非限制性外支架防治移植静脉狭窄的早期形态学观察

目的 探讨非限制性外支架防治移植静脉内膜增生的效果及其可能的作用机制。方法新西兰白兔36只随机分成两组，每只均实施颈外静脉-颈总动脉移植术，支架组（S组）在移植静脉外套以直径6mm的非限制性涤纶外支架，对照组（NS组）移植静脉外无外支架，分别于术后7、14、28d取材进行观察。术后应用彩色多普勒超声观察移植静脉的通畅情况。组织切片进行HE和弹力VG染色和抗α-平滑肌肌动蛋白（α-SMA）免疫组织化学染色。采用计算机图像分析系统测量移植静脉内膜、中膜的厚度和面积，管腔面积，并计算内膜增值率（即内膜面积，内弹力板包围面积）。结果（1）S组术后死亡1只，闭塞性血栓形成1只，在支架与移植静脉之间有“果冻样”物质（新外膜）形成；NS组术后偏瘫并死亡1只，血栓形成1只。超声检查移植静脉通畅情况与取材时结果完全一致。（2）染色显示：术后7-28d，S组和NS组移植静脉内膜和中膜逐渐增生，S组新外膜为肉芽肿样增生，内有较多炎症细胞浸润。（3）计算机图像分析结果：S组和NS组内膜、中膜的厚度和面积均逐渐增加，术后7d时，S组的内膜厚度、面积和内膜增生率与NS组的差别无统计学意义，P〉0．05；术后14、28d，S组的内膜厚度、面积和内膜增生率均小于NS组，P〈0．05；术后1-4周，S组的中膜的厚度、面积均小于NS组，P〈0．05。结论非限制性外支架可以抑制移植静脉内膜和中膜增生；在非限制性外支架和移植静脉之间可以生成新外膜，新外膜的生成在防治内膜增生的过程中可能发挥了重要作用。     

低能量红激光局部照射对自体移植静脉内膜增生的影响

目的探讨低能量红激光局部照射对自体移植静脉内膜增生的影响.方法取80只大鼠,随机分为单纯自体静脉移植组(对照组,n=40)和低能量红激光局部照射组(激光组,n＝40).两组大鼠分别于术后第3 d、7 d、14 d及28 d取移植静脉段(每时相组各l0只)固定,行HE染色、弹力纤维染色及增殖细胞核抗原(PCNA)免疫组化染色,应用光学显微镜和计算机图像分析系统分析测定其内膜厚度和管腔面积.结果术后第3 d,两组管腔横截面积及内膜平均厚度差异无显著性意义(P＞0.05);激光组术后第7 d、14 d、28 d内膜平均厚度低于对照组(P＜0.05),管腔横截面积明显大于对照组(P＜0.05);PCNA免疫组化染色结果显示,激光组移植静脉平滑肌细胞(VSMC)增殖受到明显抑制(P＜0.01).结论低能量红激光局部照射可以抑制自体移植静脉内膜及VSMC的增生,减少再狭窄的发生.     

兔颈动脉无缝线胶黏吻合与传统缝线吻合的对比研究

目的　对比研究兔颈动脉无缝线胶黏吻合与传统缝线吻合的手术操作情况和吻合口通畅情况。方法　将 16只新西兰大白兔随机分为对照组和实验组 ,记录每个吻合口的吻合时间及出血量 ,术后 1、2、4、12周分别取材观察其通畅情况 ,并对吻合口内膜增生情况行病理切片和计算机图像分析。结果　与对照组相比 ,实验组的手术时间明显缩短 [(8.19± 6.5 1)min比 (2 0 .5 0± 14 .3 5 )min] ,术中出血量明显减少 [(2 .44± 5 .83 )ml比 (10 .3 8± 17.49)ml] ,通畅率也较高 (93 .8%比87.5 % ) ,内膜增生程度明显减轻 ,术后 1、2、4、12周时其内膜厚度分别降低了 3 1.4%、2 4.5 %、2 3 .9%和 3 1.9% (P <0 .0 1) ,其内膜面积分别降低了 3 6.2 %、2 9.1%、3 1.3 %和 40 .0 % (P <0 .0 1)。结论　中小血管的无缝线胶黏吻合较传统的缝线吻合操作省时省力 ,术中出血少 ,避免了缝针和缝线对血管吻合口处的透壁性损伤 ,消除了缝线等异物对管壁的持续性刺激所致的增生性反应 ,使吻合口处内膜增生减轻 ,吻合口通畅率提高。     

造血干细胞动员对移植静脉近期通畅率的影响

目的 研究造血干细胞动员对移植静脉近期通畅率和吻合口内膜增生程度的影响.方法 将24只新西兰大白兔随机分为实验组和对照组,每组12只,每只兔建立双侧颈动-静脉移植模型,其中一侧移植静脉于移植前采用0.25%胰蛋白酶去内皮细胞处理.实验组兔静脉移植后24h开始皮下注射分泌型基因重组人粒细胞集落刺激因子(rhG-CSF,100μg/kg),连续10d;对照组兔注射等量生理盐水.术后观察造血干细胞动员情况,包括外周血有核细胞计数,单个核细胞比率,移植静脉的近期通畅和吻合口内膜增生情况.结果 实验组术后5d外周血有核细胞计数(t=8.406,P=0.000)和单个核细胞比率(t=31.267,P=0.000)较对照组明显增加.两组内皮完整移植静脉均有较高的通畅率;去内皮移植静脉的通畅率明显降低,实验组通畅率高于对照组(67%vs.30%).实验结束实验组去内皮移植静脉吻合口搏动指数(PI)明显低于对照组(t=2.958,P=0.009).术后4周病理检查显示,两组移植静脉吻合口内膜均有不同程度地增生,去内皮移植静脉内膜增生程度较重,实验组去内皮移植静脉再内皮化完全,吻合口内膜增生程度明显轻于对照组(t=3.413,P=0.004).结论 造血干细胞动员对移植静脉有保护作用,可促进移植静脉的再内皮化,提高近期通畅率,预防吻合口内膜增生引起的再狭窄.     

小血管端侧镶嵌缝合法的实验研究与临床应用

在６０只Ｗｉｓｔｅｒ大白鼠股动脉分支血管模型上，设计与主于血管顺血流方向４５°和９０°角端侧镶嵌缝合法吻会的实验研究，与传统吻合法作为对照。术后９周内分别做解剖血管，测定血管外径和血流量，动脉造影，组织学检查等。结果证明，实验组术后１～９周内通畅率高于对照组。实验组无吻合口狭窄，其内膜光滑，增生轻，愈合良好。对照组有１／５的动物吻合口严重狭窄。半数以上的内膜高度增生，通血不良。经临床初步应用，证明此法有明显优点。     

碱性成纤维细胞生长因子对胆肠吻合口愈合的影响

目的　观察碱性成纤维细胞生长因子( basic fibroblast growth factor,b FGF)对胆肠吻合口愈合过程的影响,预防术后吻合口狭窄。　方法　选用健康杂种犬31只,随机分为实验组16只,对照组15只。通过制作犬胆总管十二指肠吻合模型,术后1周内吻合口局部应用b FGF(实验组)及生理盐水(对照组)。术后3d,1、3周,3、6个月( n=3)分别取材行HE及Masson染色组织学观察,吻合口瘢痕组织羟脯氨酸含量测定。　结果　实验组较对照组愈合时间明显缩短。组织学见实验组肉芽组织中成纤维细胞及毛细血管增生,上皮增生明显加快,1周时开始修复,3周时基本完成,瘢痕亦已基本定型,胶原纤维排列整齐有序,较快( 2～3周左右)进入塑形期;对照组术后3周时胶原纤维排列杂乱,呈旋涡状。电镜观察实验组肉芽组织中细胞功能旺盛,胞浆丰富,粗面内质网发达。瘢痕组织羟脯氨酸含量术后各时间点实验组均小于对照组,差异有统计学意义( P<0 .0 5 )。　结论　吻合口局部应用b FGF可预防术后胆肠吻合口狭窄     

羧甲基壳聚糖-羧甲基纤维素膜对结肠吻合口愈合的影响

目的 评估羧甲基壳聚糖(carboxymethyichitosan,CMCH)-羧甲基纤维素(carboxymethylcellulose,CMC)膜预防结肠吻合口粘连的效果及其对吻合口愈合能力的影响. 方法 取64只成年健康雄性SD大鼠随机分为对照组和实验组(n=32),按Buckenmaier等的方法 制备鼠结肠吻合口动物模型.对照组吻合口不作任何处理;实验组用3cm×2cm的CMCH-CMC膜包裹结肠吻合口部位.于术后7 d和14 d观察吻合口粘连情况;测定吻合口抗张强度,并与6只正常大鼠结肠抗张强度进行比较;检测吻合口羟脯氨酸(hydroxyproline,HP)含量. 结果 术中及术后共死亡5只大鼠,实验组2只,对照组3只.术后7、14 d粘连评分对照组分别为(1.67±0.15)、(2.29±0.18)分(P<0.05),实验组分别为(0.50±0.16)、(0.45 ±0.14)分(P>0.05);两组比较差异均有统计学意义(P<0.01).术后7、14 d吻合口抗张强度对照组分别为(138.67±16.65)、(178.36±20.10)mmHg(1 mmng=0.133 kPa,P<0.01);实验组分别为(130.81±18.38)、(172.74±22.18)mmHg(P<0.01);两组比较差异无统计学意义(P>0.05).术后7 d两组吻合口抗张强度与正常大鼠比较差异有统计学意义(P<0.01).术后7、14 d吻合口HP含量对照组分别为(55.47±12.89)、(137.14±16.81)lag/mg干重组织(P<0.01);实验组分别为(84.47±11.87)、(146.07 ±14.81) tg/mg干重组织(P<0.01);术后7 d两组差异有统计学意义(P<0.05),术后14d差异无统计学意义(P>0.05). 结论 CMCH-CMC膜在预防结肠吻合口周围粘连形成的同时不干扰吻合口的愈合.     

Fas—配体在移植物动态硬化血管平滑肌细胞中的表达

目的：为探讨移植物动脉硬化形成过程中,血管内膜和外膜增生的平滑肌细胞中是否有Fas-配体（Fas-L)表达。方法：健康纯系Wistar大白鼠为供者,306只;SD大白鼠为受者,162只,根据受者血管移植后有无明显排斥反应分为3组。急性排斥组：受者90只,分别于术后14天、28天、56天处死,每次处死30只;免疫耐受组;受者72只,分别于术后28天、56天、84天处死,每次处死24只;对照组：供者和受者均为Wistar大白鼠,受者72只,处死方法同免疫耐受组。采用同种异体大鼠胸主动脉腹腔移植模型。切取标本经处理后进行Masson染色和免疫组织化学染色,比较移植术后不同时间Fas-L在增生外膜和内膜平滑肌细胞上的表达水平。结果：术后14天、28天、56天急性排斥组外膜Fas-L的表达程度逐渐增高（P＜0．01）,其在外膜增生的平滑肌细胞中表达比内膜更早且广泛。Fas-L在急性排斥组的表达程度和范围亦比免疫耐受组和对照组明显增高和广泛（P＜0．05）。结论：在移植动物硬化形成过程中,Fas-L在增生平滑肌细胞中高度表达,其参与移植物动脉硬化的发生和发展。     

小承气合剂促进结肠吻合术后吻合口组织愈合的实验研究

目的评价小承气合剂对促进结肠吻合术后吻合口组织愈合的作用。方法选用Wistar大鼠40只,采用随机数字表法分为实验组(n=20)与对照组(n=20),2组均行结肠切除吻合术造模。实验组大鼠术后早期灌服小承气合剂,对照组大鼠同期灌服净化自来水。分别于术后第3、7和14天每组取相同数量大鼠进行剖腹探查,取吻合口及周围肉芽组织,检测羟脯氨酸含量和胶原纤维密度(Masson染色)。结果术后第3天,吻合口胶原已经开始增生,但纤维纤细,尚未形成束状纤维束,实验组大鼠羟脯氨酸含量及胶原纤维密度较对照组增高(P<0.05);术后第7天开始出现明显纤维化,但纤维束较细,纤维排列紊乱,实验组大鼠羟脯氨酸含量及胶原纤维密度明显高于对照组(P<0.01)。术后第14天,吻合口组织呈现广泛纤维化,且纤维束较粗,排列较整齐,2组大鼠羟脯氨酸含量及胶原纤维密度差异无统计学意义(P>0.05)。结论小承气合剂可促进术后胃肠吻合口愈合,可能有益于结肠吻合口漏的预防。     

单边内翻套入缝合法吻合兔颈动脉的实验研究

目的：探寻一种新的安全、快捷的小血管吻合方法。方法成年新西兰白兔45只，一侧颈动脉行单边内翻套入缝合法为实验组，另一侧行常规对端缝合法为对照组，比较两组的血管吻合时间、血管通畅率，术后1周，2周行血管吻合口的大体观察、组织学及扫描电镜观察。结果血管吻合时间：实验组为（12±2） min，对照组（16±2） min，差异有显著性（P＜0.05），实验组明显低于对照组。术后两组的血管即刻通畅率均为100%，近期通畅率均为98%，两组间差异无显著性（P＞0.05）。组织学及扫描电镜观察示两组血管吻合口愈合过程及时间相似。结论单边内翻套入缝合法吻合小血管快捷、简单，效果可靠。     

Oxygen tensions in healing anastomosis of rabbit aorta.

Tissue oxygen tensions in healing anastomoses of rabbit abdominal aortas were measured with ultramicro-oxygen cathodes with 1 to 3 mum tips. Two days after constructing the anastomosis, the over-all profile of intramural oxygen tension was different markedly from that of normal aortic wall, showing a progressive fall of Po2 from adventitia to media and no increasing gradient from media to intima. One week after operation to intimal Po2 increased and the oxygen gradient due to diffusion from the lumen was re-established. By the end of the second week adventitial and medial oxygen tensions reached their minimum. Six weeks after operation the oxygen tensions in the anastomosis resembled those of an intact aortic wall, suggesting that the availability of oxygen to the injured area had been re-established fully.     

Histological changes in the rat common carotid artery induced by aneurysmal wrapping and coating materials

Histological changes in and around the arterial walls of rats were investigated following topical application of aneurysmal wrapping and coating materials, including a fibrin glue, a cyanoacrylate glue (Biobond), and cotton fibers (Bemsheet). Bilateral common carotid arteries were exposed using sterile techniques, and one of the test materials was applied to the right artery. The left artery was used as the control. Changes in arterial histology were evaluated at 2 weeks, 1 month, 2 months, and 3 months after surgery. The fibrin glue was surrounded by intense inflammation at 2 weeks after surgery. Both the fibrin glue and inflammation had disappeared at 2 months, but the glue had induced mild inflammation in the adventitia. Biobond caused chronic inflammation, necrosis of the media, and thickening of the arterial wall due to fibrosis in both the media and adventitia. Bemsheet produced chronic inflammation, progressive fibrosis, and granuloma. Connective tissue increased in the adventitia, but no major changes were observed in the media. The Bemsheet fibers remained unchanged, and adhered to the arterial wall. Although arterial stenoses were not observed in the present study, the results suggest that cyanoacrylate glue can cause the arterial occlusive lesions observed following aneurysm surgery.     

Aorta transplantation as a model to study hyperacute, acute, and chronic rejection of xenografts

Abstract: To explore the mechanism of rejection of vascularized xenografts, we performed discordant and concordant transplantation of aortic grafts. Forty-one guinea pig-to-rat and 50 hamster-to-rat aortic transplantations were performed successfully. Recipient rats were either untreated or treated three times per week with 10 mg/kg of cyclosporine (CsA) starting the day before transplantation. Recipients were sacrificed at various timepoints after transplantation and the grafts were processed for histology and immunohistochemistry. Guinea pig aortic grafts were rejected hyperacutely in both the control and CsA treated group. Four hours after transplantation all endothelial cells and some of the medial smooth muscle cells had disappeared. Seven days after transplantation the media were totally acellular, whereas the adventitia was enlarged due to infiltrating cells, consisting mainly of macrophages. At day 56, only traces of the original graft could be identified.
Hamster aortic grafts developed signs of chronic rejection. In control rats, the intimal lesions could already be demonstrated in 17% of the rats at day 14, and in all rats from day 28. CsA treatment inhibited the development of the intimal lesions. At days 56 and 84 the difference in intimal thickness between the control group and the CsA treated group was statistically significant. The cellularity of the media of the hamster grafts remained constant during the first 21 days in both groups but declined sharply thereafter as a consequence of migration or necrosis of myocytes. The thickness of the adventitia in both groups increased after transplantation, due to infiltrating macrophages and T cells, reaching a peak at day 14. In conclusion, the aorta transplantation model provides useful information with regard to the development of chronic rejection in concordant grafts. Discordant aortic grafts are rejected hyperacutely just like discordant heart grafts.     

Vein to artery grafts: a morphological and histochemical study of the histogenesis of intimal hyperplasia.

Failure of vein to artery grafts has been associated with intimal thickening (hyperplasia) and atherosclerosis. Current theories of intimal development, derived from arterial studies, show that smooth muscle cells migrate from the media to the intima after endothelial damage, where they proliferate and produce intimal hyperplasia. However, little is known of the histogenesis of these lesions in vein grafts. Experimental ilio-lumbar vein to iliac artery autografts were placed in 52 rats and analysed by light microscopy and histochemistry from 2 to 140 days after surgery. On day 2 the grafts and adjacent artery were severely damaged. Regeneration of damaged arterial tissue occurred by day 5, and thickening was already evident in the arterial intima. The intimal cells had histochemical characteristics of smooth muscle. By day 15, this hyperplastic intima was continuous across the anastomosis from the artery into the graft. After day 28 a wedge of densely packed cells was present in the vein graft intima for approximately 2 mm into the graft. By day 140, all the grafts were fully re-endothelialized. Intimal hyperplasia was present in all grafts and varied in thickness from 3 to 20 cells. Histochemical staining of these cells showed them to be of smooth muscle origin.     

VEIN TO ARTERY GRAFTS: A MORPHOLOGICAL AND HISTOCHEMICAL STUDY OF THE HISTOGENESIS OF INTIMAL HYPERPLASIA

Failure of vein to artery grafts has been associated with intimal thickening (hyperplasia) and atherosclerosis. Current theories of intimal development, derived from arterial studies, show that smooth muscle cells migrate from the media to the intima after endothelial damage, where they proliferate and produce intimal hyperplasia. However, little is known of the histogenesis of these lesions in vein grafts. Experimental ilio-lumbar vein to iliac artery autografts were placed in 52 rats and analysed by light microscopy and histochemistry from 2 to 140 days after surgery. On day 2 the grafts and adjacent artery were severely damaged. Regeneration of damaged arterial tissue occurred by day 5, and thickening was already evident in the arterial intima. The intimal cells had histochemical characteristics of smooth muscle. By day 15, this hyperplastic intima was continuous across the anastomosis from the artery into the graft. After day 28 a wedge of densely packed cells was present in the vein graft intima for approximately 2 mm into the graft. By day 140, all the grafts were fully re-endothelialized. Intimal hyperplasia was present in all grafts and varied in thickness from 3 to 20 cells. Histochemical staining of these cells showed them to be of smooth muscle origin.     

人组织因子途径抑制因子基因转染对移植静脉新生内膜的影响

目的 为减少冠状动脉旁路移植术后移植静脉再狭窄,探讨人组织因子途径抑制因子(tissue factor pathway inhibitor,TFPI)基因转染对移植静脉内膜增生的影响. 方法 构建真核表达质粒pCMV-(Kozak)TFPI.将48只日本大耳白兔随机分为3组,每组16只,即TFPI转染组、空载体对照组和空白对照组.建立颈总动脉旁路移植模型.吻合前,TFPI转染组移植静脉内采用阳离子脂质体pCMV-(Kozak)TFPI(400μg)和腔内加压灌注法(30 min)转染,空载体对照组以空质粒pCMV(400 μg)代替pCMV-(Kozak)TFPI,空白对照组不予干预.术后3 d,用RT-PCR、Westernblot和免疫组织化学法检测外源基因在移植静脉中的表达.术后30 d,血管多普勒测最移植静脉管腔内径和管壁厚度;组织病理标本测量内膜面积和中膜面积,并计算其比值;透射电镜观察移植静脉新生内膜的细胞构成. 结果 TFPI转染组移植静脉中有人TFPI基因mRNA和蛋白表达,两对照组未见表达.TFPI转染组移植静脉管腔内径为(2.68±0.32)mm,大于空载体对照组(2.41±0.23)mm和空白对照组(2.38±0.21)mm,差异均有统计学意义(P＜0.05).TFPI转染组管壁厚度为(1.09±0.11)mm,小于空载体对照组(1.28±0.16)mm和空白对照组(1.34±0.14)mm,差异均有统计学意义(P＜0.01).TFPI转染组移植静脉内膜面积和内膜、中膜面积比值分别为(0.62±0.05)mm2及0.51±0.08,均小于两对照组的(0.70±0.05)mm2、0.58±0.06及(0.72±0.04)mm2、0.59±0.08(P＜0.05);中膜面积各组差异无统计学意义(P＞0.05).透射电镜观察,TFPI转染组移植静脉内膜未见甲滑肌细胞,两对照组均见甲滑肌细胞. 结论 人TFPI基凶转染减少移植静脉内膜增生.     

The effect of hyperbaric oxygen on medial collateral ligament healing in a rat model

Hyperbaric oxygen has been shown to promote healing in bone and some soft tissues. This study was undertaken to determine its effect on ligamentous healing. Forty-eight Sprague-Dawley rats underwent a standardized surgical laceration of the right (divided) medial collateral ligament, whereas the left (undivided) medial collateral ligament was not surgically lacerated. A control group of 24 rats recovered without intervention. An experimental group consisting of the other 24 rats was exposed to hyperbaric oxygen at 2.8 atmospheres for 1.5 hours a day for 5 days after the surgery. Six rats from each group were euthanized at 2, 4, 6, and 8 weeks. The stiffness and final force to failure were recorded for the divided and undivided medial collateral ligaments. At 4 weeks, a statistically greater force was required to cause failure of the previously divided ligaments that had been exposed to hyperbaric oxygen than those that had not. The stiffness and force to cause failure of previously divided ligaments were statistically greater at 4 weeks than at 2 weeks, whether or not hyperbaric oxygen was used. No additional statistical increases in stiffness or force were observed at 6 weeks.     

Zum Nachweis von Kollagenen in experimentellen arteriellen Anastomosen

Aim: To investigate the distribution of collagens in experimental microvascular surgery. Material and methods: Autografts (4 mm) of the left common carotid artery in 20 Wistar rats were harvested up to 4 weeks after surgery. The specimens were investigated immunohistochemically for the demonstration and distribution of collagen III and IV. Results: The demonstration and distribution pattern of collagens was a function of the accuracy of each single suture. In the intima, the organisation and amount of collagen IV was directed to the lumen and dependent on the distance and vitality of the vessel segments. The media had in its axis direction the lowest reparative potential for regenerating the continuity break. The adventitia formed a thick cuff around the anastomosis, in which collagen III and IV-positive vasa vasorum had grown in a circular fashion. The marked myointimal hyperplasia in the area around the anastomosis and in the entire autograft was made up of collagen-positive extracellular matrix. Conclusions: Our results support the demand for a careful and atraumatic suture technique in microvascular surgery. The identification of collagens in rat vessels is a valuable tool for studying wound healing in experimental microsurgery.     

移植动脉慢性排斥反应的病理组织学观察

目的 了解慢性排斥反应时移植动脉硬化的病理变化。方法 采用病理图象定量分析及电镜等检测手段,观察大鼠动脉移植后3、7、14、20、30及60d的病理变化。结果 同系移植对照组除供者血管冷缺血超过1h的2只术后14d内膜轻度增生外,基余移植动脉与受者自身的正常动脉比较,差异不显著;异系移植实验组术后3d血管外膜有大量炎性细胞浸润,7d时局部内皮剥脱,14d内膜中层细胞通过弹力膜裂隙向内膜迁移,内膜增生,20d内膜全层或局部呈8半月形增生,平滑肌细胞形态由收缩型转变为合成型,30d内膜细胞数达峰值,60d内膜持续增厚,基质纤维成分增多,内膜修复。结论 移植体动脉硬化具有内皮剥脱、炎性细胞浸润、中层坏死、平滑肌细胞迁移及内膜增生4大特点。     

Hyperbaric oxygen as an adjunct to acute revascularization of the brain

Two recent cases suggest that hyperbaric oxygen may be an important adjunct to the surgical treatment of occlusion of major cerebral arteries within the first few hours after onset of neurological deficit. In both patients, one with an embolus to the right middle cerebral artery and one with a surgical occlusion of the left internal carotid artery, circulation to the ischemic area was restored more than eight hours after occlusion. In the patient with the middle cerebral artery embolus, hemiplegia cleared after a six-minute exposure to hyperbaric oxygen. The patient with occlusion of the internal carotid artery was revascularized by anastomosis of a superficial temporal artery less than 1 mm in diameter to a branch of the middle cerebral artery. Her hemiplegia and aphasia cleared rapidly and concomitantly with intermittent exposure to hyperbaric oxygen during the first nine postoperative days. Postoperative angiograms demonstrated patency in both cases. The implications of these observations are discussed.