Human aortocoronary grafts and nitric oxide release: Relationship to pulsatile pressure

被引:31
作者
Bilfinger, TV [1 ]
Stefano, GB [1 ]
机构
[1] SUNY Stony Brook, Hlth Sci Ctr, Dept Surg, Div Cardiothorac Surg, Stony Brook, NY 11794 USA
关键词
D O I
10.1016/S0003-4975(99)01083-8
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background. Short and long-term failure of saphenous Vein grafts continues to be a significant problem for cardiac surgeons. The purpose of this study was to elucidate the early adaptive changes of human artery and vein conduits with respect to nitric oxide (NO) production under various pressure and pulsatile distention conditions. Methods. Real-time amperometric NO determinations were made in an in vitro model using human saphenous vein segments (n = 12) and internal thoracic artery segments (n = 8) between 70 and 170 mm Hg, under static conditions recorded with a pressure transducer. Exposing the tissue to morphine (10(-6) M) also stimulated NO release. Under conditions in which the conduits were exposed to the respective pressures for 1 hour, they were then examined for their granulocyte-adhering potential using computer-assisted imaging techniques. Results. A pressure-dependent decrease of NO release was found after 32 minutes of pulsatile pressure (170 mm Hg) in artery and vein, the latter of which appeared to be affected more negatively (p < 0.05; because many more observation points differed significantly after 32 minutes compared to 110 mm Hg values). In vessels maintained for 1 hour at these different pressures and then exposed to morphine (1 mu M), stimulated NO release significantly diminished in the veins (artery 37.4 nM NO versus vein 18.1 nM NO; p < 0.05). Increased pressures also correlated with an increase in granulocyte adhesion to veins that could not be reduced following morphine exposure. Conclusions. Increased pressure and cyclic distention lead to loss of NO release and increased immunocyte adhesion, which are significantly more pronounced in saphenous vein than in internal thoracic artery, suggesting that in the long term this may contribute to the failure of saphenous vein conduits in coronary revascularization. (C) 2000 by The Society of Thoracic Surgeons.
引用
收藏
页码:480 / 485
页数:6
相关论文
共 26 条
[1]   Cryopreserved veins in myocardial revascularization: Possible mechanism for their increased failure [J].
Bilfinger, TV ;
Hartman, AR ;
Liu, Y ;
Magazine, HI ;
Stefano, GB .
ANNALS OF THORACIC SURGERY, 1997, 63 (04) :1063-1069
[2]  
CALVER A, 1992, J HYPERTENS, V10, P1025
[3]  
CAMPEAU L, 1983, CIRCULATION, V68, P1
[4]   Flow-induced release of endothelium-derived relaxing factor during pulsatile bypass: Experimental study in the fetal lamb [J].
Champsaur, G ;
Vedrinne, C ;
Martinot, S ;
Tronc, F ;
Robin, J ;
Ninet, J ;
Franck, M .
JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY, 1997, 114 (05) :738-744
[5]   Nitric oxide modulation of neutrophil-endothelium interaction: Difference between arterial and venous coronary bypass grafts [J].
Chello, M ;
Mastroroberto, P ;
Perticone, F ;
Celi, V ;
Colonna, A .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 1998, 31 (04) :823-826
[6]   LONG-TERM HUMAN VEIN GRAFT CONTRACTILITY AND MORPHOLOGY - A FUNCTIONAL AND HISTOPATHOLOGICAL STUDY OF RETRIEVED CORONARY VEIN GRAFTS [J].
CROSS, KS ;
DAVIES, MG ;
ELSANADIKI, MN ;
MURRAY, JJ ;
MIKAT, EM ;
HAGEN, PO .
BRITISH JOURNAL OF SURGERY, 1994, 81 (05) :699-705
[7]   CONSTITUTIVE NITRIC-OXIDE SYNTHASE IS EXPRESSED AND NITRIC OXIDE-MEDIATED RELAXATION IS PRESERVED IN RETRIEVED HUMAN AORTOCORONARY VEIN GRAFTS [J].
DAVIES, MG ;
BERKOWITZ, DE ;
HAGEN, PO .
JOURNAL OF SURGICAL RESEARCH, 1995, 58 (06) :732-738
[8]  
GOTTLIEB AI, 1991, LAB INVEST, V65, P123
[9]   ENDOTHELIUM-DEPENDENT RESPONSES IN LONG-TERM HUMAN CORONARY-ARTERY BYPASS GRAFTS [J].
KU, DD ;
CAULFIELD, JB ;
KIRKLIN, JK .
CIRCULATION, 1991, 83 (02) :402-411
[10]   Endogenous but not exogenous nitric oxide decreases TNF-alpha-induced leukocyte rolling [J].
Kubes, P ;
Sihota, E ;
Hickey, MJ .
AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY, 1997, 273 (03) :G628-G635