规范其治疗措施,能较好的提高急性脑梗死患者救治的成功率,降低死亡率和致残率。     

早期动脉内超选择性溶栓治疗急性缺血性脑梗死

目的观察动脉内超选择性尿激酶溶解血栓治疗急性缺血性脑梗死的疗效及并发症。方法对6例发病于4～12h内的急性缺血性脑梗死患者行动脉内超选择性尿激酶溶解血栓治疗。结果经溶解血栓治疗后完全再通4例，部分再通2例；溶解血栓治疗后14d基本痊愈1例，显著进步3例，进步1例，死亡1例。溶栓后无颅内出血。结论早期动脉内超选择性尿激酶溶解血栓能明显提高闭塞血管再通率，改善预后，是治疗急性缺血性脑梗死的一种有效和相对安全的方法。     

大剂量尿激酶早期静脉溶栓治疗急性脑梗死临床应用研究

目的：探讨大剂量尿激酶（UK）早期静脉溶栓治疗急性脑梗死（ACT）的临床疗效,治疗时机及副作用发生率。方法：分析55例ACI患者的溶栓疗效。结果：55例ACI患者分为发病0－6小时（A组）和6－12小时（B超）。两组溶栓前后神经功能缺损评分积分差分别为：18．07＋6．13、19．12＋5．13。溶栓前后积分相比及两组溶栓结果相比有显著性差异（P＜0．01,P＜0．05）,总基本痊愈42例（76．3％）显著进步4例（7．6％）,进步3例（5．5％）,总有效率89％,血管再通率83．6％。2例合并颅内出血死亡。2例大面积梗死死亡,1例出现皮肤淤癍。结论：大剂量尿激酶（UK）早期溶栓治疗急性脑梗死（ACI）疗效肯定,超早期疗效更好,12小时内仍然有效。     

接触溶栓结合球囊机械扩张治疗急性脑梗死

目的观察和总结急性脑梗死的动脉接触溶栓结合球囊机械扩张开通栓塞血管的可行性和安全性.方法对15例急性脑梗死病人（栓塞血管分别为大脑中动脉6例,大脑前动脉3例,颈内动脉主干5例,基底动脉1例）均在发病9 h内进行超选择动脉接触溶栓治疗,其中6例结合球囊机械扩张开通颅内栓塞动脉.结果主要栓塞动脉100%再通,病人恢复较好.6例随访1～12个月,病情稳定.结论超选择动脉接触溶栓加球囊机械扩张治疗急性脑梗死安全有效,明显提高了栓塞动脉的再通率.     

罂粟碱开放血脑屏障动脉化疗96例恶性胶质瘤长期效果

目的观察和分析罂粟碱可逆性开放血脑屏障动脉注药化疗恶性胶质瘤的效果。方法对96例恶性胶质瘤病人经颈动脉穿刺注入罂粟碱可逆性开放血脑屏障后,动脉注入卡莫司汀(BCNU)进行治疗,连续观察20~23年。结果 96例中5年生存率25%,10年生存率11.45%,20年生存率10.4%。目前仍有10例生存,最长23年多。结论罂粟碱可逆性开放血脑屏障动脉注药化疗恶性胶质瘤可作为术后化疗的一种方式。     

Ischemic threshold of brain protein synthesis after unilateral carotid artery occlusion in gerbils

The threshold of the relation between regional cerebral blood flow and regional cerebral protein synthesis was investigated in gerbils submitted to a 1-hour occlusion of the left common carotid artery. Blood flow was measured with [131I]iodoantipyrine and protein synthesis with [14C]leucine using double-tracer autoradiography and trichloroacetic acid wash-incubation for removal of nonincorporated tracer radioactivity. Specific activity of blood and brain leucine and [14C]leucine incorporation into brain proteins was also measured by conventional high-performance liquid chromatography to validate the autoradiographic approach. In control gerbils, gray matter blood flow ranged between 180 and 220 ml/100 g/min and fractional amino acid incorporation was approximately 80%. Unilateral carotid artery occlusion resulted in graded ischemia with blood flow between 10 and 100 ml/100 g/min. Regional cerebral protein synthesis gradually declined at blood flows of less than 100 ml/100 g/min and approached 0 at a blood flow of 40 ml/100 g/min. This threshold for complete suppression of protein synthesis is much higher than that for maintenance of tissue energy state and suggests that the size of an infarct after focal ischemia is determined by the suppression of protein synthesis rather than by the breakdown of energy metabolism.     

Effect of hemodilution on cerebral hemodynamics and oxygen metabolism.

BACKGROUND AND PURPOSE: To evaluate the effects of hemodilution on cerebral hemodynamics and oxygen metabolism in the normal human brain, we measured regional cerebral blood flow, oxygen extraction fraction, oxygen metabolic rate, and regional cerebral blood volume in eight normal volunteers before and after hemodilution using positron emission tomography and oxygen-15-labeled gas inhalation technique. SUMMARY OF REPORT: Hemodilution was accomplished by phlebotomy of 400 ml and drip infusion of 500 ml low molecular weight dextran, which reduced hematocrit from 42.5% to 37.2% and arterial oxygen content from 19.1 to 16.9 ml/dl (both p less than 0.005). It also increased mean cerebral blood flow from 45.2 to 47.7 ml/100 ml/min (p less than 0.025), but decreased tissue oxygen delivery from 8.7 to 8.0 ml/100 ml/min (p less than 0.05) and cerebral blood volume from 4.9% to 4.6% (p less than 0.025) in the overall cortical gray matter. CONCLUSIONS: Our results indicate that hemodilution in the tested range does not improve oxygen transport or tissue oxygenation in the normal human brain, although it increases cerebral blood flow.     

Threshold relationship between cerebral blood flow, glucose utilization, and energy metabolites during development of stroke in gerbils.

Focal brain ischemia was produced in halothane-anesthetized Mongolian gerbils by occluding the right common and the left external carotid artery. Ninety minutes after vascular occlusion the following regional hemodynamic and metabolic parameters were evaluated in adjacent cryostat sections taken from seven different coronal planes of each brain: cerebral blood flow (CBF), glucose utilization (CMRG), and the tissue content of ATP and glucose. NADH fluorescence was recorded from the surface of the cryostat block. In addition, tissue slices were taken from each brain to determine the rate of phosphorylation of 2-deoxyglucose in ischemic and nonischemic regions. Depending on the density of ischemia, the following metabolic disturbances were observed. At CBF values below 35 ml x 100 g-1 x min-1 CMRG increased and at values below 25 ml x 100 g-1 x min-1 it declined sharply. Glucose content declined when CBF was below 35 ml x 100 g-1 x min-1 and ATP fell at CBF below 20 ml x 100 g-1 x min-1. At 10 ml x 100 g-1 x min-1 ATP was completely depleted. NADH fluorescence was found elevated at flow rates that caused an increase of glucose utilization and was maximal when CBF stopped. The ischemic thresholds for the initial increase in CMRG and the complete depletion of ATP content represent the metabolic equivalent of the penumbra zone and provide a basis for the evaluation of therapeutic procedures for the treatment of stroke.     

Phenylephrine-induced hypertension reduces ischemia following middle cerebral artery occlusion in rats

We studied the influence of phenylephrine-induced hypertension on the area of ischemia during brief middle cerebral artery occlusion. Rats were anesthetized with 1.2 minimal alveolar concentration (MAC) isoflurane, and the middle cerebral artery was occluded via a subtemporal craniectomy. Immediately thereafter, in one group (n = 9) arterial blood pressure was increased 30-35 mm Hg above the preocclusion level by intravenous infusion of phenylephrine. In a second, control, group (n = 10) there was no manipulation of blood pressure. Local cerebral blood flow was determined autoradiographically 15 minutes after occlusion. The areas (expressed as a percentage of the total coronal cross-sectional area) in which local cerebral blood flow decreased to three ranges (0-6 ml/100 g/min [rapid neuronal death probable], 6-15 ml/100 g/min [delayed neuronal death probable], and 15-23 ml/100 g/min [electrophysiologic dysfunction with prolonged survival probable]) were measured. The areas in which local cerebral blood flow decreased to the two more severely ischemic ranges were smaller in the phenylephrine group than in the control group. For example, in the coronal section in the center of the middle cerebral artery distribution, local cerebral blood flow was 0-6 ml/100 g/min in 6.7 +/- 1.4% of the section in normotensive rats but was in that range in only 1.7 +/- 0.6% of the section during phenylephrine-induced hypertension (p less than 0.05). For the 6-15 ml/100 g/min range, the areas were 6.8 +/- 0.8% and 3.8 +/- 0.7%, respectively (p less than 0.05). For the 15-23 ml/100 g/min range, there were no differences between groups.(ABSTRACT TRUNCATED AT 250 WORDS)     

Prognostic value of ICP, CPP and regional blood flow monitoring in diffuse and focal traumatic cerebral lesions

Forty patients with severe traumatic brain injury (GCS score 8 and less) aged 16-54 years treated in our clinic were analyzed. Correlations between clinical symptoms, CT signs of diffuse and focal traumatic lesions, intracranial hemorrhage, indices of cerebral blood flow (CBF) according to perfusion CT study, intracranial pressure (ICP) and cerebral perfusion pressure (CPP) were assessed. Main mechanism of injury in 27 of 40 (67.5%) patients was acceleration-deceleration due to traffic accidents which usually leads to diffuse axonal injury (DAI) of different severity. In the other 13 (32.5%) cases injury was associated with coup-countercoup mechanism which caused focal contusions mostly. Not only GCS score but CT-signs of DAI severity, intracranial hemorrhage and minimal levels of CPP had significant prognostic value. Results of perfusion CT studies demonstrated that in 37 of 40 (92.5%) patients cerebral blood flow decreased (below 28.6 ml/100 g/min) in one or more arterial blood distribution areas. Increase of CBF was registered in 9 cases (over 69 ml/100 g/min), in 6 of them elevation of CBF in one arterial distribution area was associated with reduction in the other. Generally, mean CBF values were higher in the middle cerebral artery circulation than in the other. The lowest CBF levels (16.3 +/- 6 ml/100 g/min) were observed in cortical and subcortical hemorrhagic foci while these values were significantly higher in the same contralateral intact zones (36.0 +/- 10.0 ml/100 g/min; p < 0.01). In 3 patients with DAI the CBF in the midbrain varied from 12.5 to 30.1 ml/100 g/min with the lowest levels in hemorrhagic focus in cerebral peduncle. It corresponded to cystic-atrophic alterations found on subsequent follow-up MRI. Thus, reduction of CBF and episodes of low CPP were the leading pathophysiological phenomena of diffuse and focal brain damages.     

恶性滋养细胞肿瘤脑转移12例临床分析

目的探讨恶性滋养细胞肿瘤脑转移的临床特点、治疗方法、疗效、预后影响因素。方法回顾性分析154例恶性滋养细胞肿瘤中发生脑转移的12例患者的临床资料。除1例未及时治疗死亡外,其余11例均接受多药联合的全身及局部化疗3~10个周期,3例还进行了放射治疗。结果脑转移的发生率为7.8%,11例经正规治疗后的缓解率为72.7%,脑栓期、脑瘤期和脑疝期的病死率分别为0%、37.5%及100%。发生脑转移时未曾化疗、曾行化疗患者的缓解率分别为100%、62.5%。结论恶性滋养细胞肿瘤脑转移预后较差,重视脑转移的临床特点及早期诊断是改善预后的关键,曾否接受过化疗是影响其预后的重要因素,多药联合全身和局部化疗加放疗是治疗的主要手段。     

Ischemic thresholds of cerebral protein synthesis and energy state following middle cerebral artery occlusion in rat

The ischemic threshold of protein synthesis and energy state was determined 1, 6, and 12 h after middle cerebral artery (MCA) occlusion in rats. Local blood flow and amino acid incorporation were measured by double tracer autoradiography, and local ATP content by substrate-induced bioluminescence. The various images were evaluated at the striatal level in cerebral cortex by scanning with a microdensitometer with 75 microns resolution. Each 75 x 75 microns digitized image pixel was then converted into the appropriate units of either protein synthesis, ATP content, or blood flow. The ischemic threshold was defined as the flow rate at which 50% of pixels exhibited complete metabolic suppression. One hour after MCA occlusion, the threshold of protein synthesis was 55.3 +/- 12.0 ml 100 g-1 min-1 and that of energy failure was 18.5 +/- 9.8 ml 100 g-1 min-1. After 6 and 12 h of MCA occlusion, the threshold of protein synthesis did not change (52.0 +/- 9.6 and 56.0 +/- 6.5 ml 100 g-1 min-1, respectively) but the threshold of energy failure increased significantly at 12 h following MCA occlusion to 31.9 +/- 9.7 ml 100 g-1 min-1 (p less than 0.05 compared to 1 h ATP threshold value; all values are mean +/- SD). In focal cerebral ischemia, therefore, the threshold of energy failure gradually approached that of protein synthesis. Our results suggest that with increasing duration of ischemia, survival of brain tissue is determined by the high threshold of persisting inhibition of protein synthesis and not by the much lower one of acute energy failure.(ABSTRACT TRUNCATED AT 250 WORDS)     

Cerebrovascular and cerebrometabolic effects of intracarotid infused platelet-activating factor in rats

Platelet-activating factor has been implicated in a variety of disease processes including ischemic brain injury and endotoxic shock, but its effects on cerebral blood flow (CBF) and metabolism in normal brain have not been described. The effects of platelet-activating factor on global CBF (hydrogen clearance) and the global cerebral metabolic rate for oxygen (CMRO2) were studied in halothane-N2O anesthetized Wistar rats. Hexadecyl-platelet-activating factor infused into the right carotid artery (67 pmol/min) for 60 min decreased mean arterial pressure (MAP) from 122 +/- 4 (x +/- SEM) to 77 +/- 6 mm Hg and CBF from 159 +/- 12 to 116 +/- 14 ml/100 g/min (p less than 0.002). In contrast, CMRO2 increased from 9.7 +/- 0.9 to 11.7 +/- 1.1 ml/100 g/min after 15 min (p less than 0.05). In controls rendered similarly hypotensive by blood withdrawal and infused with the platelet-activating factor vehicle, CMRO2 was unchanged, whereas CBF transiently decreased then returned to baseline at 60 min. These cerebrovascular and cerebrometabolic effects of PAF are reminiscent of and may be relevant to hypoperfusion and hypermetabolism observed after global brain ischemia and in endotoxic shock.     

Selective enhancement of tumor blood flow and drug delivery to brain tumors in experimental rat gliomas under angiotensin II-induced hypertension

Regional blood flow of brain tumors and normal brain tissue of rats before and during angiotensin II (AT II)-induced hypertension were measured using an electrolytic flowmeter and a laser flowmeter. Etoposide concentration in the tumor and brain tissue after intracarotid administration were also measured in brain tumor bearing rats with or without AT II-induced hypertension. A suspension of 5 x 10(5)/10 microliters 9L gliosarcoma cells was inoculated into the left caudate-putamen of CD Fischer 344 rats. Before induced hypertension, regional blood flow of the tumor (28.2 +/- 2.6 ml/100 g/min; mean +/- SEM) and the contralateral caudate-putamen (23.0 +/- 1.8 ml/100g/min) in the tumor bearing rats were significantly lower than that of the caudate-putamen (43.9 +/- 4.1 ml/100g/min) in the normal rats (p less than 0.01). Intravenous administration of AT II at a dose of 0.4-0.6 microgram/body/min increased the mean arterial blood pressure from 96.5 +/- 4.7 mmHg to 138.0 +/- 3.6 mmHg. AT II-induced hypertension resulted in an approximate 1.8(1.1 - 3.6)-fold increase in the regional tumor blood flow. On the other hand the regional blood flow of the contralateral caudate-putamen was slightly decreased at the rate of 6%. The mean concentration of etoposide with AT II-induced hypertension in the tumor tissue was 2.2-fold higher than that without AT II-induced hypertension. However, etoposide delivery to normal brain tissue was small. From these results, induced hypertension with intravenously administrated AT II selectively increase the tumor blood flow and drug delivery to brain tumor tissue. Intracarotid chemotherapy with AT II-induced hypertension might contribute to enhance therapeutic effect of malignant brain tumors.