Differential inhibition by hyperglycaemia of shear stress- but not acetylcholine-mediated dilatation in the iliac artery of the anaesthetized pig

被引:26
作者
Kelly, R. [1 ]
Ruane-O'Hora, T.
Noble, M. I. M.
Drake-Holland, A. J.
Snow, H. M.
机构
[1] Natl Univ Ireland Univ Coll Cork, Biol Serv Unit, Cork, Ireland
[2] Natl Univ Ireland Univ Coll Cork, Dept Physiol, Cork, Ireland
[3] Univ Aberdeen, Dept Med & Therapeut, Aberdeen, Scotland
[4] Robert Gordon Univ, Sch Pharm, Aberdeen AB9 1FR, Scotland
来源
JOURNAL OF PHYSIOLOGY-LONDON | 2006年 / 573卷 / 01期
关键词
D O I
10.1113/jphysiol.2006.106500
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Clinical hyperglycaemia affects vascular endothelial function, but the effect on shear stress-induced arterial dilatation has not yet been established. We hypothesized that hyperglycaemia would inhibit this response via impaired glycocalyx mechanotransduction. Experiments were carried out in the anaesthetized pig in which pressure, blood flow and diameter of the left iliac artery were measured at two sites: proximal (d1) and distal (d2). Infusion of glucose, sufficient to raise blood glucose to 16-30 mm along the whole length of the artery, attenuated the shear stress-dependent dilatation in both sections of the artery with preservation of the responses to acetylcholine. The distal site was then isolated using snares and the lumen exposed to blood containing 25-35 mm glucose for 20 min. In the control situation, after exposure of both sections to normoglycaemia (5.7 mm glucose), both sections of artery showed increases in diameter in response to shear stress and acetylcholine. Hyperglycaemia attenuated the shear stress-dependent dilatation in the distal section only (P < 0.25), but not the response to acetylcholine. It is concluded from these results that the hyperglycaemia-impaired dilatation is consistent with loss of mechanotransducing properties of the endothelial glycocalyx by hyperglycaemia. These findings offer a possible explanation for the increased incidence of vascular disease in diabetic patients.
引用
收藏
页码:133 / 145
页数:13
相关论文
共 52 条
[1]   Insulin causes endothelial dysfunction in humans - Sites and mechanisms [J].
Arcaro, G ;
Cretti, A ;
Balzano, S ;
Lechi, A ;
Muggeo, M ;
Bonora, E ;
Bonadonna, RC .
CIRCULATION, 2002, 105 (05) :576-582
[2]  
ARISAKA T, 1995, ANN NY ACAD SCI, V748, P543
[3]   HEMODYNAMIC ACTIONS OF INSULIN [J].
BARON, AD .
AMERICAN JOURNAL OF PHYSIOLOGY, 1994, 267 (02) :E187-E202
[4]   Mechanisms for early microvascular injury in obesity and type II diabetes [J].
Bohlen, HG .
CURRENT HYPERTENSION REPORTS, 2004, 6 (01) :60-65
[5]   Acute hyperglycemia does not affect the reactivity of coronary microcirculation in humans [J].
Capaldo, B ;
Galderisi, M ;
Turco, AA ;
D'Errico, A ;
Turco, S ;
Rivellese, AA ;
de Simone, G ;
de Divitiis, O ;
Riccardi, G .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2005, 90 (07) :3871-3876
[6]   Insulin stimulates both endothelin and nitric oxide activity in the human forearm [J].
Cardillo, C ;
Nambi, SS ;
Kilcoyne, CM ;
Choucair, WK ;
Katz, A ;
Quon, MJ ;
Panza, JA .
CIRCULATION, 1999, 100 (08) :820-825
[7]   Vasodilator response to systemic but not to local hyperinsulinemia in the human forearm [J].
Cardillo, C ;
Kilcoyne, CM ;
Nambi, SS ;
Cannon, RO ;
Quon, MJ ;
Panza, JA .
HYPERTENSION, 1998, 32 (04) :740-745
[8]  
Chien S, 2003, PROG BIOPHYS MOL BIO, V83, P131, DOI [10.1016/S0079-6107(03)00053-1, 10.1016/s0079-6107(03)00053-1]
[9]   Endothelial cell glycocalyx modulates immobilization of leukocytes at the endothelial surface [J].
Constantinescu, AA ;
Vink, H ;
Spaan, JAE .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2003, 23 (09) :1541-1547
[10]  
CONSTANTINESCU AA, 2002, THESIS ACAD MED CTR