术中预缺血对猪骨骼肌保护作用的实验研究

目的研究术中预缺血对骨骼肌缺血坏死的保护作用及相关的肌肉代谢变化。方法 10只猪背阔肌瓣在4h 缺血前先进行3个循环10min 的术中预缺血,48h 后用染色法记录肌肉成活率,于肌肉缺血前、缺血后2,4h 和再灌流1.5h 分别作肌肉活检。结果 4h 缺血后的肌瓣,术中预缺血组成活率高出对照组44％,肌肉活检三磷酸腺苷(ATP)增加和乳酸降低(P<0.05)。结论术中预缺血可增加骨骼肌对缺血坏死的保护作用,这与肌肉中能量代谢的减低相关。     

腺苷延长肌瓣缺血耐受时间的实验研究

目的研究缺血前局部使用腺苷对猪背阔肌瓣缺血耐受的促进作用和机理。方法用不同剂量（０，０．５，２．０ｍｇ）的腺苷从腋动脉穿刺注入肌瓣，肌瓣缺血４，４８小时后切取肌瓣，染色后测定肌瓣成活率，腺苷注射前、后，缺血后分别采取肌肉标本做三磷酸腺苷（ＡＴＰ）定量分析。结果腺苷注射组肌肉坏死率明显低于对照组（对照组：４０．３％±２．２％），０．５ｍｇ组：２０．６％±１．６％，２ｍｇ组：１８．２％±１．０％）。腺苷注入组缺血后肌肉ＡＴＰ水平明显高于对照组。结论缺血前局部使用小剂量腺苷对缺血肌瓣有保护作用，并伴随肌肉ＡＴＰ分解水平的减低     

腺甘延长肌瓣缺血耐受时间的实验研究

目的 研究缺血前局部使用腺苷对猪背阔肌瓣缺血耐受的促进作用和机理。方法 用不同剂量（０，０．５，２．０ｍｇ）的腺苷从腋动脉穿刺注入肌瓣，肌瓣缺血４，４８小时后切取肌瓣，染色后测定肌瓣成活率，腺苷注射前、后，缺血后分别采取肌肉标本做三磷酸腺苷（ＡＴＰ）定量分析。结果 腺苷注射组肌肉坏死率明显低于对照组（对照组：４０．３％±２．２０％），０．５ｍｇ组：２０．６％±１．６％，２ｍｇ组；１８．２％±１．０     

腺苷延长肌瓣缺血耐受时间的实验研究

目的研究缺血前局部使用腺苷对猪背阔肌瓣缺血耐受的促进作用和机理。方法用不同剂量(0,0.5,2.0mg)的腺苷从腋动脉穿刺注入肌瓣,肌瓣缺血4,48小时后切取肌瓣,染色后测定肌瓣成活率,腺苷注射前、后,缺血后分别采取肌肉标本做三磷酸腺苷(ATP)定量分析。结果腺苷注射组肌肉坏死率明显低于对照组(对照组:40.3％±2.2％),0.5mg 组:20.6％±1.6％,2mg 组:18.2％±1.0％)。腺苷注入组缺血后肌肉 ATP 水平明显高于对照组。结论缺血前局部使用小剂量腺苷对缺血肌瓣有保护作用,并伴随肌肉 ATP 分解水平的减低。     

骨肌瓣移植治疗股骨头缺血坏死的远期随访（附96例分析）

骨肌瓣移植治疗股骨头缺血坏死的远期随访（附９６例分析）王毅张震宇杨卫良于维良张波辛风赵承斌关国发于占革纪青我院１９８４年４月～１９９４年８月以髓心减压骨肌瓣移植治疗股骨头缺血坏死９６例（１３２髋）。平均随访６４年（５～１０年），优良率６５３％（８...     

缺血预处理减轻骨骼肌缺血再灌注损伤

目的 观察缺血预处理对骨骼肌缺血再灌注损伤的保护作用。方法 选择２４只健康兔,随机等分为实验组和对照组。实验组先进行缺血预处理,再持续阻断后肢血流４ｈ;对照组直接阻断后肢血流４ｈ,制作骨骼肌缺血再灌注损伤模型。测定再灌注期血清中肌酸磷酸激酶（ＣＰＫ）和天门冬氨酸氨基转移酶（ＡＳＴ）,镜下观察骨骼肌变化。结果 实验组血清中ＣＰＫ和ＡＳＴ的含量均明显低于对照组（Ｐ〈０．０５）。实验组骨骼肌线粒体空泡变     

缺血预处理时间对大鼠骨骼肌缺血再灌注损伤保护作用的影响

目的探讨缺血预处理时间与骨骼肌缺血再灌注损伤保护作用之间的关系. 方法 36只大鼠随机分成 6组,制成切断患肢皮肤、肌肉和神经,仅保留股动静脉的动物模型.A组:直接缺血4 h再灌注;B、C、D和E组:分别缺血5、10、15和20 min,再灌注5、10、15和20 min,重复3次后缺血4 h再灌注;F组:制成仅保留股动静脉的左大腿组织块模型,未经过缺血处理.通过测定丙二醛(malondialdehyde, MDA)、骨骼肌水肿和坏死程度,观察不同预缺血时间对骨骼肌缺血再灌注损伤的保护作用. 结果对骨骼肌缺血后再灌注,预缺血5 min对骨骼肌即有保护作用,肌肉存活面积达82.47%;预缺血10和15 min肌肉存活面积增至最高,达89.03%和89.49%;预缺血20 min肌肉存活面积降至78.27%.预缺血5 min即可减轻骨骼肌水肿;预缺血10 min骨骼肌水肿程度最轻;预缺血15 min水肿程度又加重,预缺血20 min水肿程度继续加重.预缺血5、10和15 min MDA水平均降低,预缺血20 min MDA水平与单纯缺血再灌注组相同. 结论预缺血时间对大鼠骨骼肌缺血再灌注损伤的保护作用呈现先增强后减弱的趋势,以预缺血10 min保护作用最强.     

缺血预处理改善骨骼肌功能的研究

目的：探讨缺血预处理法改善缺血骨骼肌功能的临床价值。方法：用ＳＤ大鼠１２只，以右后肢为动物实验模型。分为缺血组（对照组，鼠６只），即缺血４小时后再灌注１小时的方法；缺血预处理组（实验组，鼠６只），缺血过程同对照组，但在缺血前预先经过２次缺血５分钟、再灌注１０分钟的处理。实验时，分别于缺血前、缺血１、４小时及再灌注１小时时，测定两组实验侧肢体腓肠肌最大肌张力的变化。实验结束后分别测量血ＭＤＡ、ＣＰＫ及大鼠右后肢９９ｍＴｃ亚甲基二磷酸计数。结果：实验组最大肌张力的变化（缺血４小时、再灌注１小时时）较对照组有明显改善；血ＭＤＡ、ＣＰＫ及肌肉９９ｍＴｃ亚甲基二磷酸较对照组显著降低。结论：缺血预处理不仅能改善骨骼肌的缺血耐受性，而且能有效地改善骨骼肌的功能     

肢体缺血再灌注导致脂质过氧化增强和血栓素A2合成增加的研究

骨骼肌缺血再灌注可导致肌肉微血管的实质损伤，观察了肌肉缺血再灌注时脂质过氧化物（ＬＰＯ）和ＴｘＡ２与ＰＧＩ２的代谢状况。缺血组家兔（ｎ＝６）。双后肢缺血２小时。再灌注２小时后，左股薄肌丙二醛（ＭＤＡ）含量，下腔静脉血ＭＤＡ和乳酸浓度均显著高于对照组（ｎ＝６）。再灌注后１０和３０分钟，缺血组血中ＴｘＢ２水平和ＴｘＢ２／６－ｋｅｔｏ－ＰＧＦ１ａ比率明显增高，再灌注后血中ＳＯＤ活性和６－ｋｅｔｏ－ＰＧＦ     

缺血预处理对骨骼肌缺血再灌物保护机制及其与腺苷关系研究

目的：探讨骨骼肌缺血预处理保护作用机制及其腺苷的关系。方法：采用兔右后肢缺血模型，将２８史兔随机分为４组，对照组：持续缺血４ｈ，再灌注１ｈ；缺血５ｍｉｎ再灌注５ｍｉｎ重复３次后，持续缺血４ｈ再灌注１ｈ。腺苷治疗组：于血再灌注前经股动脉注入０．５ｍｇ腺苷。腺苷受体拮抗剂８－ＰＴ处理组；在３次循环ＩＰＣ处理前，经股动脉注射３．０ｍｇ８－ＰＴ，再缺血４ｈ，再灌注１ｈ。通过高铲液相色谱法测定处理胶、缺血４     

术中预缺血对猪骨骼肌保护作用的实验研究

OBJECTIVE: The aim of this study was to investigate metabolism of ischemic muscle and the efficacy of acute ischemic preconditioning for protection of skeletal muscles against infarction. METHODS: The efficacy of preconditioning was tested by subjecting pig latissimus dorsi muscle to 3 cycles of ischemia reperfusion, each for 10 min, before 4 h of global ischemia. Infarction was assessed at 48 h reperfusion using nitroblue tetrazolium dye. Muscle biopsies were taken from the latissimus dorsi before ischemia, at the end of 2 and 4 h of ischemia and 1.5 h of reperfusion. RESULTS: Preconditioning reduced the total infarct size by 44% in the latissimus dorsi. The muscle contents of ATP were maintained higher and the lactate lower (P < 0.05) in the preconditioned than in the non-preconditioned muscle at the end of 2 h, 4 h of ischemia and 1.5 h of reperfusion. CONCLUSION: Preconditioning of pig skeletal muscle is associated with a lower energy metabolism during sustained ischemia. At the present time, it is not known if this energy sparing effect is a major mechanism of ischemia preconditioning against infarction in the skeletal muscle.     

Late‐phase ischemic preconditioning in skeletal muscle: is the phenomenon protective?

Reports in the literature on the effectiveness of late-phase Ischemic preconditioning (IPC) in skeletal muscle are controversial. The purpose of this study was to determine in the same muscle flap model the effectiveness of various IPC protocols in inducing late-phase protection. Rat latissimus dorsi muscle (LDM) flaps were preconditioned with either 30 or 60 min of total ischemia, divided as follows: single cycles of either 30 or 60 min, two cycles of 15 or 30 min, and three cycles of 10 or 20 min. Ischemia cycles were separated by 10 min of reperfusion. A day after IPC, flaps were elevated and challenged with 4 h of ischemia. Three days later, flaps were assessed for viability. We found that IPC protocols of different total durations and comprised of two or three cycles of ischemia elicited a protective effect against necrosis. We conclude that IPC induces late-phase protection against necrosis in skeletal muscle, and that the protection requires more than one ischemia/reperfusion cycle.     

Ischemic preconditioning of skeletal muscle: duration of late-phase protection

BACKGROUND: The time course of the late phase of ischemic preconditioning (IPC) was determined in latissimus dorsi muscle (LDM) flaps using viability and function as the endpoints. MATERIALS AND METHODS: LDM flaps from Sprague-Dawley rats were allocated into 6 groups. LDMs were preconditioned with 2 30-minute periods of ischemia separated by 10 minutes of reperfusion and subjected to a 4-hour ischemic insult after 24, 48, 72, and 96 hours from IPC. LDMs were evaluated for percent necrosis and muscle contractile function and compared with controls. RESULTS: The late phase of IPC provides significant protection against necrosis up to 72 hours. Conversely, when the end point used was muscle contractile function, the protection only lasted 48 hours. CONCLUSION: The time course of late-phase protection in skeletal muscle is 2-3 days. Late phase IPC appears to protect muscle flaps during the most critical time period following elevation.     

Preconditioning: a new technique for improved muscle flap survival.

Musculocutaneous regional and distal flaps have become an important tool available to the head and neck surgeon. Vascularized autogenous muscle transplants allow single-stage reconstruction of complex defects. Ischemic muscle necrosis is a well-recognized complication with serious potential morbidity. It has been shown that myocardial muscle is protected from ischemic damage by brief periods of coronary artery occlusion and reperfusion subsequent to prolonged ischemia. This is called preconditioning. To our knowledge, this technique has never been extrapolated to skeletal muscle. This article presents a discussion of preconditioning and the potential benefits of this new technique as a means to enhance skeletal muscle survival to sustained normothermic global ischemia. Theories behind ischemic muscle injury are presented. A review of the development of preconditioning in myocardial muscle is discussed. Experimental models used to investigate this phenomenon are also presented. In addition, results of our laboratory investigations using the latissimus dorsi porcine model are discussed. Preconditioning is a new, nonpharmacologic means to improve muscle flap survival. This simple technique may have great clinical application in reducing ischemic muscle necrosis in regional and distal muscle transplantation.     

缺血后处理和预处理对大鼠骨骼肌缺血-再灌注损伤的作用

目的 探讨缺血后处理( IPost)和缺血预处理(IPC)对大鼠骨骼肌缺血再灌注(IR)损伤的影响.方法 将40只大鼠随机分成缺血再灌注组(A组)、缺血后处理组(B组)、缺血预处理组(C组)、缺血预处理加缺血后处理组(D组)以及对照组(E组),采用切断患肢全部皮肤、肌肉和神经,保留患肢股动、静脉的动物模型,通过夹闭和开放股动、静脉造成骨骼肌缺血再灌注损伤,通过测定骨骼肌缺血4h、再灌注1h后血清丙二醛(MDA)和骨骼肌髓过氧化物酶(MPO),以及再灌注6h后骨骼肌的坏死程度来观察缺血后处理.缺血预处理及缺血预处理加缺血后处理对大鼠骨骼肌缺血再灌注损伤的影响.结果 B组、C组和D组再灌注1 h MDA和MPO水平以及再灌注6h骨骼肌坏死程度均低于A组(P＜ 0.05),但是高于E组(P＜0.05);B组和D组再灌注1 h MDA和MPO水平以及再灌注6h骨骼肌坏死程度基本相同(P＞0.05);B组和D组再灌注1 h MDA和MPO水平低于C组(P＜0.05),但再灌注6h骨骼肌坏死程度基本相同(P＞0.05).结论 应用缺血后处理和缺血预处理对大鼠骨骼肌缺血再灌注损伤有一定的保护效果,联合应用缺血后处理和缺血预处理,对骨骼肌缺血再灌注损伤的保护作用并没有明显增强.     

缺血预处理对骨骼肌缺血再灌注损伤的保护机制及其与腺苷关系研究

目的 :探讨骨骼肌缺血预处理保护作用机制及其腺苷的关系。方法 :采用兔右后肢缺血模型 ,将 2 8只兔随机分为 4组 (n =7) ,对照组 :持续缺血 4h ,再灌注 1h ;预处理组 :缺血 5min ,再灌注 5min ,重复 3次后 ,持续缺血 4h再灌注1h。腺苷治疗组 :于缺血再灌注前经股动脉注入 0 5mg腺苷。腺苷受体拮抗剂 8-PT处理组 :在 3次循环IPC处理前 ,经股动脉注入 3 0mg 8-PT ,再缺血 4h ,再灌注 1h。通过高效液相色谱法测定处理前、缺血 4h ,再灌注 10min、3 0min及6 0min时血浆腺苷浓度变化。通过血浆CPK、MDA及骨骼肌99mTcMDP吸收量的测定判断骨骼肌损伤程度。结果 :预处理组、腺苷组及 8-PT组 ,在缺血 4h和再灌注 1h期间血浆腺苷浓度明显升高 (P <0 0 1) ,再灌注 10min时达到高峰 ,并随再灌注时间延长而逐渐降低。与对照组相比 ,预处理组和腺苷组血浆CPK、MDA及骨骼肌99mTcMDP吸收量显著降低 (P <0 0 1)。结论 :腺苷参与了缺血预处理对骨骼肌的保护作用 ,腺苷受体拮抗可阻断缺血预处理对骨骼肌的保护作用。腺苷释放和腺苷受体激活在骨骼肌缺血预处理中起重要作用。     

Die Anzahl der Präkonditionierungszyklen beeinflusst die Skelettmuskelprotektion durch ischämische Präkonditionierung

Ischemic preconditioning (IP), using one or more brief periods of ischemia before a sustained ische- mia, represents a new approach in reducing ischemia-induced skeletal muscle damage. The aim of this study was to investigate the effect of IP on skeletal muscle function after 3 h ischemia and 2 h reperfusion in a rodent model. IP protocols using one, two, or three preconditioning cycles of 10 min ischemia and 10 min reperfusion each, were compared to non-preconditioned controls. IP was found to significantly improve force, performance, endurance, and contractility of postischemic skeletal muscle. The efficacy of IP- induced protection was correlated with the number of preconditioning cycles. Preconditioning with three cycles resulted in a more effective protection as compared to one or two cycles. Altogether, this study describes the efficacy of IP in improving post-ischemic muscle function and the need of more than one IP cycle to achieve this improvement. The respective clinical potential warrants further exploration.     

Ischemic preconditioning: lack of delayed protection against skeletal muscle ischemia-reperfusion

We investigated the ability of ischemic preconditioning to induce expression of heat shock protein 70 (Hsp 70) and/or to increase muscle survival after ischemia-reperfusion in the rat hind limb. Ischemic preconditioning regimens tested were; 1 x 5 min of ischemia, 4 x 5 min of ischemia interrupted by 10 min of reperfusion, 1 x 10 min of ischemia or 2 x 10 min of ischemia interrupted by 15 min of reperfusion. Western blot analysis revealed only a modest induction of Hsp 70 at 24 h after preconditioning using the latter two protocols of 1 x 10 min of ischemia or 2 x 10 min. Used at 24 h prior to prolonged ischemia, neither protocol improved muscle survival measured at 24 h after reperfusion. In conclusion, ischemic preconditioning did not produce delayed protection from ischemia-reperfusion in this model and the study suggests that ischemic preconditioning is not a useful protective strategy against skeletal muscle necrosis in the long-term.