NEUTROPHILS AS MEDIATORS OF HUMAN SKELETAL-MUSCLE ISCHEMIA-REPERFUSION SYNDROME

被引:51
作者
FORMIGLI, L
LOMBARDO, LD
ADEMBRI, C
BRUNELLESCHI, S
FERRARI, E
NOVELLI, GP
机构
[1] UNIV FLORENCE, DEPT HUMAN ANAT & HISTOL, HISTOL SECT, I-50121 FLORENCE, ITALY
[2] UNIV FLORENCE, INST ANAESTHESIOL & INTENS CARE, I-50121 FLORENCE, ITALY
[3] UNIV FLORENCE, DEPT PRECLIN & CLIN PHARMACOL, I-50121 FLORENCE, ITALY
[4] UNIV FLORENCE, CHAIR VASC SURG, I-50121 FLORENCE, ITALY
关键词
SKELETAL MUSCLE; ISCHEMIA-REPERFUSION; GRANULOCYTES;
D O I
10.1016/0046-8177(92)90317-V
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
Nine patients with aortic aneurysm undergoing arterial reconstruction with temporary aortic occlusion were studied. Since a typical condition of ischemia-reperfusion of the muscles of the lower limbs was created during this surgery, muscle biopsies from the right femoral quadriceps as well as blood samples from the homolateral saphenous vein were taken: (1) before clamping of the aorta, (2) just before declamping, and (3) 30 minutes after reperfusion. Light microscopy revealed a consistent granulocyte infiltration in the ischemic and reperfused skeletal muscle. Ultrastructural damage to the muscle fibers was seen during ischemia and became more severe upon reperfusion. The recruitment of granulocytes into the muscle tissue paralleled the activation of the blood complement system and an increase in circulating neutrophils. Although a spontaneous superoxide anion (O2) generation from such granulocytes cannot be proved, upon stimulation with formyl-methionyl-leucylphenylalanine neutrophils showed a reduced ability in O2 free radical production at the end of ischemia and enhanced O2 generation at reperfusion as compared with the controls. All these findings indicate an active role of granulocytes in the genesis of reperfusion-induced tissue injuries. © 1992.
引用
收藏
页码:627 / 634
页数:8
相关论文
共 42 条
  • [1] METABOLIC CHANGES IN BLOOD AND SKELETAL-MUSCLE IN RECONSTRUCTIVE AORTIC-SURGERY
    ANDERSSON, J
    EKLOF, B
    NEGLEN, P
    THOMSON, D
    [J]. ANNALS OF SURGERY, 1979, 189 (03) : 283 - 289
  • [2] BELLAVITE P, 1983, EUR J CLIN INVEST, V13, P363
  • [3] THE SUPEROXIDE-FORMING ENZYMATIC SYSTEM OF PHAGOCYTES
    BELLAVITE, P
    [J]. FREE RADICAL BIOLOGY AND MEDICINE, 1988, 4 (04) : 225 - 261
  • [4] BULKLEY G B, 1987, British Journal of Cancer, V55, P66
  • [5] NEUTROPHIL-MEDIATED MICROVASCULAR DYSFUNCTION IN POSTISCHEMIC CANINE SKELETAL-MUSCLE - ROLE OF GRANULOCYTE-ADHERENCE
    CARDEN, DL
    SMITH, JK
    KORTHUIS, RJ
    [J]. CIRCULATION RESEARCH, 1990, 66 (05) : 1436 - 1444
  • [6] CAVAROCCHI NC, 1986, CIRCULATION, V74, P130
  • [7] COMPLEMENT ACTIVATION DURING CARDIOPULMONARY BYPASS - EVIDENCE FOR GENERATION OF C3A AND C5A ANAPHYLATOXINS
    CHENOWETH, DE
    COOPER, SW
    HUGLI, TE
    STEWART, RW
    BLACKSTONE, EH
    KIRKLIN, JW
    [J]. NEW ENGLAND JOURNAL OF MEDICINE, 1981, 304 (09) : 497 - 503
  • [8] FREE-RADICALS IN ISCHEMIC AND REPERFUSION MYOCARDIAL INJURY - IS THIS THE TIME FOR CLINICAL-TRIALS
    COHEN, MV
    [J]. ANNALS OF INTERNAL MEDICINE, 1989, 111 (11) : 918 - 931
  • [9] COMPLEMENT AND NEUTROPHIL ACTIVATION IN THE PATHOGENESIS OF ISCHEMIC MYOCARDIAL INJURY
    CRAWFORD, MH
    GROVER, FL
    KOLB, WP
    MCMAHAN, CA
    OROURKE, RA
    MCMANUS, LM
    PINCKARD, RN
    [J]. CIRCULATION, 1988, 78 (06) : 1449 - 1458
  • [10] DELMAESTRO RF, 1980, ACTA PHYSIOL SCAND, P43