Inotropic, vascular and neuroendocrine effects of dopexamine hydrochloride and comparison with dobutamine

Abstract

Dopexamine hydrochloride is a novel beta 2- and dopaminergic-receptor agonist proposed for intravenous therapy in patients with congestive heart failure. To gain a clearer knowledge of its efficacy relative to other agents, intravenous infusions of dopexamine hydrochloride (4 micrograms/kg/min) and dobutamine (10 micrograms/kg/min) were administered to 10 patients with congestive heart failure (ejection fraction less than 0.4). Both agents increased stroke volume and cardiac indexes to a similar degree, and both decreased systemic vascular resistance, with a trend toward a greater decrease with dopexamine hydrochloride. Although dobutamine had no significant effect on left ventricular systolic pressure, dopexamine hydrochloride caused a decrease from 121 +/- 8 to 110 +/- 7 mm Hg (p less than 0.01). Both dobutamine and dopexamine hydrochloride increased peak rate of left ventricular pressure development (dP/dt), and there was a trend to a greater increase with dobutamine (control 1,043 +/- 102 mm Hg/s; dobutamine 1,340 +/- 142 mm Hg/s; dopexamine hydrochloride 1,213 +/- 120 mm Hg/s, p = 0.067 vs dobutamine). Plasma norepinephrine levels increased only with dopexamine hydrochloride (+49%, p less than 0.05). Plasma renin activity increased with both agents (dobutamine +38%, p less than 0.06; dopexamine hydrochloride +41%, p less than 0.05). Dobutamine and dopexamine hydrochloride, therefore, improve cardiac function by way of both vasodilator and inotropic mechanisms. At the doses administered, dopexamine hydrochloride relies on a greater systemic vasodilator effect than dobutamine to achieve and increase in left ventricular performance. Increased levels of endogenous catecholamines may contribute to the increased inotropic state with dopexamine hydrochloride.