Amrinone: Is it the inotrope of choice?

Global myocardial function is compromised in infants with pulmonary hypertension

“…This recognition has pertinent therapeutic implications. Milrinone, a selective phosphodiesterase three inhibitor, causes relaxation of vascular smooth muscle, enhances myocardial contractility (inotropy effect) and improves myocardial relaxation (lusitropic effect) (10–12). There are recent pharmacokinetic and clinical neonatal data demonstrating its usefulness in improving oxygenation in term neonates with PPHN when used in conjunction with iNO or in PPHN refractory to iNO therapy (13,14).…”

Use of milrinone in the management of haemodynamic instability following duct ligation

“…PDE inhibitors affect myocardial function in multiple ways: (1) increased inotropy as a result of cyclic adenosine monophosphatemediated increase in trans-sarcolemmal calcium influx [21], (2) peripheral vasodilatation secondary to removal of free intracellular calcium by causing its uptake by sarcoplasmic reticulum [4], and (3) myocyte relaxation (lusitropy) possibly due to improved actin-myosin complex dissociation [23]. These non-glycoside non-catecholamine agents improve myocardial performance without raising myocardial oxygen consumption [11].…”

Effects of Amrinone on Thrombin-Induced Platelet-Derived Growth Factor-Like Protein Secretion from Endothelial Cells

“…Although catecholamines have previously been shown to inhibit thrombin-induced PDGF-like protein secretion from EC, long-term use causes tachyphylaxis with decreased number of P-receptors, uncoupling of the receptors from adenylate cyclase, and accelerated cAMP degradation (27). Because of these disadvantages, a medication such as amrinone may have potential for long-term PDGF-like protein inhibition.…”