诺维本滴注浓度对兔外周血管组织损伤的实验研究

目的 探讨不同浓度诺维本对兔耳缘血管壁及其周围组织损伤的影响,为临床采用适合的诺维本滴注浓度提供依据.方法 将36只兔随机分成A、B、C三组,均于其双耳耳缘静脉同时滴注诺维本溶液.A组左耳注射浓度0.2 mg/ml、右耳0.4 mg/ml;B组左耳注射浓度0.2 mg/ml、右耳0.6 mg/ml;C组左耳注射浓度0.4 mg/ml、右耳0.6 mg/ml.均用输液泵控制滴速40 gtt/min,输液时间3 min.分别于滴注8 h、24 h、48 h观察双耳外观后,切取兔耳缘静脉及其周围组织,常规制作组织切片,观察兔耳缘静脉及其周围组织的损伤程度.结果 滴注不同浓度的诺维本8 h时兔耳缘静脉及周围组织损伤评分比较,差异无统计学意义(均P＞0.05);24 h时评分比较,差异有统计学意义(均P＜0.01);在48 h时,0.2 mg/ml、0.4 mg/ml浓度的损伤评分比较,差异无统计学意义(P＞0.05),而0.6 mg/ml浓度评分显著高于0.2 mg/ml及0.4 mg/ml(均P＜0.01);相同浓度不同时间段的损伤评分比较,差异有统计学意义(均P＜0.01).结论 诺维本滴注浓度与血管壁组织损伤呈正比,浓度越高,血管壁及周围组织损伤越严重;诺维本滴注适宜浓度为≤0.4 mg/ml,且每天应更换输液部位进行治疗.     

诺维本滴注浓度对兔外周血管组织损伤的实验研究

目的探讨不同浓度诺维本对兔耳缘血管壁及其周围组织损伤的影响,为临床采用适合的诺维本滴注浓度提供依据。方法将36只兔随机分成A、B、C三组,均于其双耳耳缘静脉同时滴注诺维本溶液。A组左耳注射浓度0．2mg／ml、右耳0．4mg／ml;B组左耳注射浓度0．2mg／ml、右耳0．6mg／ml;C组左耳注射浓度0．4mg／ml、右耳0．6mg／ml。均用输液泵控制滴速40gtt／min,输液时间3min。分别于滴注8h、24h、48h观察双耳外观后,切取兔耳缘静脉及其周围组织．常规制作组织切片,观察兔耳缘静脉及其周围组织的损伤程度。结果滴注不同浓度的诺维本8h时兔耳缘静脉及周围组织损伤评分比较．差异无统计学意义（均P〉0．05）;24h时评分比较,差异有统计学意义（均P〈0．01）;在48h时,0．2mg／ml、0．4mg／ml浓度的损伤评分比较,差异无统计学意义（P〉0．05）,而0．6mg／ml浓度评分显著高于0．2mg／ml及0．4mg／ml（均P〈0．01）;相同浓度不同时间段的损伤评分比较,差异有统计学意义（均P〈0．01）。结论诺维本滴注浓度与血管壁组织损伤呈正比,浓度越高,血管壁及周围组织损伤越严重;诺维本滴注适宜浓度为≤O．4mg／ml,且每天应更换输液部位进行治疗。     

三黄软膏不同时段外敷防治诺维本致静脉炎的实验研究

目的探讨不同时段三黄软膏外敷防治诺维本致兔耳静脉炎的效果,以明确三黄软膏外敷防治静脉炎的最佳使用时间。方法建立诺维本所致化疗性静脉炎的兔耳模型,随机分为A、B、C三组。分别在静脉注射诺维本后即刻、24h、48h用三黄软膏外敷干预,于第7天进行观察和局部病理切片,以评价静脉损伤程度。结果 A组静脉炎发生率最低,病理损伤程度最轻,其防护效果优于B、C组,差异有统计学意义(P<0.05,P<0.01)。结论三黄软膏越早外敷防治静脉炎效果越好。     

红黄洗液预防留置针输注甘露醇致静脉损伤的实验研究

目的探讨红黄洗液外用预防留置针输注甘露醇所致外周静脉损伤的效果。方法将30只新西兰白兔随机分为A、B两组各15只,取其双侧耳缘静脉置入留置针。A组左耳(红黄洗液组)注射常温(20℃)20%甘露醇,同时涂搽红黄洗液;右耳(乙醇组)涂搽75%乙醇。B组左耳(加温组)静脉注射加温至35℃20%甘露醇;右耳(对照组)静脉注射常温20%甘露醇。均为2次/d,间隔6h,连续5d。实验期间肉眼观察静脉炎发生情况,实验结束后行病理组织学分析。结果肉眼观察红黄洗液组静脉损伤评分显著低于另三组(均P0.05)。病理分析,针体段炎细胞浸润、纤维组织增生四组比较,差异有统计学意义(均P0.05);针体前段血管壁损伤、炎细胞浸润、纤维组织增生及血栓形成四组比较,差异有统计学意义(P0.05,P0.01)。结论采用留置针静脉注射20%甘露醇对兔耳缘静脉有不同程度的损伤,以针体前段更甚,用红黄洗液涂搽局部预防效果优于涂搽75%乙醇及液体加温法。     

红黄洗液预防留置针输注甘露醇致静脉损伤的实验研究

目的探讨红黄洗液外用预防留置针输注甘露醇所致外周静脉损伤的效果。方法将30只新西兰白兔随机分为A、B两组各15只,取其双侧耳缘静脉置入留置针。A组左耳（红黄洗液组）注射常温（20℃）20％甘露醇,同时涂搽红黄洗液;右耳（乙醇组）涂搽75％乙醇。B组左耳（加温组）静脉注射加温至35℃20％甘露醇;右耳（对照组）静脉注射常温20％甘露醇。均为2次／d,间隔6h,连续5d。实验期间肉眼观察静脉炎发生情况,实验结束后行病理组织学分析。结果肉眼观察红黄洗液组静脉损伤评分显著低于另三组（均P〈0．05）。病理分析,针体段炎细胞浸润、纤维组织增生四组比较,差异有统计学意义（均P〈0．05）;针体前段血管壁损伤、炎细胞浸润、纤雏组织增生及血栓形成四组比较,差异有统计学意义（P〈0．05,P〈0．01）。结论采用留置针静脉注射20％甘露醇对兔耳缘静脉有不同程度的损伤,以针体前段更甚,用红黄洗液涂搽局部预防效果优于涂搽75％乙醇及液体加温法。     

槐耳清膏诱导人直肠癌HR8348细胞凋亡的实验研究

目的　探讨槐耳清膏在体外对人直肠癌HR83 48细胞的生长抑制作用和凋亡诱导作用及其作用机理。方法　将处于对数生长期的HR83 48细胞用含槐耳清膏的培养基培养 3 6h ,用四氮唑蓝 (MTT )比色法检测吸光度 (OD)值 ,计算抑制率 ;用甲基绿 派若宁染色法及TUNEL法检测细胞凋亡指数 ;用免疫组织化学方法检测bcl 2、bcl xl、bax、bak及 p5 3基因表达的情况。 结果　槐耳清膏对HR83 48细胞的抑制率随浓度增加而上升 ,浓度为 4.0mg/ml时抑制率最大 (71.1% ) ,与 5 FU组 (浓度为 10 μg/ml)相比差异无显著性意义 (P>0 .0 5 )。甲基绿 派若宁染色法和TUNEL法均可见到典型的细胞凋亡、凋亡小体或出泡现象 ,凋亡指数随槐耳清膏浓度的增加而增加 ,当浓度达 4.0mg/ml时 ,凋亡指数迅速上升 ,甲基绿 派若宁法为 0 .162 0± 0 .0 12 8,TUNEL法为 0 .2 612± 0 .0 15 8,均大于 5 FU组的凋亡指数(0 .0 780± 0 .0 0 95和 0 .10 2 8± 0 .0 13 1) ,P<0 .0 5。槐耳清膏组bcl 2、bcl xl、bak、p5 3蛋白表达较空白对照组明显增强(P<0 .0 5 ) ,而bax变化不明显 (P>0 .0 5 )。槐耳清膏组bak/bcl 2和bak/bcl xl比值显著大于空白对照组。结论　槐耳清膏在体外对人直肠癌HR83 48细胞具有显著的抑制作用和凋亡诱导作用。槐耳清膏     

槐耳清膏联合氟尿嘧啶抑制肝癌生长转移的实验研究

槐耳清膏的主要活性成分是多糖蛋白（polysaccharide of trametes robiniophila murr，PS—T），能诱导人直肠癌细胞株（HR8348细胞）发生凋亡，对血管内皮细胞体外构建新生血管有抑制作用。但槐耳清膏对肝癌在体内的生长和转移的干预作用尚无报道。本研究利用裸鼠人肝癌转移模型LCI-D20进行了抑制肿瘤生长和转移的动物实验，现报道如下。     

反义TGF-β1抑制兔耳增生性瘢痕的实验研究

目的：探讨反义TGF-β1脱氧寡核苷酸对增生性瘢痕动物模型伤口愈合中瘢痕生成的抑制作用，研究局部使用反义。TGF-β1的有效给药途径。方法：成年日本大耳白兔20只，建立兔耳腹侧面增生性瘢痕模型。采用组织形态学的方法对比研究反义TGF-β1在兔耳增生性瘢痕形成中的影响，并用原位杂交法技术检测兔耳增生块内TGF-β1 mRNA、Ⅰ型胶原蛋白(colla-genⅠ)mRNA、Ⅲ型胶原蛋白(collagenⅢ)mRNA的表达水平。结果：兔左耳增生性瘢痕局部注射反义TGF-β1后，按时间段取材，HE和Masgon染色显示真皮层变薄，成纤维细胞数量明显减少，胶原排列趋于一致。增生块的相对增生高度低于对照组。原位杂交显示TGF-β1 mRNA、collagenⅠmRNA、collagenⅢ mRNA阳性细胞表达率明显降低。结论：反义TGF-β1能抑制兔耳增生性瘢痕的增殖过程，使瘢痕组织纤维化程度明显减轻。局部注射裸DNA治疗瘢痕的给药途径是可行的。     

二氢青蒿素抑制兔耳瘢痕增生的实验研究

目的：观察二氢青蒿素对兔耳增生性瘢痕增生的影响。方法：选取成年新西兰大耳白兔16只，建立兔耳增生性瘢痕动物模型，待上皮化后，对实验组、对照组分别给予二氢青蒿素（180mg／kg）和生理盐水（乙醇终浓度为0．1％）各10ml灌胃，术后28天和56天时观察药物对瘢痕增生指数（HI）的影响及光镜下瘢痕变化情况。结果：二氢青蒿素组与生理盐水组之间HI差异均有显著性意义（P〈0．01）；光镜下见二氢青蒿素组成纤维细胞凋亡增加及胶原纤维的含量降低。结论：二氢青蒿素可明显抑制兔耳增生性瘢痕的形成及瘢痕组织增生。     

Effects of intravenously administered hypertonic urea solution

Summary and Conclusions In 12 patients with increased intracranial pressure, caused by an expanding process, a hypertonic urea solution was intravenously administered during a craniotomy. At different times before, during and after the operation, the electrolytes, urea, glucose and total protein values were determined in various body fluids and tissues.This study disclosed that the urea administered was distributed through both the intracellular and the extracellular space after 20 minutes. The values of the electrolytes, except the calcium, in the extracellular fluid remained constant after administration of the urea solution; the total protein value, however, showed a considerable decrease.It was established that the blood-brain barrier plays no appreciable role in the mechanism of action of hypertonic urea solutions in dehydrating the brain tissue; the blood-C. S. P. and brain-C. S. F. barriers may do.

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Zusammenfassung Bei 12 Patienten mit intrakranieller Drucksteigerung infolge eines raumbeengenden Prozesses wurde Harnstofflösung intravenös während der Schädeleröffnung gegeben. Zu verschiedenen Zeitpunkten vor, während und nach der Operation wurden Elektrolyt, Harnstoff, Glukose und Gesamteiweiß quantitativ bestimmt und zwar sowohl in verschiedenen Körperflüssigkeiten wie auch in Geweben.Die Untersuchungen ergaben, daß der verabfolgte Harnstoff in 20 Minuten sich sowohl auf den intrazellulären, wie den extrazellulären Raum verteilt hat. Die Elektrolytwerte, mit Ausnahme von Kalzium, blieben nach der Harnstoffinfusion in den extrazellulären Flüssigkeiten unverändert, der Gesamteiweißwert nahm dagegen beträchtlich ab.Es wurde festgestellt, daß die Bluthirnschranke keine wesentliche Rolle für die entwässernde Wirkung des Harnstoffes auf das Hirngewebe spielt, während die Blut-Liquor-Schranke und die Hirn-Liquor-Schranke vielleicht von Bedeutung sind.

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Resumen Después de una craniectomía se administró una solución de urea hipertónica por via intravenosa a 12 pacientes que presentaban una presión intracraneal creciente a causa de una exposición de la hipófisis. Periódicamente, antes, durante y después de la operación se determinaron los valores de los electrolitos, de la urea, de la glucosa y de las proteinas totales en los diferentes líquidos y tejidos del organismo.Este estudio demostróque la urea administrada se distribuia a través del espacio intra y extracelular al cabo de 20 minutos. Los valores de los electrolitos, excepto el calcio, permanecieron constantes en el líquido extracelular después de la administración de la solución de urea; el valor de las proteinas totales, sin embargo, mostró un descenso considerable.Se concluyó que la barrera hemato-encefálica no juega ningún papel apreciable en los mecanismos de acción de las soluciones de urea hipertónica en la deshidratación del tejido cerebral; tal vez lo juegue en las barreras sangre-liquido cofalo-raquídeo y cerebro-líquido cefalo-raquídeo.

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Résumé Lors d'une craniotomie, une solution d'urée hypertonique fut administrée par voie intraveineuse chez 12 patients présentant une pression intracrânienne grandissante causée par une expansion de l'apophyse. De temps en temps, avant, pendant et après l'opération, les valeurs des électrolytes, de l'urée, du glucose et de la protéine totale étaient déterminées dans les différents liquides et tissus du corps.Cette étude démontra que l'urée administrée était distribuée à travers l'espace intra et extraecllulaire au bout de 20 minutes. Les valeurs des électrolytes, excepté le calcium, demeurèrent constantes dans le liquide extracellulaire après l'administration de la solution d'urée; la valeur de la protéïne totale, pourtant, montrait une baisse considérable.Il fut établi que la barrière hémato-encéphalique ne joue aucun rôle appréciable dans le mécanisme d'action des solutions d'urée hypertonique dans la déshydratation du tissu cérébral; les barrières sang-liquide céphalorachidien et cerveau-liquide céphalo-rachidien, peut-être.

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Riassunto In 12 pazienti con ipertensione endocranica, causata da un processo espansivo, è stata somministrata durante la craniotomia dell'urea in soluzione ipertonica per via venosa. A diversi tempi prima, durante e dopo l'intervento, sono stati dosati gli elettroliti, l'urea, il glueosio e le proteine totali in vari fluidi e tessuti corporei. Queste ricerche hanno evidenziato che l'urea viene distribuita tra spazio intracellulare ed extracellulare in 20 minuti. I livelli degli elettroliti, eccetto il calcio, rimangono costanti nel liquido extracellulare dopo la somministrazione di urea, i valori della proteinemia totali invece mostrano una notevole diminuizione.E' stato stabilito che la barriera emato-cerebrale non gioca alcun ruolo apprezzabile nel meccanismo d'azione dell'urea ipertonica nel disidratare il tessuto cerebrale; un ruolo importante potrebbe essere inveoe giocato dalla barriera emato-liquorale e tra liquor e sistema nervoso.

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This study was supported by a grant from the Netherlands Organization for the Advancement of Pure Research (Nederlandse Organisatie voor Zuiver-Wetenschappelijk Onderzoek, Z. W. O.).     

人羊膜上皮细胞培养液抑制角膜炎症的实验研究

探讨人羊膜上皮细胞(human amniotic epithelial cell,HAEC)培养液对角膜炎症反应的抑制作用及机制.方法 体外培养及鉴定HAEC和兔角膜上皮细胞,制备HAEC培养液.根据培养兔角膜上皮细胞的培养液成分不同分为无血清改良杜氏培养基(Dulbeccos modified Eagles medium,DMEM)组(DMEM组)、无血清DMEM与HAEC培养液1:1混合组(混合组)、HAEC培养液组(HAEC组).传代的角膜上皮细胞贴壁24 h后,用磷酸盐缓冲液润洗后按分组更换为上述3种培养液培养48 h后收集细胞.应用酶联免疫吸附试验(ELISA)检测HAEC培养液中白介素-1受体拮抗剂(interleukin-1 receptor antagonist,IL-1Ra)的含量.采用实时定量聚合酶链反应(PCR)检测3组培养液中兔角膜上皮细胞中的白介素(IL)-1β信使核糖核酸(messenger RNA,mRNA)的表达,采用八肽胆囊收缩素(cholecystokinin-octapeptide,CCK-8) 法检测3组细胞的增殖情况.结果 HAEC和兔角膜上皮细胞的形态学观察符合上皮细胞特征.HAEC培养液中IL-1Ra的含量为(153.56±0.36)ng/L,无血清DMEM对照中未检出IL-1Ra.3组培养液中,兔角膜上皮细胞的IL-1β mRNA表达由低至高分别为HAEC组、混合组和DMEM组,3组的IL-1β mRNA表达差异均有统计学意义(均为P<0.05).兔角膜上皮细胞分组培养24、48、72 h后,HAEC组的兔角膜上皮细胞吸光值明显高于混合组和DMEM组,DMEM组的兔角膜上皮细胞吸光值在各时间点均低于混合组(均为P<0.05).结论 HAEC可分泌IL-1Ra抑制角膜上皮细胞IL-1β的表达,减少炎症反应及移植排斥作用,并促进角膜上皮细胞增殖.     

高渗氯化钠羟乙基淀粉溶液对失血性休克兔应激反应的影响

目的国观察高渗氯化钠羟乙基淀粉溶液(HHS)对失血性休克兔应激反应的影响。方法 14只兔随机分为HHS组和乳酸盐林格液组(LBS组),每组7只。采用Wiggers改良法制作失血性休克模型,休克后45 min后分别用6 ml／kg的HHS和LRS复苏。在休克前、复苏前、复苏后30、60和120min时取血标本,测定血浆肾上腺素、胰高血糖素、胰岛素及血糖的浓度,计算胰岛素敏感指数(ISI)。结果 与休克前比较,复苏前两组动物血浆肾上腺素、胰高血糖素和血糖浓度均升高,胰岛素浓度均降低(P<0.01);复苏后,HHS组动物血浆肾上腺素、胰高血糖素水平回落,胰岛素浓度升高(P<0.05或0.01),LRS组动物血浆肾上腺素、胰岛素和血糖浓度均升高(P<0.01);HHS组复苏后各时点血浆肾上腺素、复苏后120 min时胰高血糖素、复苏后60 min时胰岛素浓度、复苏后60及120 min时血糖浓度均较低于LRS组(P<0.05或0.01)。复苏期间,两组动物胰岛素敏感指数均较休克前降低(P<0.05或0.01),但HHS组在复苏120 min时恢复至休克前水平(P>0.05)。HHS组于复苏后60、120 min ISI均高于LRS组(P<0.05或0.01)。结论 HHS复苏能够降低失血性休克应激激素水平,阻止胰岛素敏感性下降。     

可吸收膜联合口服塞来昔布防止兔肌腱粘连的实验研究

[目的]观察聚乳酸聚乙二醇共聚物[poly(l-lactic acid)-polyethylene goycol,PELA]可吸收膜与口服塞来昔布联合应用对预防兔肌腱粘连、降低局部炎症的有效性。[方法]成年雌性新西兰大白兔36只,体重2.0².5 kg,随机分为三组。制备双后足第3趾屈肌腱损伤模型:A组原位缝合作为对照,B组采用防粘连膜包裹肌腱损伤区,C组应用防粘连膜并术后口服塞来昔布[10 mg/(kg·d)]。术后3周行大体及组织学观察、肌腱功能评价和生物力学测定。[结果]3周后,肉眼下:A组腱周大量致密粘连组织,锐性分离困难;B组中度粘连,锐性分离见肌腱表面"假鞘"覆盖;C组仅少量粘连,"假鞘"薄,钝性可完全分离。镜下,C组断端愈合良好,腱周粘连少,局部炎细胞少于其他组。肌腱屈曲总角度:C组优于B组,A组最差,组间差异均有统计学意义(P<0.05)。生物力学测定示三组最大抗拉力无明显差异。[结论]PELA可吸收膜联合口服塞来昔布能有效防止肌腱粘连,抑制局部炎症,为防止肌腱粘连提供了一种新方法。     

Elimination of intravenously administered ibandronate in patients on haemodialysis: a monocentre open study.

BACKGROUND: Ibandronate is an inhibitor of osteoclast-mediated bone resorption. This therapeutic effect is utilized in the treatment of osteoporosis and metastatic bone disease. The effect of ibandronate in patients on haemodialysis with renal osteopathy has not been studied since the pharmacokinetics of ibandronate under haemodialysis are unknown. METHODS: We analysed the removal of ibandronate from the plasma by haemodialysis in 12 chronic haemodialysis patients suffering from end-stage renal disease (ESRD). After intravenous administration of 1 mg ibandronate, the plasma concentration of ibandronate was determined in plasma samples drawn before entering (inflow) and after passing through (outflow) the haemodialyser, and in the dialysate at 1, 2, 3 and 4 h during the first haemodialysis session, and after 1 and 4 h during the second and third dialysis sessions. RESULTS: The back-extrapolated initial ibandronate plasma level was 38.9+/-15.9 ng/ml; this decreased during first haemodialysis (after 4 h) to 4.9+/-0.9 ng/ml and after two subsequent haemodialysis treatments to 0.38+/-0.16 ng/ml. Ibandronate concentration was reduced by 47% with every passage through the dialyser. The total decrease of ibandronate plasma concentration during the first 4 h of haemodialysis was 78% of plasma peak levels. The ibandronate dialysis plasma clearance was determined at 92+/-19 ml/min. The total amount excreted at the first dialysis using the recovery rate measure was 364+/-98 microg and using the mean difference in inflow/outflow (arteriovenous) concentration (A-V difference method) it was 371+/-132 microg. About 36% of the total amount of ibandronate administered (1 mg) was removed by the first dialysis treatment. CONCLUSION: Ibandronate was efficiently removed by haemodialysis. After three haemodialysis sessions the ibandronate plasma levels were close to quantification limit. One monthly dose of 1 mg ibandronate would not result in elevated plasma levels in patients with ESRD on haemodialysis treatment three times a week. In haemodialysis patients, ibandronate should be administered after the haemodialysis session.     

Modulatory effects of topically administered lidocaine and pentobarbital on traumatic vasospasm in the rabbit ear artery

The effect of topical administration of 2 or 20% lidocaine and of 3% pentobarbital on traumatic vasospasm was studied in the central ear artery of the rabbit. The inner diameter of the artery was measured by in vivo microscopy. Vasospasm was induced by a standardised pinch of a 3.2 mm long arterial segment and lasted for 10-20 min. The drugs were given locally at maximal spasm, 1 min after spasm induction. All treatments caused prompt resolution of the vasospasm. This was followed by a plateau phase when the vessel diameter was reduced to about 60% of the initial pre-spasm value as a result of drug-induced vasoconstriction. The vasoconstriction lasted between 40 min and 24 h, depending on the treatment. Twenty per cent lidocaine was most effective, but caused thrombosis in microvessels surrounding the central ear artery. It is concluded that topical lidocaine and pentobarbital are both effective in resolving traumatic vasospasm but should only be used after careful consideration, since they also cause a general decrease in vascular diameter.     

Cutaneous burn diminishes beneficial effect of intravenously administered mesenchymal stem cells on acute lung injury induced by smoke inhalation in sheep

ObjectiveTo investigate effects of intravenously administered allogeneic mesenchymal stem cells (MSCs) on burn/smoke-induced lung injury.MethodsSheep were subjected to 40%, third-degree flame skin burn and smoke inhalation under deep anesthesia and analgesia. One-hour after injury, PlasmaLite A (control) or 200 million MSCs (treatment) were intravenously administered. Pulmonary oxygenation index, PaO₂/FiO₂ ratio, lung–lymph flow, and bloodless lung wet-to-dry weight ratio were measured. Distribution of MSCs and stromal cell-derived factor-1 (Sdf-1) protein level were determined in lung and skin tissues. Effects of burn exudate on MSCs migration were characterized.ResultsMSCs did not attenuate pulmonary dysfunction. The number of MSCs was significantly higher in lungs of sheep with smoke inhalation compared with those with burn/smoke injury. In contrast, number of MSCs was significantly higher beneath burned skin in sheep with burn/smoke than in unburned skin of sheep with smoke inhalation only. Expression of Sdf-1 protein was increased in the burned skin compared to unburned skin. Effects of burn exudate on cultured MSCs proliferation differed depending on collection time.ConclusionSkin burn diminishes beneficial effects of MSCs on smoke-induced lung injury, by promoting migration of MSCs from the pulmonary tissue to the injured skin area, possibly via expression of Sdf-1 protein.     

前列腺素E1透皮乳膏局部用药扩血管效应的实验研究

目的　探讨前列腺素E1 (PGE1 )透皮乳膏剂局部应用的扩血管效果 ,为临床开发理想的局部扩血管药物提供实验依据。方法　新西兰成年兔 60只 ,分为 6组 (每组 10只 ) :实验 1组 (含透皮剂的 0 .1%PGE1 乳膏组 ) ,实验 2组 (含透皮剂的 0 .2 %PGE1 乳膏组 ) ,实验 3组 (含透皮剂的 0 .4%PGE1 乳膏组 ) ,实验 4组 (含透皮剂的 0 .8%PGE1 乳膏组 ) ,不含透皮剂的 0 .4%PGE1 乳膏的药物对照组及空白对照组。全麻后 ,用 0 .1%盐酸肾上腺素注射于兔耳部制成血管痉挛模型 ,出现典型血管痉挛后于每只兔耳皮肤表面抹药。测量注射肾上腺素前、痉挛后 10min时及用药后 10 ,15 ,3 0 ,60 ,90和12 0min各时间点血管管径及血液灌流量的变化。结果　同一组内各时间段血管管径与血液灌流量成正比关系。实验 3 ,4组在用药 10min起血管管径及血液流量均已恢复注射肾素前的水平 ,且在各时间段的结果与实验 1,2组、药物对照组及空白对照组相比均有显著性差异 (P <0 .0 1) ,而第 3 ,4组间各时间段结果无显著性差异 (P >0 .0 5 )。结论　PGE1 在透皮剂作用下可透过皮肤有效缓解肾上腺素所致的血管痉挛 ,其扩血管效果与药物浓度成依赖关系。该药作为局部扩血管药物具有适应证广 ,显效快 ,副作用小 ,作用持久等特点 ,可能会成为一种     

The effect of surgical denervation on prevention of excessive dermal scarring: A study on rabbit ear hypertrophic scar model

Background

Previous reports have suggested that the extent of wound contraction, epithelisation and total healing time were influenced by denervation of tissues. In this article, we studied for the first time the effect of sensory denervation on prevention of excessive dermal scarring.

Materials and Methods

Sixteen New Zealand white rabbits were used. Denervation of the right ears was performed by surgical excision of two main sensory nerves. Dissections were also performed on left ears without any nerve excision for the control group. After 14 days of follow-up and confirmation of tissue denervation, an excessive dermal scarring model as defined by Morris et al. was made by surgery on both ears. Twenty-eight days after making the wounds, the tissues were extirpated for analyses. The scars were evaluated by the scar elevation index (SEI), epithelisation time and inflammatory cell count.

Results

The SEI of the denervated side scars was significantly lower than that of the non-denervated side. The rate and timing of total epithelisation and inflammatory cell count between groups yielded no difference.

Conclusions

In this study, the surgical denervation skin reduced scarring. It was suggested that understanding the exact role of sensory nerves and neural mediators in excessive dermal scarring is necessary for the prevention and treatment of scarring.