周围神经旁移植自体髓核对大鼠疼痛行为的影响

目的　探讨髓核在坐骨神经痛发病机制中的作用。方法　选择 16只SD雄性大鼠随机分为两组 ,分别将自体尾椎髓核混悬液注射到腰椎硬膜外腔或坐骨神经周围。测定其后肢机械刺激缩爪阈值。结果　在没有明显机械压迫下 ,腰椎硬膜外腔的髓核使大鼠后肢产生明显的痛觉过敏反应 ,坐骨神经旁的髓核不能使大鼠产生上述变化。结论　与髓核相关的炎症的介质是引起坐骨神经痛的原因之一 ,神经根缺乏神经外膜保护是引起疼痛的解剖学基础。     

异体纤维环组织硬膜外腔植入对大鼠痛阈的影响

目的 观察硬膜外腔植入异体纤维环组织对大鼠痛阈的影响,以期为椎间盘源性疼痛提供理论依据。方法 18只雄性SD大鼠（体重260-280g）随机分为假手术组、异体脂肪对照组和异体纤维环组（每组n=6）。所有大鼠在水合氯醛腹腔麻醉下于L6-S1间隙手术暴露硬膜外腔,假手术组不植入任何物质,异体脂肪对照组和异体纤维环组分别植入异体大鼠腹膜外脂肪和尾椎纤维环。在手术前、术后第3天、术后第7天、术后第15天及术后第30天分别测定尾部对伤害性电刺激、温度刺激及机械刺激的反应。结果 术后假手术组和脂肪组大鼠对各种刺激的痛阈与术前相比没有显著差异（p〉0．05）;而纤维环组在硬膜外腔植入异体髓核后对电刺激、机械刺激和温度刺激均表现为痛觉过敏（P〈0．05）。结论 异体纤维环组织硬膜外腔植入可引起大鼠痛觉过敏,这可能是椎间盘突出引起根性神经痛的原因之一。     

硬膜外腔植入髓核对大鼠脊髓背根神经节SP和CGRP表达的影响

目的 观察硬膜外腔植入异体髓核对大鼠L6-S1,脊髓背根神经节细胞SP和CGRP表达的影响,以期为椎间盘源性疼痛发病机制提供细胞生物学基础.方法 18只雄性SD大鼠(体重260-280g)随机分为三组:脂肪组、髓核组、假手术组,每组n=6.另外3只雄性SD大鼠用来提供异体脂肪和髓核.术后第30d取L4-L6脊髓背根神经节和脊髓背角,采用免疫组织化学染色方法 观察髓核对脊髓背角和背根神经节细胞肽类神经递质SP和CGRP表达的影响.结果 术后30d脂肪组大鼠与假手术组相比,脊髓背角和背根神经节细胞SP和CGRP表达没有显著性差异(P>0.05);髓核组与脂肪组和假手术组相比脊髓背角和背根神经节细胞SP和CGRP表达显著增加(P<0.05).结论 硬膜外腔植入异体髓核可引起脊髓背根神经节细胞SP和CGRP表达增加.     

脊髓神经元型一氧化氮合酶在大鼠神经病理性痛中的作用

目的 探讨脊髓神经元型一氧化氮合酶(nNOS)在大鼠神经病理性痛中的作用.方法 健康雄性SD大鼠40只,体重220～280 g,采用结扎坐骨神经干的方法建立坐骨神经慢性压迫性损伤(CCI)模型.随机分为4组(n=10),Ⅰ组及Ⅱ组暴露坐骨神经干,分别于术后1 d开始鞘内注射选择性nNOS抑制剂7-NI 60 μg[溶于20%二甲基亚砜(DMSO)]10μl)、20%DMSO 10μl,1次/d,连续6d;Ⅲ组及Ⅳ组制备CCI模型,分别于术后1 d开始鞘内注射7-NI 60μg(溶于20%DMSO 10μl)、20%DMSO 10 μl,1次/d,连续6 d.分别于CCI前1 d、CCI后1、3、5、7 d时测定大鼠机械痛阈和热痛阈.于CCI后7 d,各组分别取5只大鼠,取术侧L_(4～6)背根神经节,分别采用实时定量PCR和Western blot法测定nNOS mRNA及蛋白的表达水平.结果 与Ⅰ组和Ⅱ组比较,T_(1～4)时Ⅲ组和Ⅳ组术侧后肢机械痛阈和热痛阈降低(P＜0.05),背根神经节nNOS蛋白及mRNA的表达上调(P＜0.05);与Ⅲ组比较,T_(1～4)时Ⅳ组机械痛阈和热痛阈降低,背根神经节nNOS蛋白及mRNA的表达上调(P＜0.05).结论 脊髓nNOS参与了大鼠神经病理性痛的形成.     

鞘内注射PDTC对神经病理性痛大鼠TRPM8受体表达的影响

目的探讨NF-κB参与TRPM8受体在大鼠神经病理性痛觉调制中的作用。方法鞘内置管成功的SPF级健康雄性SD大鼠36只,4～6周龄,体重180～200g,采用随机数字表法分为三组:假手术组(S组)、神经病理性痛组(NP组)和NF-κB阻滞剂PDTC组(PDTC组),每组12只。鞘内置管成功后第3天,NP组和PDTC组采用坐骨神经缩窄性损伤(chronic constriction injury,CCI)法制备大鼠神经病理性痛模型;S组只游离坐骨神经不做损伤处理。三组大鼠术后1d开始连续鞘内注射,连续14d(2次/天),PDTC组鞘内注射PDTC 20μg/10μl(20μg PDTC溶于10μl生理盐水),注射完成后10μl生理盐水冲管,S组和NP组分别鞘内注射等容量生理盐水,三组大鼠分别于术前1d、术后1、3、7、10和14d鞘内给药后30min测定冷痛阈、热痛阈和机械痛阈。分别在术后7、14d处死大鼠,采用Western blot法检测背根神经节(DRG)中TRPM8受体和NF-κB p65蛋白含量。结果与S组比较,术后1～14dNP组冷痛阈明显降低、热痛阈明显缩短、机械痛阈明显降低(P0.05);与NP组比较,术后3～14dPDTC组冷痛阈明显增多、热痛阈明显延长、机械痛阈明显升高(P0.05)。与S组比较,术后7、14dNP组TRPM8受体和NF-κB p65蛋白含量明显升高(P0.05);与NP组比较,术后7、14dPDTC组TRPM8受体和NF-κB p65蛋白含量明显降低(P0.05)。结论大鼠DRG中TRPM8和NF-κB p65表达上调参与神经病理性痛的发生发展,抑制NF-κB活化可以减少TRPM8受体的表达上调并且改善大鼠痛觉过敏的症状。     

吗啡对非伤害性刺激后CCI大鼠脊髓c-fos表达的影响

目的　观察慢性坐骨神经收缩损伤 (CCI)大鼠触摸刺激后机械痛阈和热痛阈的变化 ,以研究吗啡 (2mg/kg)腹腔注射后对非伤害性刺激后脊髓后角c fos表达的影响 ,探讨脊髓痛觉调控机制。方法　选择雌性SD大鼠 30只 ,随机分为假手术组、CCI组和吗啡组 ,分别于术前 2d、术后 4、7、14d给予机械痛阈和热痛阈测试。大鼠处死前 3h给于非伤害性触摸刺激 ,处死后取脊髓切片 ,免疫组织化学方法检测c fos表达。结果　CCI组和吗啡组大鼠坐骨神经结扎 4d后均呈现不同程度的痛觉过敏 ,以术后 14d为甚 ,触摸刺激导致的脊髓c fos的表达明显增加 ,主要集中分布于脊髓背角表层Ⅰ～Ⅱ层的中间内侧部 ,Ⅴ～Ⅹ层也有一定程度增多。 2mg/kg腹腔注射不能有效的阻断慢性缩神经损伤大鼠痛觉过敏。吗啡组与CCI组相比c fos的表达无明显减少 ,两组相比差异无显著性意义 (P >0 0 5 )。结论　 2mg/kg吗啡腹腔注射不能有效抑制非伤害性刺激诱发痛觉过敏以及脊髓背角c fos的表达 ,可能与吗啡用药途径和用量过小有关 ,也可能与脊髓背角二级感觉神经元兴奋性增高有关     

柚皮苷硬膜外腔注射对髓核致坐骨神经痛大鼠的疼痛行为影响

目的研究柚皮苷硬膜外腔注射对致坐骨神经痛大鼠的疼痛行为学的影响。方法选择雄性SD大鼠28只,制作髓核致坐骨神经痛大鼠模型。随机分为4组,每组7只大鼠。术后第3天开始注药治疗,柚皮苷组每日硬膜外腔注入柚皮苷注射液50μl,地塞米松组每日硬膜外腔注入地塞米松注射液50μl,生理盐水组每日硬膜外腔注入生理盐水50μl,未注药组硬膜外腔无药物注入处理。检测大鼠术前,术后及给药后1、3、7、14d的疼痛行为指标（50％机械性刺激缩足阈值和热刺激缩足反应潜伏期）。结果4组大鼠在术后均对机械刺激产生明显的痛觉过敏,与术前比较差异有显著性（P〈0.05）;柚皮苷组与地塞米松组在提高疼痛行为学指标的作用方面差异无显著性（P〉0.05）。结论硬膜外腔注射柚皮苷可有效改善髓核致坐骨神经痛大鼠的疼痛反应。     

皮层躯体感觉诱发电位在监测腰神经根损伤中作用的研究

目的：利用大鼠髓核突出动物模型。探索皮层躯体感觉诱发电位（CSEP）的波幅和潜伏期变化是否与神经根性疼痛有关系。方法：取大鼠自体尾部的髓核无压迫下放置在L4和L5神经根上，制成髓核突出动物模型。分别在术后3d,1,2及4周观察大鼠术侧肢体机械刺激敏感性和热刺激敏感性和热刺激敏感性的变化，并引出大鼠后肢CSEP，观察术侧肢体CSEP的变化。结果：在无明显机械压迫的情况下，大鼠腰神经根上植入自体髓核可产生痛觉过敏，CSEP波幅增高。结论：髓核自身是引起腰腿痛的重要原因，CSEP波幅的增高与神经根性疼痛有一定相关性。     

磷酸化丝裂原活化蛋白激酶在大鼠髓核源性背根神经节炎性损伤中的变化

目的:观察背根神经节磷酸化p38丝裂原活化蛋白激酶(p-p38MAPK)表达的变化与非压迫性髓核所致的炎性反应及病理性神经痛的关系。方法:选择成年SD雄性大鼠54只随机分为假手术组(18只)和模型组(36只)。模型组在左L5神经背根神经节(DRG)应用自体髓核组织移植建立大鼠非压迫性腰椎间盘突出模型,假手术组应用自体肌肉移植。测量各组大鼠术前至术后21d时左后肢50%机械性撤足阈值(50%PWT)以测定机械痛敏的变化,假手术组术后7d及模型组术后7d、14d、21d取左L5DRG分别进行HE染色观察组织学变化和免疫组化法测定环氧化酶-2(COX-2)与p-p38MAPK的阳性细胞比率。结果:假手术组50%PWT术后无明显变化,模型组术后7d时出现明显的50%PWT下降损伤,术后14d达最低值,术后21d部分恢复。假手术组术后7d时DRG无明显组织损伤,COX-2和p-p38MAPK微弱表达。模型组术后7d时DRG组织损伤严重,COX-2、p-p38MAPK高表达;术后14d时组织损伤进一步加重,COX-2、p-p38MAPK表达更高;术后21d时组织损伤减轻,COX-2、p-p38MAPK表达减弱。结论:背根神经节p-p38MAPK的表达与非压迫性髓核所致炎性反应和病理损伤及病理性神经痛的变化密切相关。     

右美托咪定复合小剂量氯胺酮对神经病理性痛大鼠痛觉过敏及脊髓背角BDNF mRNA表达的影响

目的 探讨右美托咪定复合小剂量氯胺酮对神经病理性痛大鼠痛觉过敏及脊髓背角脑源性神经营养因子(BDNF) mRNA表达的影响.方法 SD雄性大鼠45只,8～ 12周龄,体重230 ～ 270g,采用随机数字表法,将其分为5组(n=9):假手术组(S组)、坐骨神经分支损伤组(SNI组)、右美托咪定组(D组)、氯胺酮组(K组)以及右美托咪定复合氯胺酮组(K+D组).除S组仅暴露坐骨神经外,其余各组均制备坐骨神经分支损伤模型.从术后24h开始,D组、K组和K+D组每天腹腔注射右美托咪定40μg/kg、氯胺酮10 mg/kg和右美托咪定20 μg/kg复合氯胺酮5 mg/kg,连续21 d,S组和SNI组给予等容量生理盐水.分别于术前ld、术后3、7、14、21 d时测定机械痛阈;机械痛阈测定结束后,分别于术前1d、术后7、21 d时处死3只大鼠,取L4-6脊髓背角,采用实时PCR法测定BDNF mRNA表达.结果 与S组比较,SNI组、K组、D组和K+D组术后机械痛阈均降低,脊髓背角BDNF mRNA表达上调(P＜0.05);与SNI组比较,K组、D组和K+D组术后机械痛阈升高,脊髓背角BDNF mRNA表达下调(P＜0.05);与K组和D组比较,K+D组术后机械痛阈升高,脊髓背角BDNF mRNA表达下调(P＜0.05).结论 右美托咪定复合小剂量氯胺酮对大鼠神经病理性痛具有协同镇痛作用,其机制与直接或者间接抑制脊髓背角BDNF合成有关.     

Metabolic function of grafted liver in rats

We studied the metabolic variations in grafted livers at different times after transplant by measuring the hepatic energy and redox states. Five groups of rats were studied: control ungrafted Wistar (RT1y) rats (group 1), ungrafted Wistar rats with ligature of the hepatic artery (group 2), isografted Wistar rats (group 3), allografted Wistar rats with livers from ACI (RT1a) donors (group 4, long-term surviving rat strain combination), and allografted Wistar rats with livers from BN (RT1n) rats (group 5, rejector rats). The metabolism of grafted livers was studied for 7 days in groups 2 and 3, for 2 months in group 4, and at the time of rejection in group 5. Adenine nucleotide levels (ATP, ADP, AMP) were significantly impaired at 24 hr and at 48 hr from grafting in isografted and in allografted livers, and the reestablishment of normal values began at the 7th day from grafting. Cytoplasmic NAD+/NADH ratios were lowered at 24 hr from grafting in isografted and in allografted livers. Mitochondrial NAD+/NADH ratios were lowered at 24 hr in isografted livers and at 24 hr and 48 hr from grafting in allografted livers. The metabolic studies performed for 2 months revealed a significant correlation between well-maintained metabolic functions and transplant survival. On the contrary, an important energy loss was evidenced in livers of group 5, at the time of rejection.     

Fos expression in the rat brain and spinal cord evoked by noxious stimulation to low back muscle and skin

STUDY DESIGN: Acute noxious stimulation delivered to lumbar muscles and skin of rats was used to study Fos expression patterns in the brain and spinal cord. OBJECTIVES: The present study was conducted to determine the differences in Fos expression in the brain and spinal cord as evoked by stimuli delivered to lumbar muscles and skin in rats. SUMMARY OF BACKGROUND DATA: Patients with low back pain sometimes show psychological symptoms, such as quiescence, loss of interest, decreased activities, appetite loss, and restlessness. The pathway of deep somatic pain to the brain has been reported to be different from that of cutaneous pain. However, Fos expression has not been studied in the central nervous systems after stimulation of low back muscles. METHODS: Rats were injected with 100 L of 5% formalin into the multifidus muscle (deep pain group; n = 10) and into the back skin of the L5 dermatome (cutaneous pain group; n = 10). Two hours after injection, the distribution of Fos-immunoreactive neurons was studied in the brain and spinal cord. RESULTS: Fos-immunoreactive neurons were observed in laminae I-V in the spinal cord in the cutaneous pain group, but they were not seen in lamina II in the deep pain group. In the brain, Fos-immunoreactive neurons were significantly more numerous in the deep pain group than in the cutaneous pain group in the piriform cortex, the accumbens nucleus core, the basolateral nucleus of amygdala, the paraventricular hypothalamic nucleus, the ventral tegmental area, and the ventrolateral periaqueductal gray. CONCLUSION: The finding that Fos-immunoreactive neurons were absent from lamina II of the spinal cord in the deep pain group is similar to that of the projection pattern of the visceral pain pathway. Fos expression in the ventrolateral periaqueductal gray in the deep pain group may represent a reaction of quiescence and a loss of interest, activities, or appetite. Furthermore, the detection of large numbers of Fos-immunoreactive neurons in the core of accumbens nucleus, basolateral nucleus of amygdala, paraventricular hypothalamic nucleus, and ventral tegmental area in the deep pain group may suggest a dominant reaction of dopaminergic neurons to stress, and a different information processing pathway than from that of cutaneous pain.     

Effect of nucleus pulposus on the neural activity of dorsal root ganglion

STUDY DESIGN: This study was designed to investigate, using neurophysiologic techniques in an in vivo rat model, the effect of application of nucleus pulposus to the nerve root on the neural activity of the dorsal root ganglion and the corresponding receptive fields. OBJECTIVES: To assess a further role of the dorsal root ganglion in mechanisms of radicular pain in lumbar disc herniation. SUMMARY OF BACKGROUND DATA: It has been suggested that the epidural application of autologous nucleus pulposus without mechanical compression causes nerve root inflammation and related radicular pain in lumbar disc herniation. Concerning the dorsal root ganglion, its mechanical hypersensitivity and potential for generating ectopic discharges have been reported. However, the effect of autologous nucleus pulposus on the dorsal root ganglion is uncertain. METHODS: In adult Sprague-Dawley rats spontaneous neural activity was recorded from the surgically exposed L5 dorsal root using electrophysiologic techniques, and the mechanosensitivity of L5 dorsal root ganglia and corresponding receptive fields on the hind paw were measured using calibrated nylon filaments. Autologous nucleus pulposus from the tail or fat was implanted at the L5 nerve root. Neural activity was monitored for 6 hours. RESULTS: Spontaneous neural activity in the nucleus pulposus group gradually increased and showed significant differences compared with the fat group from 2.5 to 6 hours after exposure. The mechanosensitivity of the dorsal root ganglia showed significant increases compared with the fat group. CONCLUSIONS: After application of nucleus pulposus to the nerve root, the dorsal root ganglion demonstrated increased excitability and mechanical hypersensitivity. These results suggest that nucleus pulposus causes excitatory changes in the dorsal root ganglion.     

Axon regeneration through blood vessel allografts after cyclosporine treatment

The present study describes the usefulness of blood vessel allografts to repair gaps in rat peripheral nerve after immunosuppression with cyclosporine. Isogeneic strains of rats with known histoincompatibility were used for this study. A 10-mm gap was created in the peroneal nerve of host Fischer rats. The gap was bridged by a 12-mm section of internal carotid artery removed from a Buffalo strain of rat. The host rats were divided into two groups. One group received no immunosuppression, whereas the other group was treated with cyclosporine. Untreated control rats immunologically rejected the allografted vessels and were unable to support host axonal regeneration through them. On the other hand, in cyclosporine-treated rats the allografted vessels survived. The regenerating host axons reorganized to form a functional nerve within the vessel conduit. The regenerated axons persisted even after rejection of the allografted vessel caused by cessation of immunotherapy. These results show that blood vessel allografts can serve as an effective conduit for reorganization of regenerated nerves and can bridge gaps in peripheral nerves.     

The treatment of peripheral nerve injuries using irradiated allografts and temporary host immunosuppression (in a rat model)

Irradiation of allografts prior to transplantation and host immunosuppression with cyclosporin-A were studied separately and in combination as means of lessening the rejection of transplanted peripheral nerve tissue. Lewis and Brown Norway rats were used in the animal model, as they differ at both major and minor histocompatibility loci. Sciatic nerve grafts (2.5 cm) were used and the animals were followed for 16 weeks after nerve grafting. The outcome was studied by functional measurements (sensory testing, gait analysis, joint flexion contracture, and muscle weight), as well as by measurements of biochemical and histologic parameters (hydroxyproline concentration and axon counts, respectively). Sensory testing was not reliable because of crossover innervation by the saphenous nerve. Evaluation by standard gait-testing techniques was found to be unsatisfactory. However, the allografted animals receiving cyclosporin-A had significantly smaller flexion contractures, compared to the allografted animals without immunosuppression (17 degrees +/- 12 degrees vs. 44 degrees +/- 13 degrees and 51 degrees +/- 13 degrees, p less than 0.005). Allografted animals receiving short-term cyclosporin-A had contractures that were not significantly different from those seen in isografted control animals (17 degrees +/- 12 degrees vs. 22 degrees +/- 15 degrees, NS). Muscle hydroxyproline concentration analysis revealed a lower hydroxyproline concentration among the allografted groups that received irradiated allografts, compared to groups receiving nonirradiated allogeneic grafts. The studies of muscle hydroxyproline concentration and muscle weight both showed substantial reinnervation, even in allografted animals without pretreatment of the grafts or immunosuppression of the recipient animal.(ABSTRACT TRUNCATED AT 250 WORDS)     

髓核对大鼠脊神经节非压迫性损伤的组织形态学研究

目的 观察硬膜外移植自体髓核后，大鼠脊神经节组织形态学的变化。方法 20只Sprague—Dawley(SD)雄性大鼠随机分成对照组和实验组，分别将自体肌肉混悬液和尾椎髓核混悬液注射到腰椎硬膜外腔，对脊神经节组织形态学进行观察。结果 在无机械压迫情况下，大鼠硬膜外移植自体髓核能使脊神经节组织形态产生明显改变。结论 髓核所致的炎性反应是引起脊神经节损伤和坐骨神经痛的重要原因之一。     

De-novo expression of vascular ecto-5′-nucleotidase and down-regulation of glomerular ecto-ATPase in experimental chronic renal transplant failure

Ischemic injury plays an important role in chronic renal transplant failure (CRTF). Down-regulation of ecto-adenosine triphosphatase (ATPase) in combination with up-regulation of ecto-5'-nucleotidase is a hallmark of ischemic injury. We studied the expression of renal ecto-5'-nucleotidase and ecto-ATPase in experimental renal transplantation. Fisher 344-to-Lewis allografted rats were either treated with an angiotensin-converting enzyme inhibitor (ACEi) or left untreated. Lewis-to-Lewis syngrafted rats served as controls. Untreated allografted rats developed proteinuria, glomerulosclerosis, and mild intimal hyperplasia. ACEi completely prevented focal and segmental glomerulosclerosis (FGS) and proteinuria, but significantly enhanced intimal hyperplasia. Untreated allografted rats revealed marked vascular ecto-5'-nucleotidase activity, which increased with ACEi. Vascular ecto-5'-nucleotidase activity was absent in syngrafted animals. Ecto-5'-nucleotidase activity correlated well with intimal hyperplasia. Glomerular ecto-ATPase expression was significantly reduced in untreated allografted rats compared to syngrafted rats and correlated well with the extent of FGS. ACEi prevented reduction in glomerular ecto-ATPase. We found de-novo expression of ecto-5'-nucleotidase at sites of renal intimal hyperplasia. Glomerular ecto-ATPase expression was markedly reduced in allografted rats and was prevented by ACEi. These enzyme expression patterns suggest local ischemic damage in experimental CRTF.     

神经肽Y应用对颗粒脂肪移植存活率的影响

目的：探讨神经肽Y应用对颗粒脂肪移植存活率的影响。方法将成熟颗粒脂肪组织自体移植到兔背部皮下,同时种植含有或不含有神经肽Y的小球,于2周、1个月、3个月后通过大体观察、B超、组织学、免疫组化法分组对照来评价脂肪颗粒的存活情况;同法将人体脂肪颗粒联合神经肽Y异体移植到无胸腺小鼠皮下,观测评价人体脂肪细胞在无胸腺小鼠的存活情况。结果应用神经肽Y组脂肪移植存活率明显高于其他对照组,神经肽Y可以刺激脂肪组织的生长,并且可以增加3个月兔和无胸腺小鼠异体脂肪移植物的存活和血供。结论神经肽Y应用在体内脂肪生成中起了重要作用,可增加脂肪移植存活或者刺激重新脂肪生成,明显提高颗粒脂肪移植的存活率,并可进一步应用于人体,具有良好的临床应用前景。     

The study of peripheral blood mononuclear cell MHC I and MHC II gene mRNA expression in acute graft rejection

BACKGROUND: Early diagnosis of acute graft rejection is important in the clinic. To explore a reliable diagnostic marker, we selected skin-grafted rabbits as an animal model to study peripheral blood mononuclear cell (PBMC) major histocompatibility complex 1 (MHC I) and MHC II gene mRNA in acute graft rejection (AGR). METHODS: Fifteen New Zealand white rabbits were randomly divided into three groups to observe skin graft rejection: three rabbits were in the autograft control group; six rabbits in a cyclosporine (CsA) treated allografted group; and the other six rabbits in untreated allografted group. The CsA-treated allografted group was given CsA (5 mg/kg) daily intramuscularly. PBMC samples were obtained every 2 days to detect by real-time polymerase chain reaction, PBMC MHC I and MHC II gene mRNA. RESULTS: MHC I and MHC II gene mRNA levels did not show any obvious change in the autografted controls. MHC I gene mRNA levels showed a slow increase in the CsA-treated allografted group, but no obvious change in the untreated allografted group. MHC II gene mRNA reached the highest level at 2 to 3 days before graft rejection appeared macroscopically in the CsA-treated allografted group and untreated allografted group, then decreasing to a low level. CONCLUSION: Compared with MHC I gene mRNA expression, PBMC MHC II gene mRNA expression may be considered to be an earlier marker for AGR.     

经保存的大鼠胚胎后肾同种腹腔内移植模型的建立

目的建立胚胎后肾大网膜内移植大鼠模型,并探讨其在受者体内生长、发育情况。方法取孕16d(E16)和17d(E17)的SD大鼠胚胎,切取胚胎后肾,以组氨酸色氨酸酮戊二酸盐液(HTK液)保存3d,然后移植到切除单侧肾脏的成年SD大鼠的大网膜内,另设未经保存的E16胚胎后肾直接移植对照组。术后给予环孢素A皮下注射,术后3～4周后开腹观察器官形成情况;术后8周,切除受者自体肾脏,观察移植后肾的组织学形态,测定后肾功能。结果移植后3周,移植后肾肾单位、集合管及输尿管的结构正常,组织中少有淋巴细胞浸润,电镜显示移植后肾发育的肾血管球细胞及基底膜、近端肾小管、远端肾小管和集合管上皮细胞超微结构正常。移植后8周,移植后肾的湿重、体积、分泌尿量及内生肌酐清除率与对照组比较,差异无统计学意义(P>0.05)。结论E16、E17胚胎后肾大网膜内移植,并辅以环孢素A皮下注射,可以形成器官,并发挥功能。