后装放疗照射犬外周血管神经的病理学观察

目的观察高剂量率(HDR)192Ir后装照射犬外周血管、神经病理反应，为HDR后装放疗应用于骨与软组织恶性肿瘤保肢术提供放射剂量耐受阈参考。方法健康普通犬12条，常规外科手术沿犬股神经血管束放置施源器，术后经3次HDR后装放射，每种剂量1条犬，总剂量分别为15、30、45、60、75、90Gy，照射长度1．0cm，照射后10、60d活体取材，经光镜和透射电镜进行组织学观察，自身对侧血管神经束作对比。结果照射后10d，大血管主要表现为内膜病变；照射后60d，剂量达到45Gy时，出现明显的不同程度血管增生和管腔狭窄。神经照射后改变，15Gy组变化不明显；30Gy以上组变化明显：急性期出现不同程度脱髓鞘，髓鞘和轴突崩解脱失等改变；慢性期神经萎缩明显。结论HDR后装放疗引起外周血管明显病理变化的剂量为45Gy；而30Gy足以引起明显的神经病理变化。建议临床治疗控制在总剂量30Gy以下，贴近神经处酌减剂量。     

高能电子射线局部外照射致皮肤损伤的实验研究

一、材料与方法 1.动物来源及分组:选取SD近交系雄性大鼠49只(本校实验动物中心),其中39只采用100 g/L水合氯醛腹腔注射麻醉,0.8 ml/200～250 g,周围以铅板屏蔽,以直线加速器发射高能电子射线一次性照射大鼠臀部皮肤,面积约4 cm×4 cm, 能量为6.4×10-13 J.根据照射剂量不同分为5、15、45 Gy 3组.5 Gy组14只,7只照射后2个月处死,7只3个月处死;15 Gy组15只,其中10只照射后2个月处死,5只3个月处死;45 Gy组10只,照射后2个月处死.余下10只作正常对照组,普通饲料喂养,不作任何处理.     

术前短程冲击放疗、术后后装放疗治疗原发性肝癌

目的 探讨术前短程冲击放疗和术后后装照射治疗原发性肝癌的治疗效果。方法 自1998年5月至1999年10月，将50例行肝癌切除术的原发性肝癌病人随机分为放疗组和对照组，每组25例。放疗组术前先行放疗6Gy，共3次，休息2周后再手术。术中放置施源管3－6根，确定驻留点2－8个，术后3－10d行后装照射，单次剂量10Gy，照射2－4次，总剂量20－40Gy。对照组手术前后不放疗。手术前后定期查血常规、肝功能、AFP、CT、B超、胸片，记录术中出血量。结果 放疗组术前放疗后肿瘤明显缩小（P＜0.05)；术中出血量显著低于对照组（P＜0.05)；后装照射后AFP转阴率100％（16／16），对照组63.6%（9／14）（P＜0.01)；6个月复发率0，低于对照组20％（5／25）（P＜0.01)；6个月生存率100％（25／25）无显著差异（P＞0.05)。结论 手术前短程冲击放疗和术后后装放疗是提高原发性肝癌近期治疗效果，降低复发率的有效手段。     

腹膜后非脏器恶性肿瘤的非手术治疗

腹膜后非脏器恶性肿瘤发病率不高，但病理分类复杂。除恶性淋巴瘤外，绝大多数为软组织肉瘤。对放疗、化疗均不敏感。其治疗主要为手术治疗，放疗与化疗仅为辅助治疗。腹膜后恶性淋巴瘤之治疗原则应为放疗与化疗的综合治疗。对何杰金淋巴瘤可仅照射肿瘤累及的部位；也可以扩大野照射，进行次全淋巴结照射或全淋巴结照射。因腹膜后肿瘤部位较深，宜采用穿透力强之直线加速器8～15MV高能X线为放射源；其次为60钴之γ线放射源；不宜采用常压之深部X线或电子束。肿瘤量可为40～45Gy／4～6周。化疗常用方案有MOPP方案：其推荐剂量为盐酸氮芥6…     

术前短程冲击放疗和术后后装放疗治疗原发性肝癌

目的：探讨术前短程冲击放疗和术后后装照射治疗原发性肝癌（PLC）的效果。方法：50例行肝癌切除术的PLC患者随机分为放疗组和对照组，每组25例。放疗组术前先行放疗6Gy，共3次，休息2周后再手术。术中放置施源管3－6根，确定驻留点2－8个，术后3－10d行后装照射，单次剂量10Gy，照射2－4次，总剂量20－40Gy。对照组手术前后不行放疗。结果：放疗组术前放疗后肿瘤明显缩小（P＜0．05）；术中出血量显著低于对照组（P＜0．05）；后装照射后AFP转阴率100％（16／16），对照组56．3％（9／14）（P＜0．01）；放射组术后6个月复发率（0）显著低于对照组（20．0％）（P＜0．01）；6个月生存率（100％）与对照组（92．0％）无显著差异（P＞0．05）。结论：手术前短程冲击放疗和术后后装放疗是提高PLC近期治疗效果，降低复发率的有效手段。     

大剂量体外射线照射对ePTFE人工血管吻合口的影响

目的 观察术后大剂量体外射线照射对ePTFE人工血管吻合口的影响.方法 20只杂种犬均施行肾下平面腹主动脉ePTFE人工血管置换术,术后随机分为对照组及照射组各10只.照射组术后2周予35 Gy体外射线分割照射(等效于恶性肿瘤根治性剂量70 Gy),观察照射后ePTFE人工血管吻合口大体变化以及显微镜下吻合口组织形态的改变;并应用CD34行免疫组化分析,观察射线照射对局部内皮细胞覆盖的影响.结果 与对照组比较,在术后4,8周内,照射组人工血管吻合口区域出现较明显的组织形态学改变,未见人工血管吻合口不愈合、或破裂以及局部动脉瘤形成等情况;未出现人工血管血栓形成率的增加.吻合口两侧血管CD34均为阳性.结论 短期观察内大剂量的射线对人工血管吻合口不会造成严重的影响,不会产生严重的负面效应.     

腹腔镜肝癌切除术28例报告

目的探讨腹腔镜肝癌切除术的适应证和可行性。方法回顾性分析2002年3月至2007年10月完成的腹腔镜肝癌切除术28例患者临床资料。结果28例均成功在腹腔镜下完成手术。对于位于肝左外叶的肿瘤，选择规则性肝左外叶切除术；肿瘤位于肝脏边缘或右肝表面时，选择肝脏不规则切除术。平均手术时间95min（60～150min）。平均术中出血345ml（50～800ml）。切除标本最大体积11cm×9cm×7cm。患者术后24h均能下床活动，术后2～3d即能进食。术后平均住院时间8d（5～15d）。术后病理诊断为原发性肝细胞癌24例，结直肠癌肝转移4例。结论对位于肝脏边缘、右肝表面或者左肝外叶的肝癌行腹腔镜肝癌切除术是安全可行的。     

组织间植入125I粒子诱导H22肝肿瘤细胞凋亡的研究

目的观察^125I粒子近距离照射对H22肝癌细胞凋亡的影响及其机制。方法用原位末端脱氧核苷酸转移酶标记法（TUNEL）检测^125I粒子近距离照射对H22细胞凋亡的影响；免疫组化Elivion^TM plus法检测Survivin蛋白的表达。60只小鼠分为A组：植入放射性粒子；B组：植入化疗药DDP；C组：植入放射性粒子和化疗药DDP；D组：正常对照组。结果^125I粒子近距离照射和／或化疗后对H22肝癌肿瘤体积抑制率A、B、C组分别为43．8％、40．7％和58．3％；凋亡指数（AI）分别为（25．15±10．36）、（33．42±12．25）和（42．34±13．95），与对照组D组（20．45±14．54）比较，C组其凋亡指数（AI）差异有统计学意义（P〈0．05）；Survivin蛋白的表达率分别为50．0％、55．6％和36．4％，与D组100．0％比较，C组表达率差异有统计学意义（P〈0．05）。结论^125I粒子近距离照射H22肝癌可有效诱导肝癌细胞凋亡，抑制肝癌细胞增殖；联合化疗药，其凋亡作用更强；Survivin可能参与了其中的调节作用。     

射频消融术后胆管损伤的病理学研究

目的 观察射频消融（radiofrequency ablation，RFA）犬肝内大胆管旁的病理学改变。方法 健康成年杂种犬20只，随机分4组。RFA射频针统一张开20mm，射频治疗时，能量由小到大序贯使用，开始能量为5W，以后每1min升高5W，最高可达95W的情况下，距肝内大胆管旁不同距离（1．0～2．9mm、3．0～4．9mm、5．0～7．9mm、8．0～10．0mm）行RFA，术后观察相关胆管的病理学改变。结果 在肝内大胆管旁行RFA，当距离为1．0～2．9mm时，整个胆管壁全层均坏死或部分全层坏死；距离为3．0～4．9mm时，部分胆管壁全层坏死和胆管上皮细胞空泡样改变；当距离为5．0～10．0mm时，胆管上皮细胞胆管空泡样改变或正常。结论 RFA位于肝内大胆管旁时，距离≥5．0mm时胆管上皮细胞改变损伤是轻微的、可逆的，而距离〈5．0mm时胆管损伤是较严重的、不可逆的。     

高剂量近距照射治疗高危前列腺癌

自2003年起采用^192铱高剂量近距照射（HDR—BT）联合远距照射治疗无转移高危前列腺癌42例，治疗前T2期6例、T3期36例；Gleason评分〈6分6例、≥6分36例；PAS值〈10．0ng／ml 13例、10．0—20．0ng／ml 9例、〉20．0ng／ml 20例。方法：第1、8天超声引导下HDR—BT前列腺被膜和前列腺外肿瘤各1次，每次8．5Gy，为使剂量平均分布，使用后装技术，通过3mm模板置入固定中空导针插植照射源^192铱，     

Radiobiology of radiosurgery: Part I. The normal rat brain model.

Because limited histological information is available from clinical radiosurgical experience, animal investigations are needed to answer questions regarding the biological response of both normal and pathological tissues. To determine the radiosurgical dose-response relationship of normal brain, we irradiated the right frontal lobe of 18 rats with a single 4-mm isocenter of stereotactic irradiation using the 201-source 60Co gamma unit. Maximal single-fraction doses varied from 30 to 200 Gy (2 rats per dose). All animals were observed for 90 days, killed, and histologically examined. No animal developed neurological dysfunction during that interval, regardless of dose. Animals that received 30, 40, 50, or 60 Gy had no pathological changes. In those given 70 Gy, we found occasional shrunken neurons, and at 80 Gy, rare arteriolar wall thickening. One animal that received 100 Gy had marked capillary endothelial cell degeneration and protein extravasation in the target volume, and the other had a 4-mm diameter necrotic region. Circumscribed cerebral necrosis also was identified in all 4 rats treated with either 150 or 200 Gy; astrocytosis, edema, and microhemorrhage were noted within the surrounding 1 to 2 mm of adjacent brain, and tissue outside that volume had a more normal appearance. We constructed a dose-response relationship based on the cellular, spatial, and temporal effects of focused single-fraction irradiation of the rat brain. To determine the temporal evolution of a known necrotic lesion (200 Gy), 12 other animals were killed (2 each) 1, 7, 14, 21, 30, or 60 days after radiosurgery.(ABSTRACT TRUNCATED AT 250 WORDS)     

Dose-related effects of single focal irradiation in the medial temporal lobe structures in rats--magnetic resonance imaging and histological study

The dose-related effects of single focal irradiation on the medial temporal lobe in rats were investigated by sequential magnetic resonance imaging and histological examination. Irradiation of 200 Gy as a maximum dose using 4 mm collimators with a gamma unit created an area of necrosis consistently at the target site within 2 weeks after irradiation. Irradiation of 100 Gy caused necrosis within 10 weeks, and 75 Gy caused necrosis within one year. Irradiation of less than 50 Gy did not induce necrosis consistently, although a restricted area of necrosis was created in the medial temporal structures including the intraparenchymal portion of the optic tract. 75 Gy may be the optimum dose for creating necrosis consistently in the medial temporal lobe structures. However, careful dose planning considering both dose-time and dose-volume relationships in necrosis development is necessary to avoid injury to vulnerable neural structures such as the optic tract when applying radiosurgical techniques to treat functional brain disorders in medial temporal lobe structures such as temporal lobe epilepsy.     

Anaplastic astrocytoma 14 years after radiotherapy for pituitary adenoma]

A case of anaplastic astrocytoma following radiotherapy for growth hormone secreting pituitary adenoma is presented with a review of the literature. A 43 year old female was admitted with the signs of acromegaly and hypertension. An eosinophilic pituitary adenoma was subtotally removed by transsphenoidal approach, and followed by 60 Gy irradiation using a 2 x 2 cm lateral opposed field. Fourteen years later at the age of 57, she suffered from headache, recent-memory disturbance and uncinate fits. CT scan and MRI disclosed ring-like enhanced mass lesion in the left temporal lobe, corresponding to the previous irradiated field. 18F-FDG PET showed hypermetabolism at the lesion. Left frontotemporal craniotomy was performed, and a reddish gray gelatinous tumor containing necrotic center and cyst was partially removed. Histologically, the tumor consisted of hypercellular astrocytic cells with perivascular pseudorosette. Coagulation necrosis at the center of the tumor, and hyalinosis and fibrosis of the blood vessels in and around the tumor, which might have been caused by the antecedent radiotherapy, were recognized. Postoperative radio- and chemotherapy were given, however, she expired 13 months after the operation. Seven cases, including ours, of malignant glioma following radiotherapy for pituitary adenoma were reported in the literature. A total dose of irradiation varies from 45 to 95 Gy with a mean of 50 Gy. The period of latency before tumor occurrence ranges from 5 to 22 years with a mean of 10 years. The differentiation of radiation-induced gliomas from radionecrosis of the brain is also discussed.     

Urologic complications of radiation therapy for gynecologic malignancies

Urinary symptoms are not well correlated with histologic bladder alterations from irradiation. The most common sequelae of bladder irradiation are acute, chronic and hemorrhagic cystitis and vesicovaginal fistula. Urodynamic evaluation of the bladder function postirradiation revealed a reduction in peak flow rate, volume at first desire to void, bladder capacity and bladder compliance. An increase in the volume of residual urine was noted. Most of these variables returned to normal values 6 months after the completion of irradiation. Most studies have found no significant correlation between measured irradiation doses to a specific point and bladder complications. When only external irradiation is given, bladder complications are not observed until a bladder dose of 60 Gy is delivered. Complications are noted with a dose of 55 Gy if such a dose is largely contributed by intracavitary therapy. The contribution of brachytherapy to bladder complications acquires significance with an external dose of 40 Gy or lower.     

A canine model for hepatic venoocclusive disease.

Hepatic venoocclusive disease is a frequent lethal complication of bone marrow transplantation. It has also been associated with hepatic irradiation and administration of chemotherapeutic agents without BMT. The pathogenesis and therapy of VOD are unclear. The present studies were directed at developing a canine model for VOD. Three groups of dogs were studied. Group one consisted of 8 dogs in which monocrotaline (MC) was administered at 125 mg/kg orally on an intermittent schedule. In 7 of the 8 dogs 6 to 9 doses of drug were administered between 42 and 110 days. Group 2 consisted of 6 dogs receiving busulfan 2 mg/kg/day for 17-25 days, when platelet counts decreased to less than 5 x 10(4)/mm3 or clinical bleeding occurred. Group 3 consisted of 2 dogs receiving 24 Gy and 4 dogs receiving 36 Gy of whole-liver irradiation. Seven of 8 dogs in group 1 developed significant liver function abnormalities and evidence of portal hypertension. Histologic findings of VOD were present at autopsy. Group 2 dogs failed to develop clinical or laboratory liver abnormalities, but 3 of 6 animals had minimal histologic evidence of VOD. Three of 6 dogs in group 3 receiving 36 Gy developed hepatic dysfunction and had findings of fibrosis at autopsy. It was concluded that MC administration produced consistent clinical and histologic features of VOD in dogs. Changes occurring after busulfan or total-liver irradiation administration were less reproducible. Dogs are a suitable large-animal model for studies of VOD.     

Anticonvulsant effects of gamma surgery in a model of chronic spontaneous limbic epilepsy in rats

OBJECT: The management of intractable epilepsy remains a challenge, despite advances in its surgical and nonsurgical treatment. The identification of low-risk, low-cost therapeutic strategies that lead to improved outcome is therefore an important ongoing goal of basic and clinical research. Single-dose focal ionizing beam radiation delivered at necrosis-inducing and subnecrotic levels was investigated for its effects on seizure activity by using an established model of chronic recurrent spontaneous limbic seizures in rats. METHODS: A single 90-minute period of repetitive electrical stimulation (inducing stimulus) of the hippocampus in rats elicited a single episode of status epilepticus, followed by a 2- to 4-week seizure-free period. Spontaneous recurrent seizures developed subsequently and persisted for the duration of monitoring (2-10 months). Simultaneous computerized electroencephalography and video recording were used to monitor the animals. After the establishment of spontaneous recurrent seizures, bilateral radiation centered in the ventral hippocampal formation was administered with the Leksell gamma knife, aided by a stereotactic device custom made for small animals. A center dose of 10, 20, or 40 Gy was administered using a 4-mm collimator. Control animals were subjected to the same seizure-inducing stimulus but underwent a sham treatment instead of gamma irradiation. In a second experiment, the authors examined the effects of gamma irradiation on the proclivity of hippocampal neurons to display epileptiform discharges. Naive animals were irradiated with a single 40-Gy dose, as already described. Slices of the hippocampus were prepared from animals killed between 1 and 178 days postirradiation. Sensitivity to penicillin-induced epileptiform spiking was examined in vitro in slices prepared from control and irradiated rat brains. CONCLUSIONS: In the first experiment, single doses of 20 or 40 Gy (but not 10 Gy) reduced substantially, and in some cases eliminated, behaviorally and electrographically recognized seizures. Significant reductions in both the frequency and duration of spontaneous seizures were observed during a follow-up period of up to 10 months postradiation. Histological examination of the targeted region did not reveal signs of necrosis. These findings indicate that single-dose focal ionizing beam irradiation at subnecrotic dosages reduces or eliminates repetitive spontaneous seizures in a rat model of temporal lobe epilepsy. In the second experiment, synaptically driven neuronal firing was shown to be intact in hippocampal neurons subjected to 40-Gy doses. However, the susceptibility to penicillin-induced epileptiform activity was reduced in the brain slices of animals receiving 40-Gy doses, compared with those from control rats that were not irradiated. The results provide rational support for the utility of subnecrotic gamma irradiation as a therapeutic strategy for treating epilepsy. These findings also provide evidence that a functional increase in the seizure threshold of hippocampal neurons contributes to the anticonvulsant influence of subnecrotic gamma irradiation.     

Focal hepatic ablation using interstitial photon radiation energy

BACKGROUND: Intratumoral ablative therapy is being used increasingly for the treatment of primary and secondary hepatic malignancies. The interstitial point-source photon radiosurgery system (PRS) is a novel ablative technique that uses radiation therapy similar in dosimetry to interstitial brachytherapy. STUDY DESIGN: To determine the feasibility, toxicity, and local tissue destructive capabilities of the PRS in the liver, preliminary studies in a nontumor-bearing canine model were examined. A 6-month survival study was conducted. Each animal received three radiation treatments, in the right, central, and left hepatic regions. Three low-dose treatments were delivered to each of six animals (group A), generating a 2.0-cm-diameter radiated sphere with a dose of 20 Gy at the lesion edge. Three high-dose treatments were delivered to each of six animals (group B), generating a 3.0-cm-diameter radiated sphere with 20 Gy at the lesion edge. RESULTS: The treatment reproducibly generated sharply demarcated hepatic ablative lesions proportional to the administered dose. Mean lesion diameter at 1 month was 1.6+/-0.2 cm in group A and 3.4+/-1.0 cm in group B. Lesion size was independent of intrahepatic location, including near vascular structures. PRS therapy, when applied to portal structures, resulted in hilar damage. Hilar damage appeared to be associated with arteriolar thrombosis and bile duct injury. Treatment of regions adjacent to large hepatic veins and the IVC was not associated with vessel thrombosis or stricture. CONCLUSIONS: PRS ablation is a generally well-tolerated method that results in consistent, well-demarcated, symmetric lesions of complete necrosis with minimal adjacent parenchymal injury. Application of such an approach for the treatment of liver tumors is promising.     

Postoperative radiation protocol for keloids and hypertrophic scars: statistical analysis of 370 sites followed for over 18 months

BACKGROUND: Before 2002, keloids and intractable hypertrophic scars were treated at our facility with postoperative irradiation of 15 Gy (the traditional protocol). Analysis of the therapeutic outcomes of patients treated with this protocol showed that the recurrence rates of keloids and intractable hypertrophic scars in the anterior chest wall, as well as the scapular and suprapubic regions, were statistically higher than at other sites, while the recurrence rates in earlobes were lower. Thus, we customized doses for various sites. This report describes our trial of postoperative radiation therapy. METHODS: Between January 2002 and September 2004, 109 patients with 121 keloid and intractable hypertrophic scar sites were treated with surgical excision following the new protocol: electron-beam irradiation at total doses of 10, 15, or 20 Gy, depending on the site. The recurrence rates and toxicities were historically followed in 218 patients with 249 keloid and intractable hypertrophic scar sites treated with the old protocol of surgical removal followed by irradiation at 15 Gy (without variation by site). The minimal follow-up time was 18 months. Statistical analysis was performed using Fisher exact probability test. RESULTS: Total recurrence rates were 29.3% before 2002 and 14.0% after 2003. The recurrence rate in the anterior chest wall was statistically reduced. Outcomes of earlobe did not differ between irradiation with 15 Gy or 10 Gy. CONCLUSIONS: Keloids and intractable hypertrophic scars should be treated with dose protocols customized by site. Our results suggest that keloid and intractable hypertrophic scar sites with a high risk of recurrence should be treated with 20 Gy in 4 fractions over 4 days and that earlobe should be treated with 10 Gy in 2 fractions over 2 days.     

造血干细胞移植前清髓及非清髓性照射预处理对小鼠血管内皮的影响

目的 探讨在造血干细胞移植前清髓及非清髓性全身照射(TBI)预处理对小鼠血管内皮的影响.方法 将6～8周龄雌性Balb/c小鼠随机分为正常对照组(正常小鼠)、致死剂量TBI组(~(60)Co 8.5 Gy)和减低剂量TBI组(~(60)Co 5.0 Gy).TBI后定期观察小鼠的生存状态,计数外周血白细胞;采用流式细胞术检测外周血中内皮细胞和内皮祖细胞的变化;通过病理切片及透射电镜观察小鼠小肠及肝脏的组织结构和血管内皮的超微结构.结果 致死剂量TBI组小鼠外周血白细胞减少,同时内皮细胞及内皮祖细胞增加,与正常小鼠相比,差异有统计学意义(P<0.05).减低剂量TBI组小鼠外周血白细胞先降后升,内皮细胞与内皮祖细胞同样也出现增加,与正常小鼠相比,差异有统计学意义(P<0.05);与致死剂量TBI组比较,其外周血内皮细胞和内皮祖细胞增加幅度明显降低(P<0.05).两个TBI组小鼠的病理切片均可见肝脏实质细胞水肿及小肠炎症细胞浸润,肝脏的超微结构可见血管内皮完整性受损,致死剂量TBI组受损更为显著.结论 清髓及非清髓性剂量TBI预处理均可引起小鼠血管内皮早期损伤,其损伤程度与剂量相关,且外周血中内皮细胞的变化可以反映血管内皮损伤的程度.     

Radiosurgery-induced microvascular alterations precede necrosis of the brain neuropil

OBJECTIVE: Radiosurgery is used as a therapeutic modality for a wide range of cerebral disorders. It is important to understand the underlying causes of deleterious side effects that may accompany gamma-irradiation of brain tissue. In this study, structural alterations in rat cerebral vessels subjected to gamma knife irradiation in vivo were examined, for elucidation of their potential role in necrosis formation. METHODS: A maximal center dose of 75 Gy was delivered to the rat parietal cortex with a 4-mm collimator, and changes occurring before necrosis formation were assessed 3.5 months after irradiation. Transmission electron microscopy, using horseradish peroxidase as a tracer, and scanning electron microscopy with vascular casting were performed. RESULTS: The capillary network in the irradiated area exhibited thickening and vacuolation of the basement membrane. The capillary density in the irradiated area was lower and the average capillary diameter was larger, compared with the nonirradiated side. These results indicate that substantial changes in the neuropil do not occur 2 weeks before the time of definite necrosis formation, whereas changes in the basement membrane are prominent. CONCLUSION: The necrotic response to intermediate doses of focused-beam irradiation appears after a considerable latency period and then progresses rapidly. This contrasts with previously reported responses to fractionated whole-brain irradiation, in which damage occurs slowly and gradually. Alterations in the microvascular basement membrane precede overt cellular changes in neuronal and vascular cells and provide an early index of cerebrovascular dysfunction in regions destined to undergo necrosis.