Dobutamine increases myocardial contractility without inducing marked tachycardia or greatly changing peripheral arterial resistance, making it useful for treating acute cardiac failure.
Dobutamine is introduced as a synthetic intravenously administered catecholamine that increases myocardial contractility without marked tachycardia, useful for treating acute cardiac failure.
Dobutamine* is a new, synthetic, intravenously administered catecholamine that acts directly to increase myocardial contractility without inducing marked tachycardia or greatly changing peripheral arterial resistance.1 These features make it useful for treating acute cardiac failure characterized by low cardiac output and elevated diastolic filling pressures, and in July, 1978, it was approved for clinical use in this country.Norepinephrine is the endogenous catecholamine that is synthesized and stored in granules in adrenergic nerve endings in the myocardium. When sympathetic nerves to the heart are activated, norepinephrine is released from its stores and stimulates specific sites on the myocardial cell surface, . . .
Koch‐Weser et al. (1979) conducted a review in acute cardiac failure. Dobutamine was evaluated. Dobutamine increases myocardial contractility without inducing marked tachycardia or greatly changing peripheral arterial resistance, making it useful for treating acute cardiac failure.