Dopamine hemodynamic effects

Dopamine produces dose-dependent hemodynamic effects because of its relative affinity for cq-, /Jr, /J2-, and Dr (vascular dopaminergic) receptors. Positive inotropic effects mediated primarily by / -receptors become more prominent with doses of 2 to 5 mcg/kg/min. At doses between 5 to 10 mcg/kg/min, chronotropic and -mediated vasoconstricting effects become more prominent. Especially at higher doses, dopamine alters several parameters that increase myocardial oxygen demand and potentially decrease myocardial blood flow, worsening ischemia in some patients with coronary artery disease. 

Introduction of chlorine or bromine into the 3- and/or 4- positions of the side chain yields more potent compounds in terms of hypotension in rats and dopamine p- hydroxylase inhibition (31. 32). The analog YP-279 (XXXV) is also hypotensive in rats but is said not to affect brain norepinephrine biosynthesis unlike fusaric acid or dibromofusaric acid (33-35). Fusaric acid amide (bupicomide, Sch 10595, XXXVI) is clinically effective at 300 to 1800 mg per day and is said to have hemodynamic effects similar to hydralazine (36. 37). The amide is... 

Seri I, Abbasi S, Wood DC, Gerdes JS. Regional hemodynamic effects of dopamine in the sick preterm neonate. J Pediatr 1998 133 728-34. 

Dobutamine, a synthetic catecholamine, is a - and 82-receptor agonist with some a -agonist effects (see Table 14—14). Unhke dopamine, dobutamine does not cause release of NE from nerve terminals. The overall hemodynamic effects of dobutamine are the result of its effects on adrenergic receptors and reflex-mediated actions. Its P2-receptor-mediated effects are greater than those of dopamine, and /82-receptor-mediated vasodilation will tend to offset some of the -receptor-mediated vasoconstriction. Thus the uet vascular effect is usually vasodilation. The positive inotropy is primarily a P -receptor-mediated effect. Cardiac -receptor stimulation by dobutamine causes an increase in contractility but generally no significant change in heart rate and may provide an explanation for the apparently more modest chronotropic actions of dobutamine compared with dopamine. 

Dopamine often is recommended as the initial catecholamine in sepsis because it increases blood pressure by increasing myocardial contractility and vasoconstriction. Dopamine has been described to have dose-related receptor activity at DAj-, DA2-, fi -, and i-receptors. Unfortunately, this dose-response relationship has not been confirmed in critically ill patients. In patients with septic shock, there is a great overlap of hemodynamic effects even at doses as low as 3 mcg/kg per minute. Tachydysrhythmias are common owing to the release of endogenous norepinephrine by dopamine entering the sympathetic nerve terminal. Dopamine may increase the PAOP through pulmonary vasoconstriction. This drug also may depress ventilation and worsen hypoxemia in patients dependent on the hypoxic ventilatory drive. 

Stein E, Pankiewicz J, Harsch HH, Cho JK, Fuller SA, Hoffmann RG, Hawkins M, Rao S, Bandettini PA, Bloom AS (1998) Nicotine-induced limbic cortical activation in the human brain a functional MRI smdy. Am J Psychiatry 155 1009-1015 Sziraki I, Lipovac MN, Hashim A, Sershen H, Allen D, Cooper T, Czobor P, Lajtha A (2001) Differences in nicotine-induced dopamine release and nicotine pharmacokinetics between Lewis and Fischer 344 rats, Neurochem Res 26 609-617 Terborg C, Birkner T, Schack B, Witte OW (2002) Acute effects of cigarette smoking on cerebral oxygenation and hemodynamics a combined study with near-infrared spectroscopy and transcranial Doppler sonography, J Neurol Sci 205 71-75 Thompson JC, WUby G, Stough C (2002) The effects of transdermal nicotine on inspection time. Hum Psychopharmacol 17 157-161... 

The clinical utility of dopamine as a vasopressor in the setting of septic shock is limited because large doses frequently are necessary to maintain cardiac output and blood pressure. At doses exceeding 20 mcg/kg per minute, there is limited further improvement in cardiac performance and regional hemodynamics. Its clinical use frequently is hampered by tachycardia and tachydysrhythmias, which may lead to myocardial ischemia. Although tachydysrhythmias theoretically should not be expected to occur until 5 to 10 mcg/kg per minute of dopamine, these fii effects are observed with doses as low as 3 mcg/kg per minute. They seem to be more prevalent in patients... 

Day NP, Phu NH, Mai NT, et al. Effects of dopamine and epinephrine infusions on renal hemodynamics in severe malaria and severe sepsis. Crit Care Med 2000 28 1353-1362. 

Hoogenberg K, Smit AJ, and Girbes AR. Effects of low-dose dopamine on renal and systemic hemodynamics during incremental norepinephrine infusion in healthy volunteers. Crit Care Med 1998 26 260-265. 

Dopamine hydrochloride is a vasopressor that stimulates beta receptors in the heart, causing more complete and forceful contractions (inotropy). It also acts on alpha receptors (dose-dependent) and has dopaminergic effects. Dopamine hydrochloride is indicated in the correction of hemodynamic imbalances present in shock syndrome after MI, trauma, endotoxic septicemia, surgery, and renal failure or imbalances in conditions of chronic refractory cardiac decompensation (e.g., CHF). 

Dopexamine (Dopacard) is a synthetic analog related to dopamine with intrinsic activity at dopamine Dj and D2 receptors as well as at P2 receptors it may have other effects such as inhibition of catecholamine uptake. It appears to have favorable hemodynamic actions in patients with severe CHF, sepsis, and shock. In patients with low cardiac output, dopexamine infusion significantly increases stroke volume with a decrease in systemic vascnlar resistance Tachycardia and hypotension can occnr, bnt nsnally only at high infusion rates. 

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