Abstract
Although a large number of studies have been performed regarding the renal and hemodynamic effects of the infusion of low-dose dopamine (LDD) in severely ill patients, there is still controversy on this subject. To evaluate the effects of dopamine (2 microg/kg/min) on systemic hemodynamics (lowest mean arterial pressure, MAP, highest heart rate, HR, central venous pressure, CVP), creatinine clearance (CLcr), diuresis and fractional sodium excretion (FENa+). A non-randomized, open, prospective clinical trial. An intensive care unit in a tertiary university hospital. 22 patients with hemodynamic stability admitted to the intensive care unit. Patients were submitted to three two-hour periods: without dopamine (P1), with dopamine (P2) and without dopamine (P3). The above mentioned variables were measured during each period. CLcr was assessed based upon the formula U x V/P, where U is urinary creatinine (mg/dl), V is diuresis in ml/min and P is serum creatinine (mg/dl). FENa+ was calculated based upon the formula: urinary sodium (mEq/l) x P/plasma sodium (mEq/l) x U) x 100. Results were presented as mean and standard deviation. The Student t test was used and results were considered significant if p was less than 0.05. Twelve patients (seven males and five females) were included, with a mean age of 55.45 years. There was no significant variation in MAP, HR, CVP, CLcr or FENa+ with a dopamine dose of 2 microg/kg/min. On the other hand, diuresis significantly increased during P2, from 225.4 to 333.9 ml. Infusion of 2 microg/kg/min of dopamine for 2 hours increases diuresis. At the doses studied, dopamine does not induce significant alterations in MAP, HR, CVP, CLcr and FENa+.
Highlights
Dopamine is an endogenous catecholamine, and is the immediate metabolite of norepinephrine and epinephrine
APACHE score results and diagnoses upon admission to the intensive care unit are presented in Tables 2 and 3, respectively
This is in agreement with many other studies on humans that have not demonstrated the prevention of acute renal failure in highrisk patients or an improved outcome for those with established acute renal failure
Summary
Dopamine is an endogenous catecholamine, and is the immediate metabolite of norepinephrine and epinephrine. DA1 receptors are post-synaptic and are located in the smooth muscle cells of renal, mesenteric and coronary gastric vessels and in hepatic arteries.[1] DA2 receptors are pre-synaptic and are located in the adrenal medulla and sympathetic nerve endings.[1] Binding of dopamine to these two specific receptors causes arterial vasodilation, 2 as well as increased glomerular filtration, renal blood flow and fractional sodium excretion.[3,4]. Acute renal failure is relatively frequent among severely ill patients. The introduction of biocompatible membranes into hemodialysis has contributed towards increasing the survival rate of acute renal failure patients, this condition is associated with poor prognosis, especially when associated with multiple organ dysfunction.[2]
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