Stack R K, Patterson R E
Department of Medicine (Cardiology), Emory University School of Medicine Carlyle Fraser Heart Center, Crawford Long Hospital of Emory University, Atlanta, Georgia 30365.
Cardiovasc Res. 1991 Sep;25(9):757-63. doi: 10.1093/cvr/25.9.757.
Neuropeptide Y is a peptide isolated from brain and neural tissue around human coronary arteries. It has been shown to produce coronary vasoconstriction and myocardial ischaemia. The purposes of this study were (a) to determine whether the vasoconstriction induced by neuropeptide Y was mediated by alpha adrenergic receptors in vivo, and (b) to determine the time course of the effect and whether it was reproducible with a second administration.
Neuropeptide Y (200 micrograms over 2 min) was given by intracoronary injection on two occasions 1 h apart to group I dogs (control). In group II the second dose was preceded by treatment with the alpha blocker phenoxybenzamine (4-10 mg.kg-1). The time course and magnitude of the effect was studied in the two groups to determine the effects of alpha blockade and of repeated neuropeptide Y dosage.
14 mongrel dogs (n = 7 per group) were anaesthetised with chloralose for a left thoracotomy to measure coronary blood flow, aortic pressure, left ventricular pressure, and heart rate.
Reproducible prolonged increases in coronary vascular resistance occurred after the first [33(SD 18)%] and second [34(17)%] doses of neuropeptide Y. At this infusion rate mean aortic pressure increased with each dose by 21% and coronary blood flow decreased by 7%. In group II dogs, phenoxybenzamine given intravenously 20 min after the first dose of neuropeptide Y reduced mean aortic pressure by 15-20 mm Hg. In this group neuropeptide Y also caused reproducible increases in coronary vascular resistance before (36%) and after (46%) alpha blockade.
Neuropeptide Y constricts coronary arteries in vivo by mechanisms that do not require intact alpha adrenergic receptors, and the coronary vasoconstriction was prolonged and reproducible.
神经肽Y是从人脑及冠状动脉周围神经组织中分离出的一种肽。研究表明它可引起冠状动脉收缩和心肌缺血。本研究的目的是：（a）确定神经肽Y诱导的血管收缩在体内是否由α肾上腺素能受体介导；（b）确定该效应的时间过程以及再次给药时是否可重现。
给I组犬（对照组）冠状动脉内注射神经肽Y（2分钟内注射200微克），两次注射间隔1小时。II组在第二次给药前先用α受体阻滞剂酚苄明（4 - 10毫克/千克）治疗。研究两组效应的时间过程和强度，以确定α受体阻断及神经肽Y重复给药的影响。
14只杂种犬（每组7只）用氯醛糖麻醉后行左胸切开术，以测量冠状动脉血流量、主动脉压、左心室压和心率。
首次[33（标准差18）%]和第二次[34（17）%]注射神经肽Y后，冠状动脉血管阻力出现可重现的持续增加。在此输注速率下，平均主动脉压每次给药升高21%，冠状动脉血流量降低7%。在II组犬中，首次注射神经肽Y后20分钟静脉注射酚苄明使平均主动脉压降低15 - 20毫米汞柱。在该组中，神经肽Y在α受体阻断前（36%）和阻断后（46%）均引起冠状动脉血管阻力可重现的增加。
神经肽Y在体内通过不依赖完整α肾上腺素能受体的机制使冠状动脉收缩，且冠状动脉血管收缩是持续且可重现的。
