Townend J N, Virk S J, Qiang F X, Lawson N, Bain R J, Davies M K
Department of Cardiovascular Medicine, University of Birmingham, Queen Elizabeth Hospital, Edgbaston, U.K.
Eur Heart J. 1993 Feb;14(2):243-50. doi: 10.1093/eurheartj/14.2.243.
To determine the effect of ACE inhibitor therapy on lymphocyte beta-adrenoceptor function and density, as well as the in vivo myocardial response to beta-agonist stimulation, we studied 12 patients with chronic severe heart failure before and after 16 weeks' treatment with quinapril. Lymphocyte beta-adrenoceptor function (intracellular cAMP production in response to isoprenaline) was studied as a surrogate tissue for myocardium, and increased significantly after quinapril at concentrations of isoprenaline between 10(-3) and 50 mmol.l-1. Lymphocyte beta-adrenoceptor density (six patients) measured by [125I] iodocyanopindolol binding, increased from 242 +/- 72 (mean +/- SEM) to 884 +/- 17 receptors/cell (P < 0.05). Changes in functional myocardial beta-adrenoceptor status were determined by measuring changes in haemodynamic responses to exercise and to incremental dobutamine infusion. Following quinapril there were significant improvements in cardiac index, stroke volume and cardiac power output during sub-maximal exercise testing and dobutamine infusion; stroke work index in response to dobutamine (but not exercise) improved significantly. ACE inhibitors cause lymphocyte beta-adrenoceptor upregulation in heart failure, which is associated with an improved cardiac pumping capacity in response to beta-agonist stimulation.
为了确定血管紧张素转换酶（ACE）抑制剂治疗对淋巴细胞β-肾上腺素能受体功能和密度的影响，以及体内心肌对β-激动剂刺激的反应，我们对12例慢性重度心力衰竭患者在使用喹那普利治疗16周前后进行了研究。淋巴细胞β-肾上腺素能受体功能（对异丙肾上腺素的细胞内环磷酸腺苷生成）作为心肌的替代组织进行研究，在喹那普利治疗后，当异丙肾上腺素浓度在10⁻³至50 mmol·L⁻¹之间时，其功能显著增强。通过[¹²⁵I]碘氰吲哚洛尔结合法测定的淋巴细胞β-肾上腺素能受体密度（6例患者）从242±72（平均值±标准误）增加到884±17个受体/细胞（P<0.05）。通过测量运动和递增多巴酚丁胺输注时血流动力学反应的变化来确定功能性心肌β-肾上腺素能受体状态的变化。使用喹那普利后，在次最大运动试验和多巴酚丁胺输注期间，心脏指数、每搏量和心脏功率输出有显著改善；对多巴酚丁胺（而非运动）的每搏功指数显著改善。ACE抑制剂可导致心力衰竭患者淋巴细胞β-肾上腺素能受体上调，这与β-激动剂刺激后心脏泵血能力的改善有关。
