白细胞在缺血—再灌流损伤中的作用

近年来中性白细胞与缺血－再灌流损伤的关系引起人们的广泛重视，但国内有关这方面的临床研究尚未开展。本文就这方面的研究工作作一综述，并探讨了抗白细胞粘附防治缺血－再灌流损伤的前景。     

粘附分子与皮瓣缺血再灌注损伤

缺血-再灌注损伤是指组织在绎历了一段时间的缺血后，由于血流恢复所造成的组织继发性损伤，由于其发病机理复杂，尚不十分清楚，是很多学者关注的热点。目前已有资料表明，氧自由基产生增加，钙离子超负荷在其损伤中起着重要作用。近年来，研究发现中性粒细胞在缺血．再灌注损伤中发挥着极为重要的作用，而粘附分子是调节这种作用的关键因素。     

皮瓣缺血再灌注损伤适应性治疗

皮瓣缺血再灌注损伤是目前研究的热点,减轻缺血再灌注损伤引起的组织损害是提高皮瓣存活率的关键.随着分子生物学技术的发展及对缺血再灌注损伤机制的进一步认识,一些新的治疗皮瓣缺血再灌注损伤的方法如远距离缺血预适应、药物预适应、再灌注后适应等逐渐应用于动物实验治疗,可给予组织有效的抗缺血保护.此外,高压氧预适应、低浓度氧预适应也可有效地提高微循环灌注,增加皮瓣存活率.皮瓣抗缺血再灌注损伤的研究重点将从动物实验研究转向临床试验研究,从基础理论研究转向临床应用.     

地塞米松减轻皮瓣缺血再灌注损伤的实验研究

皮瓣修复创面，常伴随缺血－再灌注损伤，影响了皮瓣的成活。其发病机制复杂，目前有不少处理方法，但效果常不满意。地塞米松对其防治作用，目前尚少见报道。本文以地塞米松防治皮瓣缺血－再灌注损伤，取得了满意效果。材料与方法取健康Ｗｉｓｔａｒ大鼠（２５０～３００...     

硫酸锌对皮瓣缺血再灌注损伤保护作用的研究

目的 观察外源性锌对皮瓣缺血再灌注（ischemia—reperfusion，IR）损伤的保护作用，并探讨其机制。方法 48只大鼠随机分为非-IR组、IR组和补锌-IR组。在大鼠以腹壁浅血管为蒂的岛状皮瓣缺血再灌注模型上，分别测定皮瓣组织中丙二醛（MDA）含量和髓过氧化物酶（MPO）活性。观察免疫组化切片中金属硫蛋白（metallothionein，MT）的表达，并对切片进行图像分析。应用透射电镜观察皮瓣缺血再灌注损伤后超微结构的改变，观察皮瓣成活率。结果 补锌-IR组在再灌注1h和24h，皮瓣组织中MDA含量分别较IR组降低11．3％、33．2％（P〈0．05），MPO活性分别较IR组降低14．2％、22．7％（P〈0．05），MT含量分别较IR组高41．5％、44％（P〈0．01）。在补锌-IR组掀起皮瓣即刻的标本中有一定量的MT表达。MT表达在皮瓣组织多种细胞的细胞浆中。补锌-IR组皮瓣的超微结构改变较IR组减轻，皮瓣成活率较IR组升高27．2％（P〈0．05）。结论 外源性锌能诱导皮瓣内MT产生，MT通过细胞保护作用对皮瓣缺血再灌注损伤产生一定的保护作用。     

皮瓣缺血-再灌注损伤的治疗

目的综述皮瓣缺血-再灌注损伤治疗方法及技术。方法广泛查阅皮瓣缺血-再灌注损伤治疗技术的相关文献,对其治疗方法进行系统性综述。结果缺血-再灌注损伤是导致皮瓣术后坏死的主要因素之一。对缺血-再灌注损伤机制任一环节的干预均可有效减轻损伤,提高皮瓣术后成活率。结论皮瓣缺血-再灌注损伤的主要机制包括活性氧物质生成、中性粒细胞聚集、浸润等。可采用药物治疗、物理干预等方法对缺血-再灌注损伤中的某一或某些环节进行有效干扰或阻断,从而减轻动物皮瓣模型缺血-再灌注损伤,提高皮瓣成活率。     

雌二醇与皮瓣缺血再灌注损伤

皮瓣缺血再灌注损伤是组织缺血后血流恢复所造成的组织继发性损伤,常导致皮瓣部分或全部坏死,严重影响手术疗效。近年研究发现,皮瓣缺血再灌注损伤发病机制非常复杂,涉及多种细胞分子的病理性损伤变化。雌二醇是重要的甾体类激素,能有效增加皮瓣组织内微循环灌注,抑制氧自由基对组织的氧化损害,减轻中性粒细胞介导的炎性损伤,促进皮瓣成活。该文就皮瓣缺血再灌注损伤机制及雌二醇对其治疗作用研究进展作一综述。     

皮瓣缺血-再灌注损伤的机制研究进展

缺血-再灌注损伤是导致皮瓣移植术后皮瓣坏死的主要因为之一.目前研究显示,氧自由基等活性氧物质生成、中性粒细胞聚集介导炎症反应、一氧化氯作用、钙超载及能量代谢障碍、细胞凋亡等因素是造成皮瓣缺血-再灌注顿伤的可能机制,这些机制相互协同促进,形成连锁反应并不断扩大化,加重皮瓣组织损伤.该文就皮瓣缺血一再灌注损伤机制作一综述.     

缺血再灌注损伤皮瓣组织中金属硫蛋白的免疫组化研究

目的：观察缺血再灌注损伤皮瓣组织中金属硫蛋白(Metallothionein MT)的表达部位及表达量的变化规律。方法：16只大鼠随机分为对照组(n=8)和缺血再灌注组(n=8)。在大鼠以腹壁浅血管为蒂的岛状皮瓣缺血再灌注模型上，用硫代巴比妥法和比色法分别测定皮瓣组织中丙二醛(MDA)含量和髓过氧化物酶(MPO)活性。观察免疫组化切片中MT的表达部位，并对切片进行图像分析，以积分光密度代表MT的含量。结果：缺血再灌注组再灌注1h和24h，皮瓣组织中MDA含量分别较对照组高46.5％、147.8％，MPO活性分别较对照组高1169．5％、408．6％，MT含量分别较对照组高119．9％、234．6％。在发生缺血再灌注损伤的皮瓣中MT表达在表皮基底层细胞、皮下组织及肉膜下组织血管壁细胞、成纤维细胞，毛囊、皮脂腺、汗腺和肌细胞的细胞浆中。结论：皮瓣发生缺血再灌注损伤后，MT表达在皮瓣组织的多种细胞内，MT含量增加可能和皮瓣在发生缺血再灌注损伤时的某些代谢产物有关。     

皮瓣缺血再灌注损伤的防治进展

在整形外科,皮瓣被常规地应用于修复由外伤、肿瘤、切除手术或者先天畸形等引起的组织缺损。经过多年来的基础和临床研究,皮瓣移植的成活率已有所增加,但临床上仍存在部分或全部坏死的病例。究其原因,缺血再灌注（ischemia/reperfusion,I/R）损伤是皮瓣坏死的主要机制,学者们在研究中提出了一些治疗措施,如通过应用血管生长因子和干细胞移植来改善皮瓣血液循环、缺血预处理、氧自由基和炎性介质抑制剂减轻皮瓣缺血再灌注损伤等,本文将其最新研究进展综述如下。     

The effect of prostaglandin E1 versus ischemia-reperfusion injury of musculocutaneous flaps

The purpose of this study was twofold. To evaluate whether prostaglandin El can increase the survival of the flap, and to determine its function against ischemia-reperfusion injury in musculocutaneous flaps. Thirty-five Sprague-Dawley rats weighing 250 to 350 g were analyzed. The transverse rectus abdominis musculocutaneous flap was used in all rats. The rats were divided into three groups: group 1 (N = 15), the control group with 4-hour ischemic injury and intraflap injection of normal saline followed by reperfusion; group 2 (N = 15), prostaglandin E1 intraflap injection of 1 microg immediately after ischemic injury and reperfusion 4 hours later; and group 3 (N = 5), the sham-operated group. Analysis consisted of flap skin survival area measurements, immunohistochemical study using anti-intercellular adhesion molecule (anti-ICAM-1) monoclonal antibody, and histological evaluation including endothelium-sticking leukocytes at 24 hours and 5 days after reperfusion. The group treated with prostaglandin E1 showed immunohistochemical findings with decreased expression of ICAM-1 on the surface of the endothelium, and histology showed significant (p < 0.01) reduction of leukocyte adhesion at 24 hours and 5 days after reperfusion. These two factors were considered to play a role against ischemia-reperfusion injury, and led to improved survival of the flap. These results suggest that prostaglandin E1 may increase flap survival and may have a protective mechanism against ischemia-reperfusion injury by decreasing leukocyte-endothelial cell adhesion through decreased expression of ICAM-1.     

The role of proinflammatory cytokines in lung ischemia-reperfusion injury

OBJECTIVE: Proinflammatory cytokines are known to play roles in ischemia-reperfusion injury of the heart, kidney, small bowel, skin, and liver. Little is known about their roles in ischemia-reperfusion injury of the lung. This study was undertaken to define the role of 2 proinflammatory cytokines, tumor necrosis factor alpha and interleukin 1beta, in ischemia-reperfusion injury of the lung. METHODS: Left lungs of male rats were rendered ischemic for 90 minutes and reperfused for up to 4 hours. Treated animals received anti-tumor necrosis factor alpha or anti-interleukin 1beta antibody before reperfusion. Increased vascular permeability in the lung was measured by using iodine 125-labeled bovine serum albumin. Neutrophil sequestration in the lung parenchyma was determined on the basis of activity. Bronchoalveolar lavage was performed to measure cell counts. Separate tissue samples were processed for histology, cytokine protein, and messenger RNA content by using Western blotting and the ribonuclease protection assay. RESULTS: Animals receiving anti-tumor necrosis factor alpha and anti-interleukin 1beta demonstrated reduced injury compared with that seen in positive control animals (vascular permeability of 48.7% and 29.4% lower, respectively; P <.001). Vascular injury was reduced by 71% when antibodies to tumor necrosis factor alpha and interleukin 1beta were administered together. Lung neutrophil accumulation was markedly reduced among animals receiving anti-tumor necrosis factor alpha and anti-interleukin 1beta (myeloperoxidase content of 30.9% and 38.5% lower, respectively; P <.04) and combination blockade afforded even greater protection (52.4% decrease, P <.01). Bronchoalveolar lavage leukocyte content was also reduced by treatment with anti-tumor necrosis factor alpha, anti-interleukin 1beta, and combination treatment. Reductions in permeability, myeloperoxidase, and bronchoalveolar lavage leukocyte content also resulted in a decrease in a histologic injury. Finally, anti-tumor necrosis factor alpha and anti-interleukin 1beta treatment resulted in decreased messenger RNA expression for a number of early response and regulatory cytokines. CONCLUSION: Tumor necrosis factor alpha and interleukin 1beta help regulate the development of lung ischemia-reperfusion injury. They appear to promote injury by altering expression of proinflammatory and anti-inflammatory cytokines and influencing tissue neutrophil recruitment.     

The role of nitric oxide in testicular ischemia-reperfusion injury

PURPOSE: This study was designed to determine the role of nitric oxide (NO) in the ischemia-reperfusion (I/R) injury process in testes. METHODS: Fifty prepubertal male rats were divided into 5 groups each containing 10 rats. After 4-hour torsion and 4-hour detorsion, bilateral orchiectomies were performed for measurement of tissue malondialdehyde (MDA) level and histopathologic examination. The results were compared statistically. The groups were labeled as group 1, basal values of biochemical parameters in testes; group 2 (control group), torsion plus detorsion; group 3, torsion plus N-monomethyl-L-arginine (L-NMMA) plus detorsion; group 4, torsion plus L-arginine plus detorsion; group 5, sham operation. RESULTS: The highest MDA values were determined in the L-arginin group in ipsilateral testes. Group 3 and group 4 were statistically different from control group. Histological examination showed that specimens from group 4 had a significantly (P < .05) greater histological injury than group 3, and contralateral testes showed normal testicular architecture in all groups. CONCLUSIONS: These results suggest that NO plays an important role in damaging the testis with I/R. Although inhibition of NO synthesis with L-NMMA significantly improves I/R injury in testes, enhancing NO production by providing excess of L-arginine increases such damage. In the early periods of detorsion, there is no damage to contralateral testes after unilateral testicular torsion.     

外源性锌对缺血再灌注损伤皮瓣超微结构的影响

目的:观察外源性锌对缺血再灌注(ischemia-reperfusionIR)损伤皮瓣的保护作用。方法:48只大鼠随机分为对照组(n=16)、缺血再灌注组即IR组(n=16)和补锌缺血再灌注组即补锌-IR组(n=16)。在大鼠以腹壁浅血管为蒂的岛状皮瓣缺血再灌注模型上,用硫代巴比妥法和比色法分别测定皮瓣组织中丙二醛(MDA)含量和髓过氧化物酶(MPO)活性。应用透射电镜观察皮瓣缺血再灌注损伤后超微结构的改变,并观察皮瓣成活率。结果:补锌-IR组在再灌注1h和24h,皮瓣组织中MDA含量分别较IR组降低11.3%、33.2%,MPO活性分别较IR组降低17.9%、21.4%。补锌-IR组皮瓣的超微结构改变较IR组明显减轻,皮瓣成活率较IR组升高27.2%。结论:外源性锌能显著减轻缺血再灌注损伤皮瓣中组织细胞超微结构的病理改变,对皮瓣缺血再灌注损伤产生一定的保护作用。     

The effects of protease inhibitor upon the ischemia-reperfusion injury]

The purpose of the study is to investigate the effects of protease inhibitor (Nafamostat mesilate: NM) upon myocardial protection. Hearts were subjected to 20 min working control perfusion followed by 3 min cardioplegic infusion with the St. Thomas Cardioplegic Solution (ST) contained various concentrations of NM, and global ischemia for 33 min at 37 degrees C (Exp. 1) or 150 min at 20 degrees C (Exp. 2). Hearts were then converted to Langendorff reperfusion (the leakage of Creatine Kinase (CK) and Cathepsin B (Cat-B) ware measured) and 20 min working reperfusion. Various concentrations of NM added during Langendorff reperfusion (Exp. 3). During working perfusion cardiac functions (aortic flow (AoF), coronary flow (CoF), heart rate (HR), aortic pressure (AoP)) were measured, and expressed as the percent recovery of pre-ischemic control value. Post-ischemic recovery of AoF (%AoF) showed the bell-shaped dose-response curve, and the optimal dose was 3 microM (Exp. 1) and 10 microM (Exp. 2) respectively. There was a significant (p < 0.05) increase of %AoF in optimal dose compared with that in controls (64.2 +/- 1.2% vs 52.3 +/- 2.5% in Exp. 1, 68.9 +/- 3.1% vs 54.1 +/- 1.4% in Exp. 2). These increase of functional recovery reflected in the values for CK and Cat-B leakage. The addition of NM in ST reduced CK and Cat-B leakage significantly in the concentration of 5 microM (in Exp. 1) and 10 microM (in Exp. 2) respectively. But the addition of NM in reperfusate did not reduced CK leakage significantly.(ABSTRACT TRUNCATED AT 250 WORDS)