Davies M G, Kim J H, Barber L, Dalen H, Svendsen E, Hagen P O
Department of Surgery, Duke University Medical Center, Durham, North Carolina 27710.
J Surg Res. 1994 Jul;57(1):106-21. doi: 10.1006/jsre.1994.1118.
Hypertension and hypercholesterolemia are known risk factors for the development of atherosclerosis and are considered to influence the development of vein graft intimal hyperplasia. This study examines the effect of hypertension (two-kidney, one-clip model for 8 weeks) and hypercholesterolemia (1% cholesterol diet for 8 weeks) individually and in combination on the formation of intimal hyperplasia and the vasomotor function of vein grafts. Forty New Zealand White rabbits underwent a carotid vein bypass graft. Ten were controls, 10 were hypertensive, 10 were hypercholesterolemic, and 10 had both hypertension and hypercholesterolemia. Hypertension and/or hypercholesterolemia were present for 4 weeks prior to and for 4 weeks after surgery. All vein grafts were harvested at 4 weeks postoperatively for histology (n = 6) or contractility studies (n = 4). Compared to controls, hypercholesterolemia increased intimal but not medial thicknesses of the vein grafts and enhanced smooth muscle cell contractility. Hypertension did not increase vein graft intimal or medial thicknesses but did augment vein graft contractility compared to controls. Hypertension with hypercholesterolemia increased intimal and medial thicknesses and enhanced vasoreactivity in vein grafts. The results show that hypertension influences the vasoreactivity but not the development of intimal hyperplasia in vein grafts. When hypertension is combined with hypercholesterolemia, there is both an increase in the medial thickness and an attenuation of vasomotor function compared to hypercholesterolemia alone, although there is no further increase in intimal hyperplasia formation. Therefore, this study suggests that the combination of both atherogenic risk factors does not act synergistically in promoting either the formation of intimal hyperplasia or vasomotor dysfunction in vein grafts.
高血压和高胆固醇血症是动脉粥样硬化发展的已知危险因素，被认为会影响静脉移植物内膜增生的发展。本研究分别及联合研究高血压（双肾一夹模型，持续8周）和高胆固醇血症（1%胆固醇饮食，持续8周）对静脉移植物内膜增生形成和血管舒缩功能的影响。40只新西兰白兔接受了颈动脉静脉搭桥手术。10只为对照组，10只为高血压组，10只为高胆固醇血症组，10只为高血压合并高胆固醇血症组。高血压和/或高胆固醇血症在手术前4周和手术后4周存在。所有静脉移植物在术后4周采集用于组织学检查（n = 6）或收缩性研究（n = 4）。与对照组相比，高胆固醇血症增加了静脉移植物的内膜厚度但未增加中膜厚度，并增强了平滑肌细胞收缩性。高血压未增加静脉移植物的内膜或中膜厚度，但与对照组相比增强了静脉移植物的收缩性。高血压合并高胆固醇血症增加了静脉移植物的内膜和中膜厚度，并增强了血管反应性。结果表明，高血压影响静脉移植物的血管反应性，但不影响内膜增生的发展。当高血压与高胆固醇血症合并时，与单独的高胆固醇血症相比，中膜厚度增加且血管舒缩功能减弱，尽管内膜增生形成没有进一步增加。因此，本研究表明，这两种动脉粥样硬化危险因素的组合在促进静脉移植物内膜增生形成或血管舒缩功能障碍方面没有协同作用。
