title: Different effects of propranolol, phenylephrine, and saline volume loading on catecholamine-induced left ventricular outflow tract obstruction in acute coronary syndrome.
abstract: Hemodynamic deterioration due to left ventricular outflow tract (LVOT) obstruction can occur during catecholamine infusion in patients with acute coronary syndrome (ACS). The purpose of the present study was to compare the utility of propranolol, phenylephrine infusion, and rapid saline loading for reversal of dobutamine-induced LVOT obstruction in a canine model of ACS. ACS was induced via left anterior descending artery ligation in 21 open-chest anesthetized dogs, and LVOT obstruction, defined as an LVOT gradient > 30 mmHg, was induced by dobutamine infusion (20 to 40 microg/kg/min). Subsequently, the effects of propranolol infusion (0.7 to 1.0 microg/kg/min, n = 8), phenylephrine infusion (10 to 200 microg/kg/min, n = 7), and saline loading (200 to 400 mL/hr, n = 6) were assessed by serial hemodynamic measurements. All interventions produced significant and comparable improvements in the LVOT pressure gradient (propranolol: 60 +/- 16 to 15 +/- 12; phenylephrine: 68 +/- 15 to 12 +/- 10; saline loading: 58 +/- 18 to 22 +/- 10 mmHg; P < 0.001 for baseline versus postintervention; P = NS for comparison between interventions). Phenylephrine produced the greatest elevation in aortic pressure (propranolol: +15 +/- 13; phenylephrine: +51 +/- 36; saline loading: +15 +/- 15 mmHg; P < 0.05), while saline loading produced the greatest increase in cardiac output (propranolol: +0.05 +/- 0.12; phenylephrine: +0.28 +/- 0.37; saline loading: +0.73 +/- 0.48 L/min; P < 0.05). Propranolol was the only intervention that produced a significant decrease in diastolic pulmonary artery pressure (16 +/- 5 to 11 +/- 3 mmHg, P < 0.05). Propranolol, phenylephrine infusion, and saline volume loading were similarly effective in reversing dobutamine-induced LVOT obstruction in this canine model of ACS. However, each intervention produced different hemodynamic effects with potentially different clinical indications.
authors.affiliation: First Department of Internal Medicine, Kagoshima University School of Medicine, Japan.
authors.forename: Ichiro
authors.initials: I
authors.lastname: Ohba
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Otsuji
authors.forename: Kensaburo
authors.initials: K
authors.lastname: Shiki
authors.forename: Shuichi
authors.initials: S
authors.lastname: Hamasaki
authors.forename: Shinichi
authors.initials: S
authors.lastname: Minagoe
authors.forename: Chuwa
authors.initials: C
authors.lastname: Tei
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000494:pharmacology*; D000789:Angina, Unstable / Q000150:complications; D000818:Animals; D003324:Coronary Artery Disease / Q000150:complications*; D004280:Dobutamine; D004285:Dogs; D006439:Hemodynamics / Q000187:drug effects*; D010656:Phenylephrine / Q000494:pharmacology*; D011433:Propranolol / Q000494:pharmacology*; D012965:Sodium Chloride / Q000494:pharmacology*; D014694:Ventricular Outflow Obstruction / Q000139:chemically induced / Q000503:physiopathology*
chemical_list: D000319:Adrenergic beta-Antagonists; D010656:Phenylephrine; D004280:Dobutamine; D012965:Sodium Chloride; D011433:Propranolol