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     

不同时间的缺血预处理对肝脏缺血再灌注损伤的影响

我们通过观察不同时间的缺血预处理对肝脏缺血再灌注损伤的影响,旨在探讨ＰＣ对肝脏缺血再灌注损伤的保护作用所需要的适合的预处理时间。一、材料与方法１．动物模型：雄性ＳＤ大鼠６０只,体重１８０～２２０ｇ,参照Ｊａｅｓｃｈｋｅ和Ｍｅｔｚｇｅｒ法制备成右肝全部缺血、左肝部分缺血后再灌注大鼠模型［１］。２．预处理方案：本实验共设５组,每组１２只大鼠;假手术组（Ｓ组）：仅行假手术;缺血再灌注组（ＩＲ组）：肝脏持续缺血６０分钟,再灌注３０分钟;预处理组分为３组,在肝脏持续缺血之前分别进行５分钟缺血及５分钟的再灌…     

卡托普利抗心肌缺血再灌注损伤的实验研究

用兔体外循环心肌再灌注损伤模型，研究卡托普利（ｃａｐｔｏｐｒｉｌ，Ｃａｐ）的心肌保护作用。２０只兔随机均分为２组，建立体外循环后在主动脉阻断同时灌注４℃心脏停跳液，对照组为Ｓｔ．ＴｈｏｍａｓＩ号液，实验组在Ｓｔ．ＴｈｏｍａｓＩ号液中加入Ｃａｐ（０．５ｍｇ／ｋｇ）。心脏缺血９０分钟和再灌注６０分钟后结果显示，实验组心肌Ｃａ＋＋、丙二醛（ＭＤＡ）、心肌酶（ＬＤＨ，ＣＰＫ）较对照组显著降低，心肌超微结构损伤明显减轻。结论：Ｃａｐ对缺血再灌注心肌起到了良好的保护效果。     

丹参对肢体缺血再灌注脂质过氧化反应影响的临床观察

目的：临床观察丹参对肢体缺血再灌注脂质过氧化反应的效果。方法：选择１６例肢体手术需充气带加压肢体止血的患者，随机分为对照组（ｎ＝８）和治疗组（ｎ＝８）。治疗组病人术前１０分钟静脉滴入复方丹参注射液（４００ｍｇ／ｋｇ），对照组病人给等量平衡液。肢体缺血前、再灌注后３０分钟、９０分钟、１８０分钟分别检测血ＭＤＡ、ＣＰＫ和ＳＯＤ。结果：肢体缺血再灌注３０分钟、９０分钟、１８０分钟与缺血前比较，血ＭＤＡ和ＣＰＫ含量升高，ＳＯＤ含量下降。治疗组缺血再灌注同时间，血ＭＤＡ含量明显低于对照组（Ｐ值＜０．０１）；ＣＰＫ值低于对照组（Ｐ值＜０．０５）；ＳＯＤ活性逐渐上升，１８０分钟高于对照组（Ｐ值＜０．０５）。结论：丹参有抗脂质过氧化作用，降低ＣＰＫ值，提高ＳＯＤ活性，能有效防治肢体缺血再灌注损伤。     

脂质过氧化抑制剂对大鼠全脑缺血后海马CA1区诱发电位的影响

目的：选脂质过氧化抑制剂（Ｕ７４３８９Ｆ）作为脑保护剂，观察其对大鼠全脑缺血后的海马ＣＡ１区诱发电位的影响。方法：雄性ＳＤ大鼠２０只，随机分三组，对照组（６只），缺血组（７只）与治疗组（７只）均脑缺血１０分钟后患，再灌注７小时，治疗组缺血前１小时腹脸注射Ｕ７４２８９Ｆ１０ｍｇ／ｋｇ。结果：大鼠全脑缺血再灌注６小时后，海马诱发电位中兴奋性突触后电位（ＥＰＳＰ）的斜率与缺血前相比显著增加（Ｐ〈０．０５     

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     

失血性休克状态下肢体缺血再灌注影响休克发展的研究

目的：研究失血性休克状态下骨骼肌缺血再灌注对休克发展的影响。方法：雌性家兔１２只，随机等分为休克对照组（Ⅰ组）和休克伴双后肢缺血再灌注组（Ⅱ组）。戊巴比妥钠麻醉，气管切开，自主呼吸，并全身肝素化。经左颈外静脉，按１ｍｌ·ｋｇ－１·ｍｉｎ－１的速度放血５分钟，停５分钟，以左颈总动脉ＭＡＰ达４．０±０．２ｋＰａ为休克开始，此时Ⅱ组阻断腹主动脉末端，９０分钟后松开。结果：休克后１２０分钟，血中ＴＸＢ２、ＴＸＢ２／６－ｋｅｔｏ－ＰＧＦ１α、乳酸、酸性磷酸酶及Ｍｇ２＋，Ⅱ组均显著高于Ⅰ组，而休克９０分钟时，各值两组间无显著性差异。结论：失血性休克状态下肢体骨骼肌缺血再灌注可能对休克的发展产生不利影响。     

去白细胞血液预防家兔缺血心肌再灌注损伤的实验研究

用涤纶纤维滤器去除再灌注血液中的白细胞，旨在检验其对缺血心肌再灌注损伤的保护效应。３２只家兔随机分成对照组和实验组，分别用全血和去白细胞血再灌注－离体心脏在２８℃下缺血６０ｍｉｎ后再灌注２０ｍｉｎ。结果表明：对照组白细胞计数、ＣＶＲ、ＣＰＫ及ＣＰＫ－ＭＢ显著高于实验组（Ｐ〈０．００１～Ｐ〈０．０５）；ＳＯＤ活性下降，ＭＤＡ含量明显增高与实验组相比有显著差异，分别为Ｐ〈０．０２及Ｐ〈０．０５。线粒体     

1,6—二磷酸果糖对兔脑缺血再灌注损伤的保护效应

１８只成年大白鼠随机分为三组：模拟手术组、对照组和实验组。采用“四动脉阻断法”造成兔全脑缺血模型，阻断血流１５分钟后再灌注１２０分钟，测定脑水份、脑皮质Ｃａ＾２＋、ＬＰＯ含量和ＳＯＤ活性，光镜标本ＨＥ染色观察一般结构、电镜标本行透射电镜观察。结果表明：１，６－二磷酸果糖（ＦＤＰ）能够降低缺血再灌注脑组织的脑水份含量及细胞内Ｃａ＾２＋浓度，抑制ＬＰＯ的产生和提高ＳＯＤ活性，由此认为：ＦＤＰ对脑缺血再     

姜黄素对骨骼肌缺血再灌注损伤的保护作用及其机制研究

目的:观察姜黄素对肢体骨骼肌缺血再灌注损伤中血浆肌酸磷酸激酶(CPK)、乳酸脱氢酶(LDH)、丙二醛(MDA)含量及骨骼肌99m锝亚甲基二磷酸钠(99mTcMDP)吸收量的影响,探讨姜黄素对肢体骨骼肌缺血再灌注损伤的保护作用及其机制。方法:制作大鼠后肢缺血再灌注损伤模型,30只大鼠随机分为假手术组、对照组、干预组。分别于再灌注1 h后测定血浆CPK、LDH、MDA含量和腓肠肌99mTcMDP吸收量变化,透射电镜观察腓肠肌超微结构变化。结果:缺血再灌注对照组和姜黄素干预组与假手术组相比,血浆CPK(7296.18±1086.53,5168.49±975.39,3014.26±963.78)、LDH(1203.66±282.53,726.56±203.65,463.85±75.32)、MDA(10.36±2.65,6.78±2.12,3.54±1.89)含量明显增高(P<0.01),99mTcMDP吸收量(16.69±3.14,11.45±2.35,9.12±1.96)明显升高(P<0.01);腓肠肌超微结构损伤明显加重;姜黄素组血浆和骨骼肌的各项指标与缺血再灌注对照组相比显著降低(P<0.01),腓肠肌超微结构损伤明显减轻。结论:姜黄素能有效降低血浆CPK、LDH、MDA含量,减少骨骼肌99mTcMDP吸收量,减轻缺血再灌注骨骼肌坏死程度和坏死范围,改善骨骼肌再灌注损伤的超微结构,说明姜黄素对骨骼肌缺血再灌注损伤具有明显的保护作用。     

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。     

Alpha-tocopherol (Vitamin E) and iloprost attenuate reperfusion injury in skeletal muscle ischemia/reperfusion injury

BACKGROUND: The aim of this study was to clarify the role of a-tocopherol (vitamin E) and iloprost on skeletal muscle ischemia/reperfusion injury. METHODS: Setting: animal research laboratory of a university hospital. Experimental design: the iliac arteries of the 24 adult Sprague-Dawley rats were clamped and 4 hours of ischemia followed by 1 hour of reperfusion was applied. In an attempt to decrease reperfusion injury, the rats were given either a-tocopherol (n=8), iloprost (n=6) and 8 rats were given normal saline and served as control group (n=8). Measures: blood pH, pO2, pCO2, HCO3, Na, K, creatine kinase (CPK), lactate dehydrogenase (LDH) values were determined at the end of the reperfusion period. Malondialdehyde (MDA), a product of lipid peroxidation, was measured in blood, muscle and lung as an indicator of free radicals. RESULTS: Blood pO2 and HCO3 levels were significantly high (p<0.05); CPK, LDH and MDA levels were significantly low (p<0.05) in both a-tocopherol and iloprost groups when compared to the control group. Similarly, the MDA levels in the gastrocnemius muscle were significantly low in both treatment groups when compared to the controls (p<0.05). There was no significant difference between groups in other parameters. CONCLUSIONS: The results suggest that, both a-tocopherol and iloprost are useful for attenuating oxidative muscle damage occurring after a period of ischemia/ reperfusion.     

川芎嗪在骨骼肌缺血再灌注损伤中的作用

目的　探讨中药川芎嗪在骨骼肌缺血再灌注损伤中有无保护作用。方法　健康成年家兔14只 ,随机分对照组、实验组 ,每组 7只。应用家兔肢体缺血再灌注损伤动物模型 ,在恢复血流再灌注当时 ,实验组静脉输注川芎嗪注射液 ,对照组静脉输注 0 9%生理盐水。测定缺血前、缺血后、再灌注后血浆丙二醛 (MDA)、乳酸脱氢酶 (LDH)及超氧化物歧化酶 (SOD)的含量。制备骨骼肌标本进行光镜及透射电镜观察。结果　实验组在恢复血流并注射川芎嗪后 1小时 ,其血浆MDA、LDH的含量较对照组明显降低 (P <0 0 1) ,而SOD较对照组明显升高 (P <0 0 1)。光镜及电镜下观察可见实验组骨骼肌损害轻于对照组。结论　实验表明中药川芎嗪对骨骼肌缺血再灌注损伤有保护作用     

利多氟嗪加强间断缺血心停搏心肌保护作用的实验研究

报道常温下用利多氟嗪（ｌｉｄｏｆｌａｚｉｎｅ）预处理加强间断主动脉阻断心停搏心肌保护作用的实验研究。１６只犬随机分为对照组和实验组。结果发现，实验组心脏血流动力学的恢复要明显优于对照组。二组间心肌组织ＡＴＰ、腺苷和肌苷以及冠脉回流液中ＣＰＫ、ＣＰＫＭＢ、ＬＤＨ、ＳＯＤ和ＭＤＡ值均有显著性差异（Ｐ＜０．０１）。结论：冠脉搭桥术中采用间断缺血心停搏时加用利多氟嗪有利于保存心肌能量，减轻心肌再灌注损伤和术后迅即恢复心脏功能     

Increased ischemia-reperfusion blood flow impairs the skeletal muscle contractile function.

BACKGROUND: The ultimate aim of replantations and transplantations of skeletal muscle is to improve impaired function. The purpose of this study was to examine the contribution of varying durations of ischemia to postischemic blood flow in the skeletal muscle and the contribution of modulation of postischemic blood flow to skeletal muscle function and viability, using an ischemic revascularized hind limb model in rats. MATERIALS AND METHODS: Warm ischemia produced by vascular pedicle clamping was sustained for 90 min, 3 h, or 6 h. Postischemic blood flow was measured by a Doppler flowmeter or microsphere technique. In another series of experiments of 3-h ischemia, either saline or N(G)-methyl-l-arginine acetate (l-NMMA) was infused for the first 2 h of reperfusion. Postischemic blood flow was also measured. Muscle contractile function and viability were determined after 24 h of reperfusion. RESULTS: Postischemic blood flow was significantly increased during the first 10 min of reperfusion in the 90-minute ischemic group and during the first 2 h in the 3-h ischemic group compared with contralateral control blood flow. No significant increase in postischemic blood flow was noted in the 6-h ischemic group. Postischemic blood flow was significantly decreased by the l-NMMA infusion. Contractile function and viability of the tibialis anterior muscle and contractile function of the gastrocnemius muscle in the l-NMMA group were significantly increased. CONCLUSION: Reperfusion blood flow increased time dependently until 3 h of warm ischemia. Hyperemia deteriorated skeletal muscle contractile function, although it was well preserved by l-NMMA infusion to restrict the postischemic hyperemia.     

Tc-99m pyrophosphate imaging of poloxamer-treated electroporated skeletal muscle in an in vivo rat model

OBJECTIVE: This study investigates whether (99m)Tc pyrophosphate (PYP) imaging provides a quantitative non-invasive assessment of the extent of electroporation injury, and of the effect of poloxamer in vivo on electroporated skeletal muscle. METHODS: High-voltage electrical shock was used to produce electroporation injury in an anesthetized rat's hind limb. In each experiment, the injured limb was treated intravenously by either poloxamer-188, dextran, or saline, and subsequently imaged with (99m)Tc PYP. The radiotracer's temporal behavior among the experimental groups was compared using curve fitting of time-activity curves from the dynamic image data. RESULTS: The washout kinetics of (99m)Tc PYP changed in proportion to the electric current magnitude that produced electroporation. Also, (99m)Tc PYP washout from electroporated muscle differed between poloxamer-188 treatment and saline treatment. Finally, 10-kDa dextran treatment of electroporated muscle altered (99m)Tc PYP washout less than poloxamer-188 treatment. CONCLUSIONS: Behavior of (99m)Tc PYP in electroporated muscle appears to be an indicator of the amount of electroporation injury. Compared to saline, intravenous polaxamer-188 treatment reduced the amount of (99m)Tc PYP uptake. Coupled to results showing poloxamer-188 seals ruptured cellular membranes, lessens the extent of electroporation injury and improves cell viability, (99m)Tc PYP imaging appears to be a useful in vivo monitoring tool for the extent of electroporation injury.     

The effects of exogenous nitric oxide donor on motor functional recovery of reperfused peripheral nerve

PURPOSE: To investigate the effects of the nitric oxide donor S-nitroso-N-acetylcysteine (SNAC) on motor functional recovery of reperfused rat sciatic nerve. METHODS: Seventy-eight rats were divided into groups treated with SNAC (100 nmol/100 g/min), methylprednisolone 30 mg/kg/h for 15 minutes, 45-minute pause, 5.4 mg/kg/h for 1.5 h), and phosphate-buffered saline 0.2 mL/100 g/h). A 1-cm segment of sciatic nerve had 2 hours of ischemia and the results were evaluated after various reperfusion periods using a walking track test, muscle contractile testing, muscle weight, and histology. RESULTS: During reperfusion there was a significant overall improvement in sciatic functional index measurement and isometric titanic contractile force for the SNAC-treated group compared with the methylprednisolone- and phosphate-buffered saline- treated groups. The SNAC group had significantly earlier improvement in the sciatic functional index measurement between days 7 and 28. Restoration of the contractile force and muscle weight of the extensor digitorum longus muscle began earlier in the SNAC group--after day 11--whereas the other 2 groups showed progressive atrophy until day 21, with a significant difference between the SNAC group and the other 2 groups. Histologic examination showed that SNAC-treated rats had less severe degeneration and earlier regeneration of axons than the others. Although methylprednisolone-treated rats showed earlier recovery than phosphate-buffered saline-treated rats in all parameters there were no significant differences between these 2 groups. CONCLUSIONS: Supplementation of nitric oxide is effective in promoting motor functional recovery of the reperfused peripheral nerve and has potential to replace or augment steroids as therapeutic agents in treatment of nervous system ischemia/reperfusion injury.     

Addition of nitric oxide donor S-nitroso-N-acetylcysteine to selective iNOS inhibitor 1400W further improves contractile function in reperfused skeletal muscle

This study examines the effects of combination therapy with the nitric oxide (NO) donor S-nitroso-N-acetylcysteine (SNAC) and the iNOS inhibitor N-(3-(aminomethyl)benzyl) acetamidine (1400W) on contractile function in reperfused rat skeletal muscle. The right extensor digitorum longus (EDL) muscles of 104 rats were subjected to 3 h of ischemia followed by reperfusion times of 3 h, 24 h, and 7 days. For each time period, rats were further divided into sham operation, control, 1400W only, and 1400W plus SNAC groups. In vitro muscle contractile functional testing was performed in an organ chamber with electrical stimulation. The results showed that twitch and isometric tetanic forces were significantly improved in the 1400W-alone group compared to controls for 24 h and 7 days, but not 3 h of reperfusion. However, all three time periods of reperfusion showed that combination treatment of 1400W + SNAC significantly improved muscle contractile force compared to both control and 1400W-only groups. This corresponded to the decreased tissue necrosis and inflammation seen with combination therapy histologically. Our results demonstrate that combination treatment of 1400W + SNAC promotes functional recovery in reperfused skeletal muscle, supporting that manipulation of NO levels with a NO donor and an iNOS inhibitor is more beneficial than either treatment in isolation.