Gaide M S, Wiggins J R, Fitterman W S, Cameron J S, Myerburg R J, Bassett A L
J Cardiovasc Pharmacol. 1984 Mar-Apr;6(2):238-43. doi: 10.1097/00005344-198403000-00005.
The positive inotropic action of phenylephrine in cardiac muscle is mediated by alpha- and beta-adrenoceptors. Data suggest the responsiveness of myocardium to inotropic agents is altered in cardiac disease. We evaluated the actions of phenylephrine on isometric contraction and K+-induced contracture in isolated cat right ventricular muscle from normal hearts and hearts with partial pulmonary artery ligation-induced pressure overload of 5-11 days in duration. Peak contractile force (Po) and rate of force development (dP/dt) were lower (p less than or equal to 0.005) in pressure-overloaded (0.59 +/- 0.2 g/mm2 and 4.6 +/- 1.7 g/s/mm2, respectively) than in normal (1.33 +/- 0.2 g/mm2 and 10.5 +/- 1.6 g/s/mm2, respectively) muscle. Phenylephrine (10(-6), 5 X 10(-6), and 10(-5) M) significantly (p less than or equal to 0.01) increased Po and dP/dt in normal but not in pressure-overloaded muscle. Phenylephrine (5 X 10(-6) M) reduced peak K+-induced contracture force (Pc) similarly in normal (-30 +/- 8%) and pressure-overloaded (-36 +/- 11%) muscles. beta-Adrenergic blockade (nadolol, 10(-4) M) reduced, but did not abolish, the "relaxant" action of the drug on Pc in both muscle groups. The lack of a positive inotropic effect of phenylephrine in pressure-overloaded muscle suggests a derangement in both alpha- and beta-adrenoceptor function in this model of cardiac disease.
去氧肾上腺素对心肌的正性肌力作用是由α和β肾上腺素能受体介导的。数据表明，在心脏疾病中，心肌对正性肌力药物的反应性会发生改变。我们评估了去氧肾上腺素对正常心脏以及部分肺动脉结扎诱导的持续5 - 11天压力超负荷心脏的离体猫右心室肌肉等长收缩和钾离子诱导的挛缩的作用。压力超负荷肌肉（分别为0.59±0.2 g/mm²和4.6±1.7 g/s/mm²）的峰值收缩力（Po）和力发展速率（dP/dt）低于正常肌肉（分别为1.33±0.2 g/mm²和10.5±1.6 g/s/mm²）（p≤0.005）。去氧肾上腺素（10⁻⁶、5×10⁻⁶和10⁻⁵ M）能显著（p≤0.01）增加正常肌肉的Po和dP/dt，但对压力超负荷肌肉无此作用。去氧肾上腺素（5×10⁻⁶ M）在正常肌肉（-30±8%）和压力超负荷肌肉（-36±11%）中对钾离子诱导的挛缩峰值力（Pc）的降低作用相似。β肾上腺素能阻断剂（纳多洛尔，10⁻⁴ M）可降低但未消除该药物对两组肌肉Pc的“松弛”作用。去氧肾上腺素在压力超负荷肌肉中缺乏正性肌力作用，表明在这种心脏疾病模型中，α和β肾上腺素能受体功能均发生紊乱。
