肢体缺血预处理对脂多糖诱导大鼠急性肺损伤的保护作用
详细信息    本馆镜像全文|  推荐本文 |  |   获取CNKI官网全文
摘要
目的:通过检测肺功能的变化,支气管肺泡灌洗液(BALF)中白细胞和乳酸脱氢酶(LDH),血清中超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量,免疫组织化学方法检测肺组织SP-A表达水平及HE染色观察肺组织病理改变来研究非创伤性肢体缺血预处理(N-LIP)对脂多糖诱导大鼠急性肺损伤的保护作用。
     方法:将15只SD雌性大鼠随机分为对照组、急性肺损伤组(ALI组)、急性肺损伤+非创伤性双下肢缺血预处理组(ALI+N-LIP组)。戊巴比妥钠腹腔注射麻醉,ALI+N-LIP组用止血带捆绑双下肢,阻断血流5min,再开放5min,反复3次,每次捆绑以双下肢紫绀、捆绑下方腹股沟处摸不到股动脉搏动为准;之后ALI组和ALI+N-LIP组分别予以腹腔注射脂多糖(4mg/kg),对照组注射等量生理盐水;1h后用Buxco有创肺功能仪,以乙酰甲胆碱(methacholine,Mch)0.39ng/mL、0.78ng/mL、1.56ng/mL、3.12ng/mL依次激发,检测大鼠气道阻力(AR)、动态肺顺应性(Cdyn)的变化,收集肺泡灌洗液(BALF),取血及肺组织。细胞计数法测定BALF中白细胞(WBC)数量,全自动生化分析仪检测BALF中乳酸脱氢酶(LDH)含量,比色法测血清中超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量,免疫组织化学方法检测肺组织中肺泡表面活性物质相关蛋白-A(pulmonary surfactant associatedprotein,SP-A)的表达水平,HE染色观察肺组织病理变化。
     结果:1.较正常对照组相比,Mch激发后ALI组气道阻力(AR)明显增高(P<0.01),动态肺顺应性(Cdyn)明显减弱(P<0.01)。ALI+N-LIP组大鼠气道阻力(AR)的增高程度(P<0.01)、动态顺应性(Cdyn)的减弱程度(P<0.01)均明显小于ALI组。
     2.支气管肺泡灌洗(bronchoalveolar lavage fluid,BALF)中,ALI组的白细胞数(P<0.01)、LDH含量(P<0.01)比对照组明显升高;ALI+N-LIP组BALF中白细胞数(P<0.01)和LDH含量(P<0.01)也增高但增高程度均明显小于ALI组(P<0.05)。
     3.ALI组血清中超氧化物歧化酶(SOD)总活力比对照组明显降低(P<0.01);丙二醛(MDA)含量比对照组明显升高(P<0.01);ALI+N-LIP组T-SOD降低、MDA升高的程度均明显小于ALI组(P<0.05)。
     4.SP-A免疫组织化学显示:ALI组肺组织中SP-A含量较对照组明显降低;ALI+N-LIP组的SP-A的含量比对照组、AIL组明显增多。
     5.肺部HE染色显示ALI组、ALI+N-LIP组均有不同程度的肺损伤,即有肺组织毛细血管出血,肺泡间隔增宽,肺泡融合,肺泡腔内出现炎性细胞浸润。但ALI+N-LIP组损伤程度明显轻于ALI组。
     结论:非创伤性肢体缺血预处理对脂多糖诱导的急性肺损伤有保护作用,其作用机制可能与促进SP-A表达和抗氧化作用有关。
Objectives: In order to observe the protective effect of noninvasive limb ischemic preconditioning on acute lung injury induced by lipopolysaccharide (LPS) of rats, the changes of lung function, white blood cells(WBC) and lactate dehydrogenase (LDH) in bronchoalveolar lavage fluid (BALF), serum superoxide dismutase(SOD) and malondialdehyd(MDA) have been tested, and the content of pulmonary surfactant-associated protein-A(SP-A) and pathological change of pulmonary tissue were also compared with control following animal model.
     Methods: Fifteen female SD rats were divided randomly into Control Group, Acute lung injury Group (ALI Group),Acute lung injury and noninvasive limb ischemic preconditioning Group (ALI+N-LIP Group). Pentobarbital sodium was used to anesthetize by intraperitoneal injection. Both lower extremities in ALI+N-LIP Group were bind with tourniquet for 5 minutes every time. The tourniquet was released for 5 minutes. The preconditioning was repeated for 3 times. After it, ALI models were established by LPS in intraperitoneal injection in ALI Group and ALI+N-LIP Group .The normal saline (NS) in tales doses was injected in Control Group. One hour later, all rats were separately stimulated by methacholine (Mch) in four doses (0.39ng/mL、0.78ng/mL、 1.56ng/mL、3.12ng/mL)in order. The airway resistance (AR) and dynamic compliance (Cdyn) were recorded by Buxco. Blood samples and BALF were collected, the amounts of WBC in BALF were counted by cytometry and the level of LDH in BALE was also tested by automatic biochemistry analyzer. The level of seram MDA and SOD were examined by chromatometry. The lung tissues were acquired to observe the content of pulmonary surfactant-associated protein-A (SP-A) by immunohisto- chemistry and pathological changes by HE.
     Results: 1. Compared with Control Group, AR in ALI Group was significantly increased (P<0.01) and Cdyn was decreased (P<0.01) after stimulus by Mch. The increasing rate of AR and decreasing rate of Cdyn in ALI+N-LIP Group were less than in ALI Group.
     2. Compared with Control Group, the level of WBC and LDH in BALF for ALI Group and ALI+N-LIP Group were higher(P<0.01). Those in ALI+N-LIP Group were much lower than ALI Group (P<0.05).
     3. Compared with Control Group, in ALI Group, the total activity of SOD was weaker (P<0.01) and the level of MDA was higher (P<0.01). In ALI+N-LIP Group, the total activity of SOD was higher and the level of MDA was lower than ALI Group.
     4. The content of SP-A in ALI+N-LIP Group was strongest in three groups (P<0.01), while that in ALI Group was weakest (P<0.01).
     5. Acute lung injury in different extend could be observed both in ALI Group and ALI+N-LIP Group. The pathological phenomenons were capillary hemorrhage, alveolar septum widened, fusion of pulmonary alveoli and inflammatory cell infiltrate. But the degree of injury in ALI+N-LIP Group was less than ALI Group.
     Conclusion: noninvasive limb ischemic preconditioning has protective effect on acute lung injury induced by LPS in rats. Their possible mechanisms are related to by improving the secretion of SP-A and antioxidation.
引文
[1]Ng CS,Wang S,Yim AP,et al.Pulmonarydysfunction after cardiac surgery.Chest,2002,121(4):1269-1277
    [2]Sievers H,Freand K,Eleftheriadis S,et al.Lung protection during total cardiopulmonarybypass byisolated lung perfusion:result sofanovel perfusions trategy.Ann Thorac,2003,76(2):516-521.
    [3]Asimakopoulos G,Smith PL,Ratnatunga CP,et al.Lung injury and acute respiratory distress syndrome after cardiopulmonary bypass.Ann Thorac Surg,1999,68(3):1107-1115.
    [4]Massoudy P,Zahler S,Becker BF,et al.Evidence for inflammatory responses of the lungs during coronary artery bypass grafting with cardiopulmonary bypass.Chest,2001,119(1):31-36.
    [5]Sievers H,Freand K,Eleftheriadis S,et al.Lung protection during total cardiopulmonarybypass byisolated lung perfusion:result sofanovel perfusions trategy.Ann Thorac,2003,76(2):516-521.
    [6]Paparella D,Yau TM,Young E.Cardiopulmonary bypass induced inflammation:pathophysiology and treatment.An update.Eur J Cardiothorac Surg,2002;21(2):232-244
    [7]Murphy PG,Myers DS,Davies MJ,Webster NR,Jones JG.The antioxidant potential of propofol(2,6-diisopropylphenol).Br J Anaesth.1992 Jun 68(6):613-618.
    [8]Przyklenk K,Bauer B,Ovize M,Kloner RA,Whittaker P.Regional ischemic 'preconditioning' protects remote virgin myocardium from subsequentsustained coronary occlusion.Circulation 1993 87:893-899.
    [9]张洪民,李钦传,王永武,等.体外循环对内毒素影响的实验研究.同济大学学报(医学版),2001,22(4):8-10.
    [10]Bouter H.Sehippers E F,Luelmo S A,et al.No effect of preoperative Selective gutdecontamination on endotoxemia and cytokine activation during cardiopulmonary bypass:a randomized,placebo-controlled study Crit Care Med,2002,30(1):38-43。
    [11]Brandt LJ,Boley SJ.Technical review on intestinal ischemia.Gastroenterology,2000,118(5):954-968。
    [12]Welbourn CRB,Young Y.Endotoxin septic shock and acute lung injury:neutrophilsmaerophages and inflammatory mediators.Br J Surg,1992;79:998-1003.
    [13]Tsuji C,Minhaz MU,Shioya S,et al.The importance of polymorpho nuclear leukocytes in lipopolysaccharide induced superoxide anion reduction and lung injury.Lung,1998,176:1-13
    [14]Kodavanti UP,Hauser R,Christiani DC,et al.Pulmonary responses to oil fly ash particles in the rat differ by virtue of their specific soluble metals.Toxicological Science,1998,43(2):204-212.
    [15]Liu H,Zhang D,Zhao B,et al.Superoxide anion,the main species of ROS in the development of ARDS induced by oleic acid.Free Radic Res,2004,38(12):1281-1287.
    [16]Christofidou-Solomidou M,Muzykantov VR.Antioxidant strategies in respiratory medicine.Treat Respir Med,2006,5(1):47-78.
    [17]Mitaka C,Hiram Y,Nagura T,et al.Circulating endothelin-1 concentrations in acute respiratory failure.Chest,1993,104:476-478.
    [18]赵振伟,曲友直,高国栋,等.甘露醇与尼莫地平联合应用对大鼠脑缺血再灌注损伤保护机制的研究.临床神经病学杂志,2005,18(3):204-205.
    [19]Wolfrum S,Nienstedt J,Heidbreder M,et al.Calcitonin gene related peptide mediates cardioproteetion by remote preconditioning.Regulatory Peptides.2005,127(1-3):217-224.
    [20]Weinbrenner C,Schulze F,Strasser RH,et al.Remote preconditioning by infrarenal aortic occlusion is operative via δ1-opioid receptors and free radicals in vivo in the rat heart.Cardiovascular Research,2004,61(3):591-599.
    [21]Li GH,Labruto F,Chen F,et al.Myocardial protection by remote preconditioning:the role of nuclear factor kappa-Bp105 and inducible nitric oxide synthase. European Journal of Cardio-Thoracic Surgery. 2004,26 (5):968-973.
    [22] Brzozowski T, Konturek PC, Konturek SJ, et al. Ischemic preconditioning of remote organs attenuates gastric ischemia-reperfusion injury through involvement of prostaglandins and sensory nerves. European Journal of Pharmacology. 2004,499(1-2):201 -213..
    [23] Konstantinov IE, Arab S, Li J, et al. The remote Ischemic preconditioning stimulus modifies gene expression in mouse myocardium. J Thorac Cardiovasc Surg, 2005, 130(5): 1326-1332.
    [24] Jones SP, Girod WG, Palazzo AJ, et al. Myocardial ischemia reperfusion injury is exacerbated in absence of endothelial cell nitric oxide synthase. Am J Physiol, 1999, 276(5Pt2): 1567—1573.
    [25] Vuokko LK, James DC. Superoxide Dismutases in the Lung and Human Lung Diseases. Am J Respir Crit Care Med, 2003, 167: 1600—1619.
    [26] Serrano AG, P6rez. Gil J. Protein—lipid interactions and sur—face activity in the pulmonary surfactant system. Chem Phys Lipids, 2006, 141: 105 —118.
    [27] Kuroki Y, Takahashi H, Chiba H , et al. Surfactant proteinsA and D: disease markers. Biochim Biophys Acta, 1998, 1408: 334-345.
    [28] Jobe AH, lkegami M. Biology of surfactant. Clin Perinatal, 2001,28:655-669
    [29] Poynter SE, LeNine AM. Surfaetant biology and clinical aplication. Crit Care Clin, 2003, 19: 459-472.
    [30] Diniz EM . The importance of surfactant on the de—velopment of neonatal pulmonary, diseases. Clinics, 2007, 62: 181—190.
    [31] Crouch E, Hartshorn K, Ofek I. Collectins and pulmonary innate immunity Immunol Rev, 2000, 173 (1) :52 65.
    [32] Ferguson JS, Martin JL, Azad AK, et al. Surfactant protein D in creases fusion of mycobaeterlum tuberculosis-containing phagosomes with lysosomes in human macro-phages. Infect Immun, 2006, 74(12): 7005-7009.
    [33] Wright JR, Youmans DC. Degradation of surfactant lipids and surfactant protein A by alveolar macrophages in vitro.Am J Physiol,1995,268(5 pt 1):L772-L780.
    [34]Bates SR,Fisher AB.Surfactant protein A is degraded by alveolar macrophages.Am J Physiol,1996,271(2 pt 1):L258-L266.
    [35]Goss CH,Brower RG,Hudson LD,et al.Incidence of acute lung injury in the United States.Crit Care Meal,2003;31(6):1607-1611.
    [36]Gunhter A,Ruppert C,Schmidt R,et al.Surfactant alteration and replacement in acute respiratory distress syndrome.Respir Ras,2001,2:353-364.
    [1]Paparella D,Yau TM,Young E.Cardiopulmonary bypass induced inflammation:pathophysiology and treatment.An update.Eur J Cardiothorac Surg,2002;21(2):232-244
    [2]Ng CS,Wan S,Yim AP,Arifi AA.Pulmonary dysfunction after cardiac surgery.Chest,2002;121(4):1269-1277.
    [3]Asimakopoulos G,Smith PL,Ratnatunga CP,Taylor KM Lung injury and acute respiratory distress syndrome after cardiopulmonary bypass Ann Thorac Surg.1999 Sep;68(3):1107-1115
    [4]Murphy PG,Myers DS,Davies MJ,Webster NR,Jones JG.The antioxidant potential of propofol(2,6-diisopropylphenol).Br J Anaesth 1992Jun;68(6):613-618.
    [5]王婷,蒋豪,薛张纲等.异氟醚对大鼠肺缺血再灌注损伤的保护作用.中华麻醉学杂志,2006;26(2):140-143.
    [6]Hano O,Silverman HS,Blank PS,Mellits ED,Baumgardner R,Lakatta EG,Stern MD Nieardipine prevents calcium loading and "oxygen paradox" in anoxie single rat myocytes by a mechanism independent of calcium channel blockade.Circ Res,1991,69(6):1500-1505.
    [7]张宇辉,党爱民,吴海英等.钙通道阻断剂的血管内皮保护作用.中国新药杂志,1999.8:81-83.
    [8]Eren S,Esme H,Balci AE,Cakir O,Buyukbayram H,Eren MN,Erdinc L,Satici O.The effect of aprotinin on ischemia-reperfusion injury in an in situ normothermic ischemic lung model.Eur J Cardiothorac Surg.2003Jan;23(1):60-65.
    [9]Nakanishi K,Takeda S,Sakamoto A,Kitamura A.Effects of ulinastatin treatment on the cardiopulmonary bypass-induced hemodynamic instability and pulmonary dysfunction.Crit Care Med,2006.34(5):1351-1357.
    [10]Deblier I,Sadowska AM,Janssens A,et al.Markers of inflammation and oxidative stress in patients undergoing CABG with CPB with and without ventilation of the lungs:a pilot study.Interact Cardiovasc Thorac Surg,2006,5(4):387-391.
    [11]Sugita T,Watarida S,Katsuyama K,Nakajima Y,Yamamoto R,Mori A.Effect of a human urinary protease inhibitor(Ulinastatin)on respiratory function in pediatric patients undergoing cardiopulmonary bypass.J Cardiovasc Surg(Torino),2002,43(4):437-440.
    [12]魏磊,刘标等 乌司他丁在体外循环中肺保护机制的研究中国 体外循环杂志 2009 7(1) 452-456
    [13]Schroeder VA,Pearl JM,Schwartz SM,Shanley TP,Manning PB,Nelson DP.Combined steroid treatment for congenital heart surgery improves oxygen delivery and reduces postbypaas inflammatory mediator expression.Circulation,2003,107(22):2823-2828。
    [14]de Mendonea-Filho HY,Gomes RV,de Almeida Campos LA,et al.Circulating levels of macrophage migration inhibitory factor are associated with mild pulmonary dysfunction after cardiopulmonary bypass.Shock,2004,22(6):533-537.
    [15]Sundrani R,Easington CR,Mattoo A,Parrillo JE,Hollenberg SM.Nitric oxide synthase inhibition increases venular leukocyte rolling and adllesion in septic rats.Crit Care Med 2000,28(8):2898-2903.
    [16]程卫平,张海涛.吴安石.一氧化氯对人体离体中性粒细胞CD2b表达的影响.中华麻醉学杂志.1998,18:601-603.
    [17]Kawahara F,Kadoi Y.The effects of prostaglandin E1 on systemic and cerebral oxygenation before and during cardiopulmonary bypass.Masui,2002,51(2):128-133
    [18]邵永丰,梁永年,陈广明等.联合应用常规及改良超滤对儿童体外循环围手术期细胞黏附分子及细胞因子的影响 南京医科大学学报,2006,26(11):1095-1099
    [19]Sievers HH,Freund-Kaas C,Eleflheriadis S,Fischer T,Kuppe H,Kraatz EG,Bechtel JF.Lung protection during total cardiopulmonary bypass by isolated lung perfusion: preliminary results of a novel perfusion strategy. Ann Thorac Surg, 2002, 74(4): 1167-1172.
    [20] Suzuki T, Ito T, kashima I, Teruya K,Fukuda T. Continuous perfusion of pulmonary arteries during total cardiopulmonary bypass affects favorably affects levels of circulating adhesion molecules and lung function. J Thorac Cardiovasc Surg, 2001, 122(2): 242-248
    [21] Fredholm BB. Purines and neutrophil leukocytes. Gen Pharmacol, 1997, 28(3): 345-350.
    [22] Murphree LJ, Sullivan GW, Marshall MA, Linden J. Lipopolysaccharide rapidly modifies adenosine receptor transcripts in murine and human macrophages: role of NF-kappaB in A(2A)adenosine receptor induclion Biochem J, 2005, 391(Pt 3): 575-580.
    [23] Yang D, Zhang Y, Hao G, et al. The A_(2b) adensoine receptor protects against inflamnmation and excessive vascular adhesion. J Clin Invest, 2006, 116(7): 1913—1923.
    [24] Nemeth ZH, Lutz CS, Csoka B, et al. Adenosine augments IL-10 production by macrophages through an A_(2b) receptor-mediated posttranscriptional mechanism. J Immtunol, 2005, 175(12): 8260-8270.
    [25] J Sipka S, Kovacs I, Szanto S, et al. Adenosine inhibits the release of interleukin-1 beta in activated human periplheral mononuclear cells. Cytokine, 2005, 31(4): 258-263.
    [26] Ezeamuzie CI, Philips E. Adenosine A3 receptors on human eosinophils mediate inhibition of degranulation and superoxide anion release. Br J Pharmacol, 1999, 127(1): 188-194.
    [27] Bouma MG, Stad RK, Van den Wildenberg FA. Differential regulatory effects of adenosine on cytokine release by activated human monocytes. J Immunol, 1994, 153(9): 4159-4168.
    [28] Le Vraux V, Chen YL, Masson I, De Sousa M, Giroud JP, Florentin I, Chauvelot-Moachon L. Inhibition of human monocyte TNF production by adenosine receptor agonists.Life Sci,1993,52(24):1917-1924:
    [29]Rivo J,Zeira E,Galun E,Matot I.Activation of A3 adenosine receptor provides lung protection against ischemia-reperfusion injury associated with reduction in apoptosis.Am J Transplant,2004,4(12):1941-1948.
    [30]Freyholdt T,Massoudy P,Zahler S,Henze R,Barankay A,Becker BF,Meisner H.Beneficial effect of sodium nitroprusside after coronary artery bypass surgery:Pump function correlates inversely with cardiac release of proinflammatory cytokines.J Cardiovasc Pharmacol,2003,42(3):372-378.
    [31]Friedman M,Wang WY,Sellke FW,et al.Neutrophil adhesion blockade with NPC15669 decreases pulmonary injure after total cardiopulmonary bypass.Thorac Cardiovasc Surg,1996,111(2):460-468.
    [32]Gillinov AM,Devaleria PA,Stein WJ,et al.complement inhibition with soluble complement receptor tyPe-1 in cardiopulmonary bypass.Ann Thorac Surg,1993,55:619-624.
    [33]郭建极,何巍,罗玉忠等1,6一二磷酸果糖对体外循环肺保护的临床实验研究 广西医科大学学报,2005,22(4):501-503.
    [34]蒋幼凡,周向东,李敏超 甘露醇对急性肺损伤兔外周血循环内皮细胞、IL-8表达的影响 中国现代医学杂志 2006 16(22):3374-3376.
    [35]Chew MS,Brandslund 1,Brix-Christensen V,Ravn HB,Hjrotdal VE,Pedersen J,Hjortdal K,Hansen OK.Tissue injury and the inflammatory response to pediatric cardiac surgery with cardiopulmonary bypass:a descriptive study.Anesthesiology,2001,94(5):745-753
    [36]Smit JJJ,de Vries AJ,Gu YJ,et al.Filtration of activated granulocytes during cardiopulmonary bypass surgery:a morphologic and immunologic study to characterize the trapped leukocytes.J Lab Clin Med,2000,135:238-245.
    [37]Olivencia-Yuivati AH,Ferrara CA,Tierney N,Wallace N,Mallet RT.Strategic leukocyte depletion reduces pulmonary microvascular pressure and improves pulmonary status post cardiopulmonary bypass.Perfusion,2003,18(Suppl 1):23-31.
    [38]Huang H,Yao T,Wang W,Zhu D,Zhang W,Chen H,Fu W.Combination of balanced ultrafiltration with modified ultrafiltration attenuates pulmonary injury in patients undergoing open heart surgery.Chin Med J(Engl),2003,116(10):1504-1507
    [39]Darling E,Searles B,Nasrallah F,Robins M,You X,Gatto L,Clay N,Picone A,Steinberg J,Nieman G.High-volume,zero balanced ultrafiltration improves pulmonary function in a model of post-pump syndrome.J Extra Corpor Technol,2002,34(4):254-259.
    [40]王风婷,罗峰.膜式氧合器中膜材料的研究进展 中国组织工程研究与临床康复,2008,12(10):1927-1930.
    [41]曲振华 李国艳 赵砚丽等两种氧合器对心肺转流炎症反应的影响 中华麻醉学杂志 2006,22(9):649-651。
    [42]Monk TG,Goodnough LT,Birkmeyer JD.Acute noemovilemic hemodilution is a cost-effective alternative to preoperative autologous blood donation by patient undergoing radical retropublic prostatectomy Transfusion,1995,34:559-565.
    [43]舒义竹,向道康,阎兴治等 血液光量子疗法对体外循环急性肺损伤的保护作用 贵州医药 2005 29(1):19-21
    [44]Claxton BA,Morgan P,Mckeague H,et al.Alveolar recruitment strategy improves arterial oxygenation after cardiopulmonary bypass Anaesthesia,2003,58(2):111-116.
    [45]Leonard RC.Liquid ventilation.Anaesth Int Care 1998;26(1):11-21.
    [46]Cheifetz IM,Cannon ML,Craig DM,Quick G,Kern FH,Smith PK,Ungerleider RM,Meliones JN.Liquid ventilation improves pulmonary function and cardiac output in a neonatal swine model of cardiopulmonary bypass.J Thorac Cardiovasc Surg,1998;115(3):528-535
    [47]Zobel G,Rodl S.Urlesberger B,Knez I,Dacar D.Partial liquid ventilation combined with two different gas ventilatory strategies in acute lung injury in piglets:Effects on gas exchange respiratory mechanics and hemodynamics.J Pediatr Surg.2003 38(4):527-533
    [48]Schlensak C,Doenst T,Preusser S,Wunderlich M,Kleinschmidt M,Beyersdorf F.Cardiopulmonary bypass reduction of bronchial blood flow:a potential mechanism for lung injury in a neonatal pig model J Thorac Cardiovasc Surg,2002,123(6):1199-1205.
    [49]De Santo LS,Romano G,Amarelli C,Onorati F,Torella M,Renzulli A,Galdieri N,Cotrufo M.Surgical repair of acute type A aortic dissection:continuous pulmonary perfusion during retrograde cerebral perfusion prevents lung injury in a pilot study.J Thorac Cardiovasc Surg,2003,126(3):826-831.
    [50]Suzuki T,Ito T,kashima I,Teruya K,Fukuda T.Continuous perfusion of pulmonary arteries during total cardiopulmonary bypass affects favorably affects levels of circulating adhesion molecules and lung function J Thorac Cardiovasc Surg,2001,122(2):242-248
    [51]刘立明,胡建国,尹邦良等 中南大学学报医学版 体外循环中含氧血持续肺动脉灌注的肺保护作用 2005,30(4):413-416
    [52]Murry CE,Jennings RB,Reimer KA,Preconditioning with ischemia:a delay of lethal cell injury in ischemic myocardium.Circulaiton,1986,74(5):1124-1136.
    [53]Przyklenk K,Bauer B,Ovize M,Kloner RA,Whittaker P.Regional ischemic 'preconditioning' protects remote virgin myocardium from subsequentsustained coronary occlusion.Circulation 1993;87:893-899
    [54]张春芳,陈胜喜,罗万俊.缺血预处理对猪肺隔离药物灌注肺损伤的保护作用.中华实验外科杂志,2004,21:1253-1254.
    [55]李国虎,陈胜喜,罗万俊,等.体外循环心脏直视手术中心脏缺血 预处理对肺的保护作用.湖南医科大学学报,1998,23(1):41-43

© 2004-2018 中国地质图书馆版权所有 京ICP备05064691号 京公网安备11010802017129号

地址:北京市海淀区学院路29号 邮编:100083

电话:办公室:(+86 10)66554848;文献借阅、咨询服务、科技查新:66554700