Acute dopamine infusion increases renal plasma flow, urinary sodium excretion rate, glomerular filtration rate, and the functional status of patients with moderate to severe congestive heart failure. These effects result from stimulation of dopamine receptors (DA! and DA2) as well as f3 adrenergic receptors. Beregovich and co-workers  studied the dose-related hemodynamic and renal effects of dopamine in patients with classes III and IV congestive heart failure (see Fig. 5). Cardiac output and urinary sodium excretion rates rose progressively as dopamine infusion was increased from 1 to 5 and 10 /¿g/kg/min. Stroke volume and urinary flow rate, however, tended to plateau above 5 /xg/ kg/min and several patients developed sinus tachycardia or striking increases in systemic vascular resistance at the highest infused dose. These workers concluded that a dose of 5 /¿g/kg/min was optimal in terms of overall hemodynamic response in patients with congestive heart failure. While the effects of dopamine infusion on renal sodium excretion and cardiac hemodynamics are often dramatic, the natriuretic effects typically wane after 12-24 hr [3, 31].
Dopmamine, /^kg/minute Dopamine, fig/kg/minute
FIGURE 5. Effects of dopamine on cardiac output (O), systemic vascular resistance (SVR, •), urinary sodium excretion (■), and urine flow rate (□) in patients with congestive heart failure. Data from Beregovich, et al. Am. Heart J. 87:550-557,1974.
Dobutamine is a dopamine derivative with different hemodynamic effects. Dobutamine is a potent inotrope that does not cause significant mesenteric vasodilation or vasoconstriction even at high doses and has little effect on mean arterial pressure. Because dobutamine does not cause the vasoconstriction that increases cardiac work and limits the maximal dopamine dose in patients with congestive heart failure, it has become the most frequently employed inotrope in such patients. Both dopamine and dobutamine have been reported to improve cardiac output, renal perfusion, and, in some situations, urinary Na excretion. To investigate the role of specific dopamine receptors on the renal responses to dopamine in congestive heart failure, Hilberman et al.  compared the effects of dopamine and dobutamine in 12 patients who had undergone open heart surgery and developed depressed left ventricular performance postoperatively. The drugs were administered in random order in doses that increased cardiac output equally (dopamine, 5.0 ± 1.8 /¿g/kg/min; dobutamine, 3.5 ±1.8 ¿ig/kg/min). At these doses, the drugs had similar effects on renal plasma flow, renal vascular resistance, and glomerular filtration rate but, compared with dobutamine, dopamine increased urinary flow rate by 2.8-fold and Na excretion by 4.6-fold. The differences in renal effects of the drugs could not be attributed to differences in renal blood flow, although changes in intra-renal blood flow distribution could not be excluded. The authors suggested that the greater ability of dopamine to increase renal sodium and water excretion resulted from its actions to inhibit renal NaCl reabsorption at the level of the renal tubule. Other studies showed that dopamine increased urinary Na and water excretion during treatment with dobutamine in patients with congestive heart failure  and during treatment with norepinephrine  or dobutamine , in critically ill hypotensive patients. These studies strongly suggest that dopamine has unique natriuretic properties, even when added to effective doses of inotropes and vasopressors , although in a study of 6 patients with chronic stable congestive heart failure, dopamine was not more effective than dobutamine (or placebo) in increasing urine volume . The studies provide a rationale for combining low dose (2-5ju.g/kg/min) dopamine with dobutamine or vasopressors in critically ill patients.
A recent study provides cautionary data concerning the ability of dopamine to increase urinary Na and water excretion in patients with congestive heart failure. Vargo et al.  asked whether low dose dopamine would increase Na and water excretion when added to maximally effective doses of a loop diuretic in patients with congestive heart failure. They reasoned that this question was more relevant to the clinical situation in which dopamine is added to a regimen that already includes a diuretic. Most previous studies had examined the use of dopamine in patients who were either off diuretics or were on their typical regimen of oral diuretics. In this randomized cross-over study, dopamine (1 to 3 yu.g/kg/min) did not increase urinary solute and water excretion when added
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FUROSEMIDE EXCRETION RATE (ftg/min)
FIGURE 6. Comparison of furosemide excretion rate vs sodium excretion rate with and without low dose dopamine infusion in patients with stable congestive heart failure. Note that the two lines nearly superimpose. With permission from ,
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FUROSEMIDE EXCRETION RATE (ftg/min)
FIGURE 6. Comparison of furosemide excretion rate vs sodium excretion rate with and without low dose dopamine infusion in patients with stable congestive heart failure. Note that the two lines nearly superimpose. With permission from , to a maximally effective dose of furosemide (see Fig. 6). Although this study does not provide evidence supporting the use of low dose dopamine in patients with congestive heart failure, the patients studied were stable patients who did respond to furosemide alone. Whether dopamine might elicit diuresis in patients who become refractory to furosemide alone was not addressed.
Dopamine augments renal blood flow in normal individuals. This observation suggests that dopamine might be useful for preventing or treating acute renal failure. The results of trials to investigate the role of dopamine in preventing and treating acute renal failure have been reviewed recently. In general, trials of dopamine to prevent or treat acute renal failure have utilized low or "renal" doses of dopamine, doses below the inotropic range. Denton et al.  reviewed 10 clinical trials of dopamine to prevent the development of acute renal failure in high risk patients. Four studies found no effect of dopamine in preventing acute tubular necrosis following renal transplantation, and three studies found no effect of dopamine in preventing acute renal failure following cardiac or abdominal surgery. One retrospective study of patients undergoing liver trans
DOPAMINE FOR PREVENTION AND TREATMENT OF ACUTE RENAL FAILURE
plantation found evidence that dopamine reduced their incidence of acute renal failure , whereas a larger prospective study did not . Two small studies have reported that prophylactic dopamine infusion reduces the incidence of acute renal failure following intravenous radiocontrast agents [17,18], whereas another found no effect . Taken together, these results do not provide strong support for the use of dopamine to prevent acute renal failure in high risk patients, although a small effect would be difficult to exclude because the incidence of acute renal failure in these studies has generally been low .
Dopamine has also been recommended to enhance renal perfusion, increase urinary NaCl excretion, and enhance recovery from established acute renal failure. In 1970, Talley et al. reported that dopamine (4 ¿ig/kg/min) improved urine output in a small group of patients with postoperative acute renal failure. In subsequent reports [15, 28] dopamine was reported to cause diuresis and natriuresis, and in some cases an improvement in glomerular filtration rate, when administered to patients with acute renal failure undergoing treatment with loop diuretics. These reports, however, involved small numbers of patients and did not include a control group, making interpretation difficult. In one prospective controlled trial of dopamine plus furosemide in malaria induced acute renal failure , the combination was more effective than furosemide alone in reversing acute renal failure when started relatively early in the course, but the number of patients in this study was also small, weakening the conclusions. Other convincing studies supporting a role for dopamine in enhancing recovery from acute tubular necrosis in humans are still lacking.
Some additional data support a possible effect of low doses of dopamine in increasing urinary solute and water output in critically ill patients with mild to moderate renal dysfunction. In two uncontrolled studies of critically ill patients, dopamine (1.5-2.5 ¿tg/kg/min) increased urine output by 42-50% in patients with baseline urinary outputs <0.5-1 ml/kg/hr [10, 39]. In a controlled cross-over study of critically ill patients comparing dopamine (200 fig/ min) vs dobutamine (175 ¿ug/tnin) vs placebo, dopamine increased urine output significantly without affecting creatinine clearance, whereas dobutamine increased creatinine clearance significantly without affecting urine output . Taken together, these data suggest that dopamine may increase urinary Na and water excretion in some patients with mild to moderate renal dysfunction.
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