Ischemic preconditioning attenuates postischemic coronary artery endothelial dysfunction in a model of minimally invasive direct coronary artery bypass grafting
Vh. Thourani et al., Ischemic preconditioning attenuates postischemic coronary artery endothelial dysfunction in a model of minimally invasive direct coronary artery bypass grafting, J THOR SURG, 117(2), 1999, pp. 383-389
Citations number
28
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Objective: Unmodified reperfusion without cardioplegia in minimally invasiv
e direct coronary artery bypass grafting procedures causes endothelial dysf
unction that may predispose to polymorphonuclear neutrophil-mediated myocar
dial injury. This study tested the hypothesis that ischemic preconditioning
in a minimally invasive direct coronary artery bypass grafting model atten
uates postischemic endothelial dysfunction in coronary vessels. Methods: In
anesthetized dogs, the left anterior descending coronary artery was occlud
ed for 30 minutes and reperfused for 3 hours without ischemic preconditioni
ng (no-ischemic preconditioning; n = 7); in 7 dogs, the left anterior desce
nding occlusion was preceded by 5 minutes occlusion followed by 5 minutes o
f reperfusion, Relaxation responses to stimulators of nitric oxide synthase
were used to evaluate endothelial function in arteries from the ischemic-r
eperfused (left anterior descending) and nonischemic (left circumflex coron
ary artery) zones, Results: Stimulated endothelial-dependent relaxation of
epicardial left anterior descending artery to incremental concentrations of
acetylcholine in the no-ischemic preconditioning animals was shifted to th
e right, and maximal relaxation was attenuated compared with the nonischemi
c left circumflex coronary artery (117% +/- 4% vs 138% +/- 5%), In contrast
, acetylcholine-induced maximal relaxation was comparable in the left anter
ior descending artery versus left circumflex coronary artery in the ischemi
c preconditioning group (130% +/- 6% vs 135% +/- 5%), In 150- to 200-mu m l
eft anterior descending microvessels, 50% relaxation occurred with a lower
concentration (log[M]) of acetylcholine in ischemic preconditioning versus
no-ischemic preconditioning (-8.0 +/- 0.4 vs -7.0 +/- 0.1) with no group di
fferences in smooth muscle relaxation to sodium nitroprusside, suggesting e
ndothelial-specific damage. Adherence of fluorescent labeled polymorphonucl
ear neutrophils to epicardial coronary artery endothelium, used as an index
of basal (unstimulated) anti-polymorphonuclear neutrophil function, was si
gnificantly attenuated by ischemic preconditioning versus no-ischemic preco
nditioning (293 +/- 25 polymorphonuclear neutrophils/mm(2) vs 528 +/- 29 po
lymorphonuclear neutrophils/mm(2)). Conclusion: In this minimally invasive
direct coronary artery bypass grafting model, both agonist-stimulated and b
asal postischemic endothelial dysfunction were attenuated by ischemic preco
nditioning.