(Circulation. 2000;102:III-296.)
© 2000 American Heart Association, Inc.
Myocardial Protection and Vascular Biology |
Difference in Endothelium-Derived Hyperpolarizing Factor–Mediated Hyperpolarization and Nitric Oxide Release Between Human Internal Mammary Artery and Saphenous Vein
From the Cardiovascular Research Laboratory, Grantham Hospital, University of Hong Kong, Hong Kong, China (Z.-G.L., Z-D.G., G-W.H.); Cardiovascular Research, Starr Academic Center for Cardiac Surgery, St Vincent Hospital, Portland, Ore (G.-W.H.); and Xiamen University Medical College, China (G.-W.H.).
Correspondence to Professor Guo-Wei He, MD, PhD, Chair of Cardiothoracic Surgery, University of Hong Kong, Grantham Hospital, 125 Wong Chuk Hang Road, Aberdeen, Hong Kong. E-mail gwhe{at}hkucc.hku.hk
Background—The greater nitric oxide (NO) release that occurs in the internal mammary artery (IMA) when compared with the saphenous vein (SV) has been suggested by more endothelium-dependent relaxation in the IMA or measured by bioassay; however, no direct measurement of NO- or endothelium-derived hyperpolarizing factor (EDHF)–mediated hyperpolarization has been reported. The present study measured such hyperpolarization, as well as NO release, in these vessels.
Methods and Results—IMA (n=46) and SV (n=61) segments taken from patients undergoing coronary surgery were studied in the organ chamber. Hyperpolarization (by intracellular glass microelectrode) and NO release (by NO-sensitive electrode) in response to acetylcholine and bradykinin, with and without incubation with NG-nitro-L-arginine, indomethacin, and oxyhemoglobin, were measured. The resting membrane potential of the smooth muscle cells from the IMA (58±0.8 mV; n=15) was higher than that in those from the SV (-62±0.9 mV; n=23; P=0.0001). The EDHF-mediated hyperpolarization induced by acetylcholine (10-5 mol/L: -9.4±1.5 mV in IMA, n=10, versus -4.5±1.0 mV in SV, n=17; P<0.01) and bradykinin (10-7 mol/L: -10.9±1.5 mV in IMA, n=8, versus -5.1±0.5 mV in SV, n=8; P<0.01) and the basal release of NO (16.8±1.6 nmol/L in IMA, n=13, versus 9.9±2.8 nmol/L in SV, n=13; P<0.001) were significantly greater in the IMA than in the SV. The duration of acetylcholine- and bradykinin-induced NO release was longer in the IMA than in the SV.
Conclusions—The basal release of NO and EDHF-mediated hyperpolarization were significantly greater in the IMA than in the SV. In addition, the duration of the stimulated release of NO was longer in the IMA than in the SV. These differences may contribute to the superior long-term patency of IMA grafts.
Key Words: endothelium-derived factors • nitric oxide • arteries • veins • electrophysiology
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