DIMINISHED BASAL NITRIC-OXIDE RELEASE AFTER MYOCARDIAL-ISCHEMIA AND REPERFUSION PROMOTES NEUTROPHIL ADHERENCE TO CORONARY ENDOTHELIUM

被引:501
作者
MA, XL
WEYRICH, AS
LEFER, DJ
LEFER, AM
机构
[1] THOMAS JEFFERSON UNIV,JEFFERSON MED COLL,DEPT PHYSIOL,1020 LOCUST ST,PHILADELPHIA,PA 19107
[2] JOHNS HOPKINS UNIV,SCH MED,DIV CARDIOL,BALTIMORE,MD 21205
关键词
N(G)-NITRO L-ARGININE METHYL ESTER; ISOLATED CORONARY ARTERY RINGS; L-ARGININE; POLYMORPHONUCLEAR LEUKOCYTES; ENDOTHELIUM-DERIVED RELAXING FACTOR;
D O I
10.1161/01.RES.72.2.403
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
We measured changes in basal release of nitric oxide and its effect on polymorphonuclear leukocyte (PMN) adherence to endothelial cells (ECs) in a feline model of myocardial ischemia (90 minutes) and reperfusion. Basal release of nitric oxide from the left anterior descending coronary artery (LAD) after myocardial ischemia/reperfusion and from the control left circumflex coronary artery (LCX) was assessed by N(G)-nitro L-arginine methyl ester (L-NAME)-induced vasocontraction. L-NAME induced a significant EC-dependent vasocontraction in control LCX rings (0.28+/-0.04 g), which was fully reversed by L-arginine but not D-arginine. L-NAME-induced vasocontraction of LAD rings was not significantly changed after 90 minutes of myocardial ischemia without reperfusion. However, 10 minutes of reperfusion reduced the L-NAME-induced vasocontraction to 0.13+/-0.04 g (p<0.05), and this was restored by addition of 3 mM L-arginine but not D-arginine. Longer periods of reperfusion progressively decreased L-NAME-induced vasocontraction. After 270 minutes of reperfusion, L-NAME-induced vasocontraction was virtually abolished. Myocardial ischemia without reperfusion did not increase PMN adherence to ECs. However, PMN adherence to LAD ECs was significantly increased after 20 minutes of reperfusion (39+/-6 to 105+/-9 PMNs/mm2, p<0.01), and incubation of LAD segments with L-arginine significantly attenuated this increase in PMN adherence. After 270 minutes of reperfusion, PMN adherence to LAD ECs was further increased to 224+/-10 PMNS/mm2 (p<0.001). This increase in PMN adherence was almost completely blocked by MAb R15.7, a monoclonal antibody against CD18 of PMNs, and was significantly attenuated by MAb RR1/1, a monoclonal antibody against intercellular adhesion molecule-1 of ECs (p<0.01). These results indicate that decreased basal release of endothelium-derived relaxing factor after myocardial ischemia/reperfusion precedes enhanced PMN adherence to the coronary endothelium, which may lead to PMN-induced myocardial injury.
引用
收藏
页码:403 / 412
页数:10
相关论文
共 40 条
[1]  
[Anonymous], MECH VASODILATATION
[2]  
BATH PMW, 1992, J VASC RES, V29, P81
[3]   INFLAMMATION IN THE COURSE OF EARLY MYOCARDIAL-ISCHEMIA [J].
ENTMAN, ML ;
MICHAEL, L ;
ROSSEN, RD ;
DREYER, WJ ;
ANDERSON, DC ;
TAYLOR, AA ;
SMITH, CW .
FASEB JOURNAL, 1991, 5 (11) :2529-2537
[4]   THE METABOLISM OF L-ARGININE AND ITS SIGNIFICANCE FOR THE BIOSYNTHESIS OF ENDOTHELIUM-DERIVED RELAXING FACTOR - CULTURED ENDOTHELIAL-CELLS RECYCLE L-CITRULLINE TO L-ARGININE [J].
HECKER, M ;
SESSA, WC ;
HARRIS, HJ ;
ANGGARD, EE ;
VANE, JR .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1990, 87 (21) :8612-8616
[5]  
JONES LF, 1992, J PHARMACOL EXP THER, V260, P627
[6]   NITRIC-OXIDE - AN ENDOGENOUS MODULATOR OF LEUKOCYTE ADHESION [J].
KUBES, P ;
SUZUKI, M ;
GRANGER, DN .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1991, 88 (11) :4651-4655
[7]   NITRIC-OXIDE MODULATES MICROVASCULAR PERMEABILITY [J].
KUBES, P ;
GRANGER, DN .
AMERICAN JOURNAL OF PHYSIOLOGY, 1992, 262 (02) :H611-H615
[8]   DEMONSTRATION OF DEPRESSED POLYMORPHONUCLEAR LEUKOCYTE FUNCTION IN NONVIREMIC FELV-INFECTED CATS [J].
LAFRADO, LJ ;
OLSEN, RG .
CANCER INVESTIGATION, 1986, 4 (04) :297-300
[9]   NEUTROPHIL-DERIVED RELAXING FACTOR RELAXES VASCULAR SMOOTH-MUSCLE THROUGH A CGMP-MEDIATED MECHANISM [J].
LEE, DKH ;
FAUNCE, D ;
HENRY, D ;
STURM, RJ ;
RIMELE, T .
LIFE SCIENCES, 1990, 46 (21) :1531-1538
[10]   ROLE OF ENDOTHELIAL DYSFUNCTION IN THE PATHOGENESIS OF REPERFUSION INJURY AFTER MYOCARDIAL-ISCHEMIA [J].
LEFER, AM ;
TSAO, PS ;
LEFER, DJ ;
MA, XL .
FASEB JOURNAL, 1991, 5 (07) :2029-2034