兔后肢缺血再灌注后足背肌腱表面微循环变化

应用活体显微镜技术，观察了兔后肢常温止血带缺血２ｈ（ｎ＝８）及５（ｎ＝８）再灌注后最初１ｈ期间足背肌腱表面微循环动态变化，尤其是白细胞内皮粘附及微血管灌注状况的变化，旨在探讨缺血再灌注损伤的发生机制，从而指导临床治疗。结果表明：①肢体缺血再灌注后缺血组织微静脉内皮上粘附的白细胞数显著增加，而且缺血时间越长，增加越显著。②肢体缺血５ｈ再灌注后，缺血组织的微循环并不能均匀恢复，部分区域发生＂无复流现象＂，包括原发性无复流和继发性毛细血管灌注衰竭两种形式。提示：①白细胞内皮粘附参与了缺血再灌注损伤的病理生理过程。②肢体缺血５ｈ再灌注后发生的局部组织损伤并非皆属缺血再灌注损伤，部分区域可能系单纯缺血性损伤，部分区域则可能属缺血再灌注一继发性缺血损伤。     

缺血再灌注对未成熟兔心冠脉微循环结构和功能损伤的研究

在离体做功模型上观察单低温１０～１５℃与低温和ＴｈｏｍａｓⅡ号心停搏液单剂和多剂量灌注对３周龄兔全心缺血再灌注的作用，结果发现单剂组低温组和多剂组心肌线粒体丙二醛，心肌和冠脉引流液内皮素含量降低，冠脉引流液一氧化氮含量增加，再灌注微血管开放良好，内皮细胞超微结构损伤减轻，心输出量恢复优于二组，多剂组与低温组组上述改良相似。提示局部低温加Ｔｈｏｍａｓ液单剂灌注对未成熟兔心冠脉微循环结构和功能保护作用     

缺血再灌注对骨骼肌微血管及微循环的影响

为了研究缺血再灌注对骨骨各肌微血管和微循环的影响，采用气囊止血带，在常温下使兔后肢缺血２小时（ｎ＝８）和５小时（ｎ＝８）。在解除止血带后，通过活体显微镜观察再灌注最初１小时期间足背肌腱表面微循环变化，并于再灌注后１小时和７２小时，自胫前肌切取电镜和光镜标本，观察骨骨各肌微血管超微结构和组织形态变化。表现：①肢体缺血２小时再灌注后，虽然少数细静脉内可见轻度红细胞聚集和白细胞贴壁数增加，但腱外膜微循环可迅速恢复，分布也较均匀；骨骨各肌微血管仅有轻微损伤，肌纤维可存活。②肢体缺血５小时再灌注后，腱外膜微循环不能迅速而均匀地恢复，大部分区域发生无复流，细静脉内有大量白细胞粘附和聚集；骨骨各肌微血管内皮细胞显著肿胀，基底膜断裂，间质高度水肿，最终大部分肌纤维坏死。结果证明：缺血再灌注可导致微血管损伤和微循环紊乱，其严重程度取决于缺血时间的长短，并是决定缺血组织实质细胞转归的重要因素之一。     

肝缺血再灌注中微循环障碍的发生机制

肝脏微循环障碍被认为是肝缺血再灌注(ischemia-reperfusion,I/R)后组织损伤的主要因素.近年来研究认为在肝组织复流早期一氧化氮(NO)与内皮素(ET)比例失衡,白细胞与内皮细胞及kupffer细胞之间频繁作用,以及被激活的中性粒细胞、kupffer细胞合成分泌大量的黏附分子、细胞因子及氧自由基最终导致肝脏微循环障碍.本文就目前研究相关进展进行简要综述.     

肢体缺血再灌注后微循环变化及其发生机制的实验研究 1．兔足背肌腱表面微循环活体观察法的建立

我们对兔后肢趾长伸肌腱的血供系统进行了解剖观察，发现其环韧带以远接近跖趾关节的一段是制作微循环活体观察标本的理想部位。该处肌腱表面有丰富的微血管，且血管的背景为白色的肌腱，反衬明显；肌腱上方仅有皮肤和少量疏松组织覆盖，因此容易解剖。在此基础上，我们成功地创立了足背肌腱表面微循环活体观察法，为利用兔后肢缺血模型研究肢体缺血再灌注后的活体微循环变化开辟了一条新途径。     

黄腐酸钠对大白鼠肝缺血/再灌注微循环作用的实验研究

目的　探讨通过肝缺血 /再灌期 ( ischem ia and reperfusion I/ R)给予药物预处理动物模型来探索不同药物、不同给药途径防治肝脏 I/ R期损伤的有效方法。方法　 60只 Wistar大鼠分成 5组 :A组 (正常对照组 )、B组 ( I/ R期无药物干预模型组 )、C( 10 % L- arg静注干预组 )、D组 ( 1% SF静注干预组 )、E组 ( 2 % SF实验前 3 d口服干预组 ) ,动脉夹阻断肝门 4 5 min后去除动脉夹再灌注 1h。于阻断肝门前、阻断后 4 5 m in、再灌注 1h测定肝脏微循环血流量 ,检测血清 AL T、AST值 ,同时取测定点处肝脏组织病理进行光镜、电镜观察分析。分别用统计学 t检验及单因素方差析的方法比较 5组间的差异和意义。结果　阻断肝门前 E组肝脏微循环血流量明显高于 A、B、C、D组 ( P<0 .0 1) ,阻断 4 5 m in时 B、C、D、E组微循环血流量均呈一致下降趋势 ,E组再灌注 1h后回升至 2 8.3 9± 0 .83 ( V) ,与 B组 2 4 .71± 0 .4 5 ( V)比较明显增高 ( P<0 .0 5 )。病理分析证实 I/ R期肝组织损伤主要发生在再灌注初期肝小叶的中央静脉区及肝腺泡 区 ,光镜半定量分析显示 E组肝细胞坏死数目明显减少 ( P<0 .0 5 )。结论　阻断肝门后肝脏微循环明显下降 ,再灌注早期可回升 ,但不能达到正常值。黄腐酸钠 ( SF)可提高正常肝脏     

异丙基肾上腺素对热缺血再灌注大鼠肝脏微循环的影响

缺血再灌注 (Ｉｓｃｈｅｍｉａ/ＲｅｐｅｒｆｕｓｉｏｎＩ/Ｒ)损伤为临床常见的病理生理表现 ,再灌注对组织可造成严重的损伤。在肝胆外科 ,某些肝胆疾病的手术常需要完全或部分阻断肝血流 ,从而不可避免地造成肝微循环障碍 ,严重时导致肝功能衰竭 ;在肝脏移植过程中热Ｉ/Ｒ引起的肝脏微循环障碍可能是供肝失活、移植失败的一个重要原因。因此 ,我们设计了本实验 ,为肝移植及需要阻断肝门的肝脏手术探索防治热Ｉ/Ｒ期肝微循环障碍的有效药物及给药途径。材料与方法1.动物分组及药物剂量 :选择Ｗｉｓｔａｒ大鼠 2 0只 (解放军总医院实验动物…     

肢体缺血再灌注后微循环变化及其发生机制的实验研究——1.兔足背肌腱表面微循环活体观察法的建立

我们对兔后肢趾长伸肌腱的血供系统进行了解剖观察,发现其环韧带以远接近跖趾关节的一段是制作微循环活体观察标本的理想部位。该处肌腱表面有丰富的微血管,且血管的背景为白色的肌腱,反衬明显;肌腱上方仅有皮肤和少量疏松组织覆盖,因此容易解剖。在此基础上,我们成功地创立了足背肌腱表面微循环活体观察法,为利用兔后肢缺血模型研究肢体缺血再灌注后的活体微循环变化开辟了一条新途径。     

黄芪对失血性休克再灌注兔肠粘膜微循环血流量的影响

研究表明,肠屏障功能损害是多器官功能衰竭(MODS)形成的一个重要发源地,肠粘膜的解剖缺陷使其极易发生再灌注损伤,因此,防止肠粘膜再灌注损伤是保护肠屏障的中心环节。本研究旨在通过观察休克-再灌注兔肠粘膜微循环血流量,探讨黄芪抗失血-再灌注肠粘膜损伤的可能性。     

Checkrein deformity due to extensor hallucis longus hypotrophy treated with extensor digitorum longus tendon transfer

Checkrein deformity is a relatively rare condition caused by hypotrophy or adhesion of a tendon after a lower leg injury. The occurrence of this condition due to the dysfunction of the extensor hallucis longus (EHL) is extremely rare. Only a few related case reports have been published, and Z-lengthening of the EHL tendon was performed for almost all patients.We report a case of checkrein deformity due to EHL hypotrophy. The patient was involved in a traffic accident 7 years ago. He sustained left tibial and fibular closed diaphyseal fractures and underwent minimally invasive plate osteosynthesis. He continued to have left great toe symptoms characterized by dorsiflexion of the great toe during ankle plantarflexion. The EHL had become an insufficient power source because of considerable hypotrophy. Therefore, a tendon transfer using the extensor digitorum longus to the second toe was performed as a primary treatment.     

Effects of postmortem freezing on tensile failure properties of rabbit extensor digitorum longus muscle tendon complex

The tensile failures of extensor digitorum longus muscle tendon units from 16 male New Zealand White rabbits were studied in the fresh state (less than 30 minutes after death) and in the frozen/thawed state (frozen at ?80°C for 28 days and then warmed to 38°C). Frozen/thawed extensor digitorum longus muscle tendon units had significantly lower values for load to failure (p < 0.01), energy absorbed to failure (p < 0.01), and strain at failure (p < 0.01), and they tended to fail at a different anatomic location (p < 0.01) (broadly at the fascia-muscle interface as compared with horizontally at the musculotendinous junction) than fresh units. The results of this study suggest that freezing muscle tendon units significantly alters their tensile failure characteristics.     

Intratendinous ganglion cyst of the extensor digitorum longus tendon: A case report

IntroductionGanglion cysts are benign lesions, common in the hand and wrist. Intratendinous ganglion, however, are rare. We present the first reported case of an intratendinous ganglion cyst in an extensor digitorum longus (EDL) tendon of the foot.Case reportA 35-year old presented with a left-sided painful dorsolateral foot swelling. Ultrasound suggested a ganglion cyst in proximity to the EDL tendon of the 5th toe. Two distinct swellings were identified on surgical exploration, including a 6 × 1 cm ganglion lying within the EDL tendon substance that had resulted in tendon splitting. The lesions were excised and EDL tendon repaired. Histological analysis confirmed that both lesions were ganglion cysts. Post-operative recovery was uneventful.DiscussionIntratendinous ganglion cysts are rare lesions that pose a unique set of diagnostic and treatment challenges. Unlike conventional ganglion, their diagnosis may not be possible until surgical exploration. They have been reported to increase the risk of spontaneous tendon rupture. As such, a lower operative threshold should be applied to prevent their progression. A high index of suspicion should be applied to any ganglion reported radiologically to be in close contact with tendons. If diagnosed upon surgical exploration, it is essential that the operating surgeon is prepared to appropriately modify the procedure to involve primary tendon repair, tendon transfer or tenodesis.     

左旋精氨酸对再灌注期大鼠提睾肌微循环的作用

目的 探讨再灌注期肌瓣微循环的变化及其与NO的关系。方法 以体重180－220g雄性SD大鼠,制成大鼠提睾肌缺血再灌注模型（热缺血5h,再灌注2h）,应用电视显微影像系统,观察缺血再灌注期肌瓣微循环的变化。结果 ①再灌注期左旋精氨酸（L－arg)治疗组微动脉复流率较对照组明显增高（P＜0．01）,对照组于再灌注30min微动脉复流率最低,仅为53％。②再灌注期L－arg能使复流之微动脉A1、A2的血管收缩幅度明显减小（P＜0．05）,血管流速明显加快,毛细血管的灌流密度显著增加。③再灌注期微静脉内皮细胞受损,静脉回流障碍,局部形成一种“只灌不流”的病理现象,使肌瓣组织出现大片明显的漏出性出血。结论 NO生成剂能够扩张微动脉,疏通肌瓣的微循环,改善组织的灌 流;再灌注期微静脉回流障碍可能是造成组织损伤的重要因素。     

Rupture of the extensor pollicis longus tendon after wrist trauma

In the period of 1976 to 1997 our clinic treated 33 patients after Colles fracture with ruptured extensor pollicis longus tendon. The occurrence of functional loss was observed after the trauma in 3 to 9 weeks. In 30 cases the surgical treatment of extensor indicis proprius tendon, in 2 cases a direct suture of the ruptured tendon was performed as a primary repair and in one patient a palmaris longus interposition was utilised.     

Transfer of either index finger extensor tendon to the extensor pollicis longus tendon

BACKGROUND:

Extensor pollicis longus (EPL) tendon ruptures have been treated succesfully with the transfer of the extensor indicis proprius (EIP) tendon. Situations exist in which, due to intraoperative observations, another tendon transfer may be considered preferable to the standard EIP transfer method.

OBJECTIVES:

To determine whether transfer of the extensor digitorum communis II (EDC II) tendon from the index finger to the EPL tendon, leaving the EIP tendon to the index finger intact, would serve as an equally efficient transfer and not adversely affect the function of the hand.

METHODS:

Two patients who had the EDC II tendon transferred to the ruptured EPL tendon, and two patients who had the EIP tendon transferred, were retrospectively reviewed. In each transfer type, one patient had suffered an EPL tendon rupture after a Colles’ fracture, and the other had rheumatoid arthritis. The rupture occurred on the non-dominant side in one patient in each transfer type. Each patient was examined and subjected to range of motion and power testing at least one year following surgery.

RESULTS:

All four patients showed a minimal extension lag with the lift off test, but there was no noticeable difference in range of motion, pinch grip and hand grip strength between the transfer types. Both EDC II transfer patients demonstrated an 8° to 15° loss of thumb interphalangeal joint flexion compared with the unoperated side; EIP transfer patients demonstrated less than a 5° loss. Three patients demonstrated a minor extension lag in the index finger and middle finger. Extension power of the thumb and index finger in all patients varied with wrist flexion and extension and ranged from 50% to 150% of the unoperated side.

CONCLUSIONS:

These case reports suggest that either index finger tendon may be successfully transferred in EPL tendon ruptures.     

A quantitative ultrastructural study of collagen fibril formation in the healing extensor digitorum longus tendon of the rat

A study was made of collagen fibril populations in healing tendon using a window lesion in rat extensor tendon. Two environments were thus created. One (the lesion area) where stress levels were reduced; the other (the non-lesion area) where stress levels were increased. In both areas a population of small diameter (less than 50nm) collagen fibrils were synthesized. Lesion area fibrils increased their diameter only slowly. Non-lesion area fibrils added to a population which increased its diameter distribution comparatively rapidly. It is suggested that in the lesion area fibrils were synthesized in response to tissue damage and low levels of stress. These may be of type III collagen. In the non-lesion area fibrils were synthesized in response to raised levels of stress. These may be of type I collagen. Implications of these events, especially as they might relate to gap formation in flexor tendon surgery are discussed.     

Influence of nitric oxide on microcirculation in pancreatic ischemia/reperfusion injury: an intravital microscopic study

Recently, protective effects of nitric oxide donors in pancreatic ischemia/reperfusion (IRI) injury have been described. Their role in post-ischemic microcirculation was previously not investigated. Ischemia reperfusion was induced in an isolated pancreatic tail segment in situ. Animals were randomized to four experimental groups (n=7 animals/group), the control group (CO) received saline as placebo. Treatment groups received either sodium nitroprusside (SN) 5 min before until 2 h after reperfusion, l-arginine (LA) 30 min before reperfusion until 2 h after reperfusion or sodium nitroprusside and l-arginine (SNLA) together. After induction of ischemia (2 h) post-ischemic microcirculation was observed for 2 h by intravital-fluorescence microscopy. Functional-capillary density (FCD), leukocyte adherence in post-capillary venules (LAV) and histological damage were analysed. After reperfusion FCD decreased in all groups (P<0.05). FCD was significantly restored in all groups with administration of nitric oxide donors after reperfusion (P<0.05) as compared to CO without significant difference between the individual nitric oxide donor groups. Leukocyte adherence was significantly increased 1 h and 2 h after reperfusion (P<0.001) as compared to baseline, which was lower in all nitric oxide donor groups. Histological damage in the pancreatic tail-segment was significantly reduced in nitric oxide donor groups (P<0.01). Administration of nitric oxide donors might be useful in ischemia-reperfusion injury of the pancreas by its protective effect on microcirculation and inflammatory reaction.