盆腔手术病人围术期血清TNF-α、IL-6、IL-8、IL-10水平的变化

目的：观察盆腔手术病人围术期血清肿瘤坏死因子－α（TNF－α）、白细胞介素－6（IL－6）、白细胞介素－8（IL－8）、白细胞介素－10（IL－10）水平的动态变化，分析手术麻醉对患者免疫力的影响。方法：选择30例子宫手术病人，用0．25％丁卡因＋1％利多卡因理解外阻滞。于手术前、手术开台后30分钟，术结、术后1天和2天分别检测外周血清中TNF－α、IL－6、IL－8、IL－10水平。结果：与术前比较，TNF－α没有明显变化；IL－6在手术开始后30分钟及术结明显升高（P＜0．05）；IL－8在术后1天达高峰，至术后2天仍高于正常；IL－10在术后1天、2天水平较术前明显下降（P＜0．05）。结论：手术创伤要引起促炎性细胞因子释放增加，抗炎性细胞因子分泌的不足可能是重要的原因。     

前列腺素E2对急性坏死性胰腺炎大鼠IL—10，TNF—α及IL—β的调控和对肺组织损伤的影响

目的：探讨前列腺素E2（PGE2）对大鼠急性坏死性胰腺炎（ANP）中血清白介素－10（IL－10），肿瘤坏死因子（TNF－α）以及白介素－1β（IL－1β）的含量及肺组织损伤的影响，方法：将SD大鼠91只随机分4组，假手术对照组（n=7)，ANP组（n=28),PGE2前处理组（n=28),BGE2后处理组（n=28)；观察同组不同时间，不同组同时间的IL－1β，TNF－α和IL－10的动态变化，并观察各组肺组织的病理切片。结果：各指标在1h,3h,6h和12hPGE2前处理组和PGE2后处理组与ANP组相比较差异有显著性（P＜0．01），在PGE2前处理组，TNF－α，IL－1β下降更加明显，IL－10升高两组都很明显，而且有PGE2保护的两组，其肺组织损伤出现较迟，较轻，结论：IL－1β和TNF－α在大鼠ANP的全身性反应过程中起重要的递质作用，IL－10能抵抗它们的作用，PGE2能降低ANP大鼠血清中IL－1β，TNF－α含量，提高IL－10含量，减轻肺组织损伤。     

黄芪注射液对肾病综合征细胞因子及其基因表达的影响

目的：探讨儿童肾病综合征（NS）外周血白细胞介素－1（IL－1）、白细胞介素－6（IL－6）、白细胞介素－8（IL－8）和肿瘤坏死因子α（TNFα）的变化,糖皮质激素（简称“激素”）加黄芪注射液对IL－1、IL－6、IL－8和TNFα的产生及其基因表达的影响。方法：将观察对象分为四组：①治疗前组;②激素组;③黄芪组;④对照组。应用酶联免疫吸附试验（ELISA）方法检测血清中IL－1、IL－6、IL－8和TNFα的水平。应用原位聚合酶链反应（原位PCR）方法,检测外周血单个核细胞（PBMC）激素加黄芪注射液对IL－1、IL－6、IL－8和TNFαmRNA表达的影响。结果：NS患儿外周血IL－1、IL－6、IL－8和TNFα水平明显高于正常儿童,有显性差异（P＜0．01）;mRNA的表达增加。激素治疗后IL－1、IL－6、IL－8和TNFα水平明显降低（P＜0．05）,mRNA的表达下降。激素加黄芪注射液对上述细胞因子和mRNA表达其降低更加显（P＜0．01）。结论：NS患IL－1、IL－6、IL－8和TNFα水平明显增高,激素对IL－1、IL－6、IL－8和TNFα的产生与mRNA表达有抑制作用,黄芪具有辅助糖皮质激素治疗的作用。     

参附注射液对体外循环中炎性反应的影响

目的：观察参附注射液对体外循环（CPB）中肿瘤坏死因子－α（TNF－α）和白细胞介素－6（IL－6）的影响。方法：将20例人工心脏瓣膜置换术患者随机分成参附组和对照组（每组10例）。参附组分别于麻醉诱导前、CPB前及主动脉开放10分钟内分别静脉滴注参附注射液20ml、40ml和40ml，于CPB前、主动脉阻断前、主动脉阻断30分钟，主动脉开放15分钟和60分钟时采用放射免疫法测定两组血心中TNF－α和IL－6的含量。结果：主动脉阻断前、主动脉阻断30分钟、主动脉开放后15分钟和60分钟，对照组TNF－α值均明显高于参附组（P＜0．05），各时点IL－6组间比较差别无显著性意义（P＞0．05）。结论：参附注射液可降低主动脉开放后血浆TNF－α的含量，具有对抗CPB所致的炎性反应的作用，而对CPB中IL－6作用不明显。     

胰腺癌术后免疫治疗抗感染作用机制的探讨

目的：了解免疫治疗剂胸腺肽－α1在腺胰癌术后抗感染中的作用机制。方法：选择60例胰腺癌根治术病人，分为用药组和对照组。用药组病人在手术后使用胸腺肽－α1，对照组不予使用。观察临床疗效、内毒素和细胞因子（IL－2、IL－6、IL－10和TNF－α）水平的变化，以及T淋巴细胞亚群CD3^ 、CD4^ 、CD8^ 和NK细胞百分率的变化。结果：胰腺癌手术组病人使用胸腺肽α－1后肿瘤坏死因子（TNF）－α水平明显下降，白介素（IL）－2、IL－10水平明显升高；手术后1周用药组的CD3^ 、CD4^ 百分率较手术前升高，且明显高于对照组。用药组术后1周临床有效率达100％，高于对照组（80％）。结论：胸腺肽－α1在胰腺癌术后可提高免疫力的功能，有利于病人恢复。     

乌司他丁对心脏直视术中缺血-再灌注损伤的保护作用

目的：研究乌司他丁对心肺转流（CPB）心脏直视手术中缺血－再灌注损伤的保护作用。方法：20例择期CPB心脏瓣膜手术患者随机均分为对照组（C组）和乌司他丁组（U组），C组不给药，U组给予乌司他丁100万U（其中30万U为麻醉诱导前给予，40万U预充体外循环机内，30万U为开放升主动脉后给予），分别于麻醉诱导后（T1），阻断升主动脉30分钟（T2），再灌注1小时（T3），再灌注2小时（T4）及再灌注3小时（T5）各时间点取静脉血用ELISA法测定样本中下降各指标的水平。肿瘤坏死因子－α（TNF-α），白细胞介素－6（IL－6），白细胞介素－8（IL－8）。结果：两组血清中TNF－α，IL-6，IL－8的浓度，都是在再灌注后与手术前值及阻断主动脉30分钟的值相比有明显的增加（P＜0．05），在T3，T4，T5三个时点C组的TNF－α，IL－6，IL－8的释放明显低于对照组（P＜0．05），结论：在CPB过程中乌司他丁可以通过抑制炎性介质TNF－α，IL－6和IL－8的释放而减轻缺血－再灌注损伤。     

兔内毒素血症时sCD14、E-选择素和IL-10水平及其与预后的关系

目的 探讨血清可溶性CD14（sCD14)、E－选择素、白细胞介素－10（IL－10）、肿瘤坏死因子－α（TNF－α）和平均动脉压（MAP）在内毒素血症病理变化过程中的水平及其相互关系。方法 复制兔内毒素血症模型，分别于模型制作后0min、30min、60min、120min、180min、240min及300min取血测定E－选择素、IL－10、sCD14及TNF－α含量，，同时八导生理记录仪记录MAP。结果 内毒素血症组中TNF－α及sCD14含量30min后即开始增加；E－选择素和IL－10含量120min后明显增加；MAP则于120min后明显下降。对照组中各指标水平变化不明显。结论 sCD14、TNF－α、E－选择素及IL－10在内毒素血症的发病机理中起着重要的作用。sCD14和TNF－α是反映感染病理变化早期过程中的重要指标之一；E－选择素和IL－10可能与该病理变化的严重程度有关。     

淋巴细胞与肝癌细胞混合培养诱导特异性细胞毒T淋巴细胞的形成

目的 通过肝癌细胞和淋巴细胞混合培养，体外诱导产生高活性的肝癌特异性细胞T淋巴细胞（H－S－CTL）。方法 采用淋巴细胞和肝癌细胞混合培养技术，在IL－1，IL－2，IL－4和IL－6刺激下，诱导产生H－S－CTL，应用间接免疫荧光法和^51Cr释放法检测其对靶细胞的杀伤效应。结果 H－S－CTL与自身LAK相比，CD3＋，CD4＋和CD8＋细胞明显增多，抗肿瘤效应明显增强。结论 采用淋巴细胞和肝癌细胞混合培养同时应用白细胞介素可获得大量扩增的高活性的H－S－CTL。     

重组腺病毒对烫伤大鼠肝组织核因子—kB活性的调控

目的 探索腺病毒介导IkBα基因对烫伤大鼠肝组织核转录因子NF－kB活性的调控作用。方法 应用重组缺陷型腺病毒载体（AdIkBα)预处理大鼠，烫伤后不同时相点取肝组织，提取组织核蛋白，与r^-32PATP标记的NF－kB特异性探针共同反应，利用凝胶电泳迁移率改变分析方法（EMSA）检测NF－kB/DNA结合性；提取肝组织总RNA，用RT－PCR法检测IL－1β,TNFα mRNA的表达。结果 与正常对照组相比，烫伤组致伤后0．5hNF-kB/DNA结合活性显增强，致伤后24h，仍保持较强结合活性。AdIkBα预处理组，大鼠NF－kB/DNA结合活性略高于正常，但显低于烫伤组。RT－PCR分析，大鼠烫伤后0．5h与对照组相比，IL－1β，TNFα表达显升高，持续致伤后24h;AdIkBα预处理组，IL－β和TNFα表达显低于烫伤组。结论 大鼠严重烫伤后，肝组织细胞内NF－kB迅速活化，IL－1β和TNFα的表达随之显增强，经AdIkBα预处理能显抑制大鼠严重烫伤后肝组织NF－kB的活化，并下调IL－1β、TNFα的表达。     

胸腔积液中肿瘤坏死因子、白细胞介素—8和腺苷脱氨酶的变化与意义

目的 探讨和比较检测胸液中肿瘤坏死因子（TNFα）、白细胞介素－8（IL－8）和腺苷脱氨酶（ADA）对结核性胸膜炎的诊断价值。方法 化学发光酶免分析法和改良的Martinek‘s法检测30例结核性、27例恶性胸腔积液和14例漏出液中TNFα、IL－8t ADA的水平。结果 结核性胸液中TNFα、IL－8和ADA水平均显著高于恶性胸液和漏出液患者（P＜0．05）。恶性胸液中TNFα、IL－8水平高于漏出液（P＜0．05）,但ADA在这两组间无显著性差异（P＞0．05）。结论 TNFα、IL－8和ADA检测可作为结核性胸腔积液与恶性胸腔积液鉴别诊断的辅助指标,尤以ADA诊断效能最高。     

肝内抗炎与致炎反应变化及其与内毒素肝损伤的关系

目的 探讨内毒素致肝损伤过程中肝内致炎与抗炎反应的变化规律及其作用,为深入阐明内毒素肝损伤的发病机制提供实验依据。方法 于尾静脉注入不同剂量内毒素（E.coli 026:B6）复制内毒素血症或休克模型。采用ELISA法检测小鼠肝组织内TNFα、IL－4、IL－10含量,并分析其与肝损害的关系。结果 注射LPS后1h,低剂量和高剂量肝组织内致炎介质TNFα、IL－6水平即显著增高,其中IL－6在注射LPS后3h达峰值,至8h仍显著高于对照组。高剂量组肝内TNFα、IL－6水平明显高于剂量组。抗炎细胞因子IL－4、IL－10水平在注射LPS后1h虽均无明显变化,但至3h,两组肝内IL－4、IL－10水平都显著升高,并在8h仍显著高于对照组,其中高剂量组肝内L－4,IL－10水平也明显高于低剂量组。地内致炎和抗炎介质变化与肝组织结构受损、肝功能障碍呈一致性改变。结论 内毒素致肝损伤过程中,肝内相继发生致炎与抗炎反应, 两者相互作用失衡是导致内毒素肝损伤的重要机制。因此,在内毒素肝损伤的防治中应考虑到局部抗炎与致炎反应的综合作用。     

Synthetic colloids attenuate leukocyte-endothelial interactions by inhibition of integrin function

BACKGROUND: It has been suspected that synthetic colloids may interfere with leukocyte adhesion by down-regulation of endothelial cell adhesion molecules. Although inhibition of endothelial inflammation might reduce leukocyte-related tissue injury, the same mechanism may be detrimental for host defense during severe infection. Regarding the widespread use of colloids, the authors performed a laboratory investigation to determine the mechanisms by which synthetic colloids interfere with leukocyte-endothelial interactions. METHODS: Adhesion molecule expression on native and cytokine-activated endothelium from umbilical veins was measured after pretreatment with gelatin and various preparations of dextran or hydroxyethyl starch. Inhibition of neutrophil adhesion to activated endothelium was examined in a flow chamber by perfusion of untreated and colloid-treated neutrophils over colloid-pretreated endothelium at 2 dyn/cm. Comparisons were made between untreated controls, colloid-pretreated endothelium, and colloid-cotreated neutrophils. RESULTS: Intercellular adhesion molecule 1, vascular cell adhesion molecule 1, E-selectin, and P-selectin were not attenuated by any colloid. Accordingly, colloid pretreatment of endothelium alone did not reduce neutrophil adhesion. In contrast, when neutrophils were cotreated by addition of colloids to the perfusate immediately before perfusion, adhesion decreased by 31-51% (P < 0.05) regardless of the colloid type. As indicated by the twofold increased rolling fractions, this reduction was due to an inhibition of neutrophil integrins. CONCLUSIONS: This study shows that synthetic colloids inhibit neutrophil adhesion by a neutrophil-dependent mechanism rather than interfering with endothelial cell activation. This suggests that inhibition of leukocyte sequestration by volume support is a common and transient phenomenon depending on the colloid concentration in plasma.     

Antithrombin can modulate coagulation, cytokine production, and expression of adhesion molecules in abdominal aortic aneurysm repair surgery

We investigated the effects of antithrombin on coagulation, fibrinolysis, and production of cytokines and adhesion molecules in abdominal aortic aneurysm repair surgery. Sixteen patients for Y-shaped graft replacement of abdominal aortic aneurysm were divided into an antithrombin group and a control group. In the antithrombin group, 3000 U antithrombin was infused over 30 min before heparin administration and 24 h later. White blood cell counts, platelet counts, prothrombin time ratio, and serum concentrations of antithrombin, polymorphonuclear leukocyte elastase, interleukin (IL)-1beta, IL-6, IL-8, tumor necrosis factor-alpha, and adhesion molecules, and variables of coagulation and fibrinolysis were measured before surgery, at the end of surgery, and 1 and 2 days after surgery. The antithrombin concentration decreased in the control group, whereas it increased in the antithrombin group with significant differences between the groups. Prothrombin time ratio, concentrations of d-dimer, thrombin-antithrombin complex, and intercellular adhesion molecule-1 increased only in the control group and polymorphonuclear leukocyte elastase, IL-6, tumor necrosis factor-alpha, and vascular cell adhesion molecule-1 increased in both groups. They were significantly less in the antithrombin group except for intercellular adhesion molecule-1. In conclusion, antithrombin could decrease hypercoagulation and inflammatory activation during abdominal aortic aneurysm surgery, which may decrease adverse events.     

七氟烷预处理对脂多糖致大鼠急性肺损伤的保护作用

目的 评价七氟烷预处理对脂多糖(lipopolysaccharide,LPS)所致大鼠急性肺损伤(acute lung injury,ALI)的影响.方法 72只SD大鼠随机分成6组:NS组、LPS组和七氟烷预处理(S-1 h组、S-6 h组、S-12 h组、S-24 h组).通过气管内滴注LPS建立大鼠ALI模型.大鼠在气道内给予LPS或NS后6 h处死,检测不同时间点七氟烷预处理(2.4%,30 min)对支气管肺泡灌洗液(bronchoalveolar lavage fluid,BALF)中白细胞计数、细胞因子TNF-α和IL-1β水平,肺组织髓过氧化物酶(myeloperoxidase,MPO)活性,肺血管通透性及肺组织病理学等的影响.结果 与NS组相比,LPS组肺组织损伤程度,BALF白细胞计数以及TNF-α和IL-1β水平,血管通透性和肺组织MPO活性均显著增高(P<0.01).给予LPS前1 h和24 h七氟烷预处理能降低肺组织MPO活性,BALF中IL-1β水平及白细胞计数(P<0.01),而S-6h组和S-12 h组与IPS组相比无明显差别.七氟烷预处理均能够降低肺血管通透性和BALF中TNF-α水平(P<0.01),且以S-1 h和S-24h组为显著(P<0.01).提示七氟烷预处理对LPS所致肺损伤具有早期和延时的保护作用.结论 气道内给予LPS1 h和24 h前七氟烷预处理对LPS致大鼠ALI具有保护作用.     

乌司他丁后处理及其联合预先给药对CPB下心脏瓣膜置换术患者心肌炎性反应的影响

目的 评价乌司他丁后处理及其联合预先给药对CPB下心脏瓣膜置换术患者心肌炎性反应的影响.方法 择期行CPB下心脏瓣膜置换术患者80例,性别不限,年龄21～59岁,心功能分级Ⅱ或Ⅲ级.采用随机数字表法,将患者随机分为4组(n=20):生理盐水对照组(C组)、乌司他丁预先给药组(U1组)、乌司他丁后处理组(U2组)和乌司他丁预先给药联合后处理组(U3组).U1组于气管插管后至升主动脉阻断前10 min经中心静脉输注乌司他丁500～ 1000 U·kg-1·min-(剂量20 000U/kg);U2组于主动脉开放前5～7 min经主动脉根部灌注乌司他丁4000～5000 U·kg-1·min-1(剂量10 000 U/kg);U3组进行乌司他丁预先给药联合后处理;C组给予等容量生理盐水.分别于升主动脉阻断前10 min(T1)、升主动脉阻断后40 min(T2)、主动脉开放后45 min(T3)和术毕(T4)时采集动脉血样,测定血浆IL- 10、IL-1、IL-6和TNF-α的浓度,并进行中性粒细胞(PMN)计数.于主动脉开放后45min时取右心耳组织,采用免疫组化法测定IL-6和IL-1β的表达.结果 与C组比较,U1组、U2组和U3组血浆IL-10浓度升高,血浆IL-1、IL-6、TNF-α的浓度和PMN计数降低,心肌组织IL-1β和IL-6表达下调(P＜ 0.05);与U1组和U2组比较,U3组T2-4时血浆IL-10浓度升高,血浆IL-1、IL-6、TNF-α的浓度和PMN计数降低,心肌组织IL-1β和IL-6表达下调(P＜0.05).结论 乌司他丁后处理可抑制CPB下心脏瓣膜置换术患者心肌炎性反应,联合预先给药时其效应增强.     

Interleukin-10 inhibits ischemic and cisplatin-induced acute renal injury.

BACKGROUND: Acute renal failure (ARF) is caused by ischemic and nephrotoxic insults acting alone or in combination. Anti-inflammatory agents have been shown to decrease renal ischemia-reperfusion and cisplatin-induced injury and leukocyte infiltration. Interleukin-10 (IL-10) is a potent anti-inflammatory cytokine that inhibits inflammatory and cytotoxic pathways implicated in acute renal injury. Therefore, we sought to determine if IL-10 inhibits acute renal injury. METHODS: The effects of IL-10 were studied in mice following cisplatin administration and bilateral renal ischemia-reperfusion, in a rat model of renal transplantation, and in cultured mouse cortical tubule cells. RESULTS: IL-10 significantly decreased renal injury following cisplatin administration and following renal ischemia/reperfusion. Delay of IL-10 treatment for one hour after cisplatin also significantly inhibited renal damage. IL-10 and alpha-melanocyte stimulating hormone (alpha-MSH) increased recovery following transplantation of a kidney subjected to warm ischemia. To explore the mechanism of action of IL-10, its effects were measured on mediators of leukocyte trafficking and inducible nitric oxide synthase (NOS-II). IL-10 inhibited cisplatin and ischemia-induced increases in mRNA for tumor necrosis factor-alpha (TNF-alpha), intercellular adhesion molecule-1 (ICAM-1), and NOS-II. IL-10 also inhibited staining for markers of apoptosis and cell cycle activity following cisplatin administration, and nitric oxide production in cultured mouse cortical tubules. CONCLUSIONS: IL-10 protects against renal ischemic and cisplatin-induced injury. IL-10 may act, in part, by inhibiting the maladaptive activation of genes that cause leukocyte activation and adhesion, and induction of iNOS.     

Interferon-gamma improves muscle flap microcirculation in double-strand RNA-induced inflammation.

Endothelial cell (EC) activation and subsequent expression of leukocyte adhesion molecules are initial events in multiple pathological processes. Viral double-strand ribonucleic acid (dsRNA) induces EC adhesion protein expression and leukocyte adhesion in vitro. Interferon-gamma (IFN-gamma) has been demonstrated to modulate the expression of certain adhesion proteins. The purpose of this study was to measure the inflammatory response to a viral mimetic--a synthetic dsRNA, polyinosinic-polycytidylic acid (poly-I:C)-on the microcirculation of a muscle flap in a rat model and to determine whether IFN-gamma attenuated the response. Two-stage surgery to create a cremaster muscle end-organ tube flap was performed on 18 male Sprague-Dawley rats in three groups. After intra-arterial injection into the abdominal aorta, the reagents (phosphate-buffered saline-bovine serum albumin [PBS-BSA] in groups I and II, and IFN-gamma in group III) were kept for 1 hour in this end-organ system. During the second stage at 16 hours, after injection into the penile vein (PBS-BSA in group I, poly-I:C in groups II and III), the flap was prepared for intravital microscopic measurement. The following parameters were measured: red blood cell velocity; vessel diameter; number of functional capillaries; and number of rolling, sticking, and transmigrating neutrophils and lymphocytes. Wilcoxon's rank sum test was used for statistical comparison. Poly-I:C caused a 70% increase in the main artery diameter and a 7% increase in velocity. But as a consequence of dynamic activation of leukocyte interaction, a 30% drop in functional capillary perfusion was observed. Injury to the entire vascular endothelium was confirmed by a 160% increase in transmigrating leukocytes. Treatment with IFN-gamma inhibited the poly-I:C-induced inflammation, as shown by 88%, 63%, and 85% decreases in rolling, sticking, and transmigrating leukocytes respectively, and by a 28% increase in capillary perfusion. Treating the system with IFN-gamma in advance, inhibited poly-I:C-induced inflammation, shown by marked decreases in rolling, adhering, and transmigrating leukocytes, and a notable increase in perfused capillaries. These observations reflect an inhibitory effect of IFN-gamma on leukocyte adhesion molecule expression in vascular endothelium in response to dsRNA in a muscle flap at the microcirculatory level.     

Synthetic Colloids Attenuate Leukocyte-Endothelial Interactions by Inhibition of Integrin Function

Background: It has been suspected that synthetic colloids may interfere with leukocyte adhesion by down-regulation of endothelial cell adhesion molecules. Although inhibition of endothelial inflammation might reduce leukocyte-related tissue injury, the same mechanism may be detrimental for host defense during severe infection. Regarding the widespread use of colloids, the authors performed a laboratory investigation to determine the mechanisms by which synthetic colloids interfere with leukocyte-endothelial interactions.

Methods: Adhesion molecule expression on native and cytokine-activated endothelium from umbilical veins was measured after pretreatment with gelatin and various preparations of dextran or hydroxyethyl starch. Inhibition of neutrophil adhesion to activated endothelium was examined in a flow chamber by perfusion of untreated and colloid-treated neutrophils over colloid-pretreated endothelium at 2 dyn/cm2. Comparisons were made between untreated controls, colloid-pretreated endothelium, and colloid-cotreated neutrophils.

Results: Intercellular adhesion molecule 1, vascular cell adhesion molecule 1, E-selectin, and P-selectin were not attenuated by any colloid. Accordingly, colloid pretreatment of endothelium alone did not reduce neutrophil adhesion. In contrast, when neutrophils were cotreated by addition of colloids to the perfusate immediately before perfusion, adhesion decreased by 31-51% (P < 0.05) regardless of the colloid type. As indicated by the twofold increased rolling fractions, this reduction was due to an inhibition of neutrophil integrins.     

红细胞停搏液的心肌保护作用及对细胞间粘附分子-1表达的影响

目的：研究红细胞停搏液的心肌保护作用及其对细胞间粘附分子－1表达的影响。方法：应用滤器去除血液中的白细胞和血小板，配制红细胞停搏液，并应用Langendorff离体心模型，测定心率（HR）、左室收缩压峰值（LVSP）、左室舒张末压（LVEDP）、左室内压最大小升速率（dp/dtmax）、冠脉流量（CF）、肌酸激酶（CK）、电镜下观察组织结构的变化，用免疫组化方法观察粘附分子（ICAM－1）的表达情况。结果：在HR、LVSP、dp/dtmax、CF的恢复率、组织显微结构和ICAM－1表达方法，红细胞停搏液组优于全血及去白细胞停搏液组（P＜0．05）。结论：红细胞停搏液较全血停搏液和去白细胞停搏液具有更好的心肌保护作用。     

Intercellular adhesion molecule-1/leukocyte function associated antigen-1 blockade inhibits alloantigen specific human T cell effector functions without inducing anergy.

BACKGROUND: Intercellular adhesion molecule (ICAM-1) is important in leukocyte adhesion-dependent events and some data suggest that ICAM-1 provides T cell costimulation. We anlayzed the role of the ICAM-1 and leukocyte function associated antigen-1 (LFA-1) interaction in human T cell alloreactivity in vitro. METHODS: Allo-antigen-induced T cell proliferation and cytotoxic T lymphocyte lytic activity were assessed by mixed lymphocyte reaction assay and 51 Chromium release assay, respectively. Immunostaining and flow cytometry were used to assess the expression of receptors on activated T cells. RESULTS: Alloantigen-induced T cell proliferation and cytotoxic T lymphocyte activity were markedly inhibited by antibodies to ICAM-1 and LFA-1. These antibodies had to be present at the time of initial T cell receptor/antigen engagement to inhibit proliferation. Neither IL-2 nor IL-4 were involved in the observed inhibition by antibodies. Inhibition was not associated with altered cell surface expression of receptors such as CD3, CD4, ICAM-1, LFA-1, CD25, and HLA-DR however, these antibodies did impede the ability of generation of functionally active T cells. Interestingly, these antibodies inhibited soluble, but not immobilized OKT3-induced proliferation of peripheral blood leukocytes. Antibody-mediated inhibition of proliferation failed to impair the ability of T cells to subsequently proliferate in response to stimulation by the original or third party alloantigen or mobilize [Ca++]i in response to CD3 or LFA-1 receptor ligation. CONCLUSIONS: These data demonstrate that blockade of ICAM-1/LFA-1 binding at the time of allorecognition potently blocks initial T cell effector functions that could be due to lack of effective T cell/APC engagement.