Anesth Analg 1999;89:1430
© 1999 International Anesthesia Research Society
CRITICAL CARE AND TRAUMA
Effect of Small-Dose Dopamine on Mesenteric Blood Flow and Renal Function in a Pig Model of Cardiopulmonary Resuscitation with Vasopressin
Wolfgang G. Voelckel, MD*,
Karl H. Lindner, MD*,
Volker Wenzel, MD*,
Johannes O. Bonatti, MD
,
Anette C. Krismer, MD*,
Egfried A. Miller, BS*, and
Keith G. Lurie, MD
Departments of
*Anaesthesia and Intensive Care Medicine and
Surgery, Leopold-Franzens-University of Innsbruck, Innsbruck, Austria; and
Cardiac Arrhythmia Center, University of Minnesota, Minneapolis, Minnesota
Address correspondence to Dr. Wolfgang Voelckel, Department of Anaesthesia and Intensive Care Medicine, The Leopold-Franzens-University of Innsbruck, Anichstrasse 35, 6020 Innsbruck, Austria. Address e-mail to wolfgang.voelckel{at}uibk.ac.at
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Abstract
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Vasopressin (antidiuretic hormone) seems a promising alternative to epinephrine for cardiopulmonary resuscitation (CPR) in cardiac arrest victims, mediating a pronounced blood flow shift toward vital organs. We evaluated the effects of small-dose dopamine on splanchnic blood flow and renal function after successful resuscitation with this potent vasoconstrictor in an established porcine CPR model. After 4 min of cardiac arrest and 3 min of CPR, animals received 0.4 U/kg vasopressin and were continuously infused with either dopamine 4 µg · kg-1 · min-1 (n = 6), or saline placebo (n = 6). Defibrillation was performed 5 min after drug administration; all animals were observed for 6 h after return of spontaneous circulation. During the postresuscitation phase, average mean ± SD superior mesenteric artery blood flow was significantly (P = 0.002) higher in the dopamine group compared with the placebo group (1185 ± 130 vs 740 ± 235 mL/min), whereas renal blood flow was comparable between groups (255 ± 40 vs 250 ± 85 mL/min). The median calculated glomerular filtration rate had higher values in the dopamine group (70–120 mL/min) than in the placebo group (40–70 mL/min; P = 0.1 at 0 min and P = 0.08 at 360 min). We conclude that small-dose dopamine administration may be useful in improving superior mesenteric artery blood flow and renal function after successful resuscitation with vasopressin.
Implications: Long-term survival after cardiac arrest may be determined by the ability to ensure adequate organ perfusion during cardiopulmonary resuscitation and in the postresuscitation phase. In this regard, small-dose dopamine improved postresuscitation blood flow to the mesenteric bed when vasopressin was used as an alternative vasopressor in an animal model of cardiac arrest.
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Introduction
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An infusion of small-dose dopamine is used in patients suffering from cardiocirculatory failure and in patients after successful cardiopulmonary resuscitation (CPR). In this circumstance, vasopressin has been reported to be an effective alternative vasopressor (1–4), which seems to work during CPR by acutely increasing systemic vascular resistance (5) via the V1-receptor (6). When administered during CPR, vasopressin mediated a pronounced blood flow shift from muscle, skin, and gut toward vital organs, which resulted in increased myocardial perfusion (1) and cerebral oxygen delivery in an animal model (4). Accordingly, compared with epinephrine, vasopressin improved return of spontaneous circulation (ROSC) after prolonged, unsuccessful, advanced cardiac life support in patients (2) and the 24-h survival rate in a small out-of-hospital trial (3).
Once spontaneous circulation is restored, 
- and/or ß-adrenergic agonists may be required for circulatory support to overcome myocardial dysfunction with low-output and regional hypoperfusion (7). In clinical practice, small-dose dopamine is often administered as a first-line catecholamine to improve renal blood flow and function. At doses of 0.2–5 µg · kg-1 · min-1, dopamine acts on two populations of dopamine receptors—DA1 and DA2—which are located primarily in the media of smooth muscle arterial walls, the kidney, and the gastrointestinal tract (8). In these organs, dopamine is thought to cause selective DA1 receptor-mediated vasodilation and to improve regional perfusion and kidney function (9–11).
When vasopressin is administered during CPR, the splanchnic bed and the kidneys are likely to be affected by vasopressin because of an increased density of V1-receptors in intestinal vessels and vasopressin’s dose-dependent antidiuretic effects (5,12). Furthermore, intestinal ischemia during cardiac arrest and the quality of reperfusion play a major role in ischemia-related tissue injury. In this regard, mucosal dysfunction associated with ischemia-reperfusion may result in bacterial translocation and sepsis, thus affecting outcome after successful CPR (13,14). The interaction between vasopressin and dopamine receptor stimulation during and after CPR is unknown. Accordingly, the purpose of our investigation was to evaluate the effects of a continuous small-dose (4 µg · kg-1 · min-1) dopamine infusion on intestinal blood flow and renal function in an animal model of CPR with vasopressin.
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Methods
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This project was approved by the Austrian National Animal Investigational Committee, and the animals were managed in accordance with the American Physiological Society and institutional guidelines. This study was performed according to Utstein-style guidelines (15) on 12 healthy, 12- to 16-wk-old swine (Tyrolean domestic pigs) of either sex weighing 30–35 kg. The animals were fasted overnight but had free access to water. The pigs were premedicated with azaperone (neuroleptic drug; 4 mg/kg IM) 1 h before surgery, and anesthesia was induced with ketamine (20 mg/kg IM) and propofol (50 mg IV). After intubation during spontaneous respiration, the pigs were ventilated using a volume-controlled ventilator (Draeger EV-A, Lübeck, Germany) with 100% O2 at 14 breaths/min and with the tidal volume adjusted to maintain PaCO2 levels at 35 ± 3 mm Hg. Anesthesia was maintained with propofol (6–8 mg · kg-1 · h-1) and piritramid (0.3 mg/kg) as needed; muscle paralysis was achieved with 8 mg of pancuronium after intubation, and subsequently as needed. Lactated Ringer’s solution (6 mL · kg -1 · h-1) and a 3% gelatin solution (4 mL · kg -1 · h-1) were administered continuously during the preparation and study period to replace fluid loss. A standard lead II electrocardiogram was used to monitor cardiac rhythm; depth of anesthesia was judged based on blood pressure, heart rate, and electroencephalography. If electroencephalographic 95% spectral edge frequency increased to >16 Hz, or if physiological signs indicated a decreasing level of anesthesia, the propofol dose was adjusted and additional piritramid was given. Body temperature was maintained with a heating blanket at 38–39°C.
A 7F catheter was advanced into the ascending aorta via cutdown in the groin for withdrawal of arterial blood samples and measurement of arterial blood pressure. A 5F pulmonary artery catheter was placed into the pulmonary artery via cutdown in the neck to measure cardiac output using the thermodilution technique and to sample mixed venous blood. Another 7F catheter was placed into the right atrium via cutdown in the groin for measurement of right atrial pressure and for drug administration. Aortic, right atrial, and pulmonary artery pressures were measured by using saline-filled catheters attached to pressure transducers (Model 1290A; Hewlett Packard, Böblingen, Germany) that were calibrated to atmospheric pressure at the level of the right atrium; pressure tracings were recorded via a data acquisition system. Blood gases were measured by using a blood gas analyzer.
After instrumentation for hemodynamic variables, a midline laparotomy was performed, and the superior mesenteric, and left renal arteries were dissected carefully from supporting tissues, then instrumented with ultrasound flowprobes (Transonic, Ithaca, NY) to measure organ perfusion (16). Before closure of the abdomen, the bladder was surgically opened, and a catheter was inserted and sutured into the bladder to measure urine production. All pigs were instrumented in an aseptic manner under sterile conditions.
After surgery, the pigs were allowed to recover for 120 min; 15 min before cardiac arrest, 5000 U of IV heparin was administered to prevent intracardiac clot formation; a single dose of 15 mg of piritramid and 8 mg of pancuronium was given; and prearrest hemodynamic variables and blood gases were measured. A 50-Hz, 60-V alternating current was then applied via two subcutaneous needle electrodes to induce ventricular fibrillation. Cardiac arrest was defined as the point at which the aortic pulse pressure decreased profoundly to hydrostatic pressure and the electrocardiogram showed ventricular fibrillation; ventilation was stopped at that point. After 4 min of untreated ventricular fibrillation, closed-chest CPR was performed manually, and mechanical ventilation was resumed with identical ventilation variables as before cardiac arrest. Chest compression rate was 80/min and was performed by the same investigator, who was blinded to hemodynamic and end-tidal CO2 tracings, and it was guided by acoustical audiotones.
After 4 min of untreated cardiac arrest and 3 min of CPR, the animals were treated with 0.4 U/kg vasopressin (Pitressin®; Parke Davis, Berlin, Germany) diluted to 10 mL, which was administered as a central venous IV push, followed by a 20-mL saline flush. At the same time, pigs were randomly assigned to receive either a continuous infusion of dopamine (4 µg · kg-1 · min-1) or saline placebo at equal infusion rates (investigators were blinded to the drugs). The dopamine dose was chosen to reflect the usual clinical therapeutic range (8), and the drug concentration was adjusted to allow an infusion flow rate of 50 mL/h during the entire observation period. Hemodynamic variables, blood gases, and organ blood flow were measured before the induction of cardiac arrest, after 90 s of CPR, 90 s and 5 min after drug administration, and for 6 h in the postresuscitation phase. After 12 min of cardiac arrest, including 8 min of CPR, up to three countershocks were administered with a defibrillator (Theracard®; Siemens, Erlangen, Germany) with an energy of 3, 4, and 6 J/kg. If ventricular fibrillation, pulseless electrical activity, or asystole persisted, a second bolus dose of 0.4 U/kg vasopressin was administered, chest compressions were resumed for an additional 90 s, and defibrillation was performed again with an energy of 6 J/kg.
ROSC was defined as an unassisted pulse with a systolic arterial pressure of >80 mm Hg and pulse pressure of >40 mm Hg. In the postresuscitation period, hemodynamic variables, organ blood flow, and kidney function were observed for 6 h. The superior mesenteric vascular resistance (SMAR) and renal vascular resistance (RAR) were calculated according to the following formulas: SMAR = mean arterial blood pressure/superior mesenteric artery blood flow; and RAR = mean arterial blood pressure/renal artery blood flow. Urine and blood samples were collected every 60 min after the ROSC for measurement of urine sodium concentration (UNa), urine creatinine concentration (UCreat), plasma sodium concentration (PNa), and plasma creatinine concentration (PCreat). Diuresis (V) was measured with a precision of mL via a small graduated container. GFR and fractional sodium excretion (FeNa) were subsequently calculated according to standard formulas: GFR = (UCreat x V)/(PCreat x 60); FeNa = 100 x (UNa x PCreat)/(PNa x UCreat). Potassium excretion and osmolar clearance were calculated in the same manner.
After finishing the experimental protocol, the animals were killed with an overdose of piritramid and potassium chloride; all pigs were then necropsied to check correct positioning of the catheters, damage to the rib cage, and evidence of gut necrosis.
Blood flow data and hemodynamic variables are given as mean ± SD. To compare hemodynamic and calculated vascular resistance values, analysis of variance for repeated measures was used. The average renal and superior mesenteric artery blood flows were assessed by calculating the area under the curve for each group over the entire postresuscitation phase, and they were further compared by using an unpaired Student’s t-test. For paired comparisons between variables measured before and 60 and 120 min after CPR, a two-tailed paired Student’s t-test was used. Calculated renal function data are reported as median (25th and 75th percentiles) and were analyzed by using the Mann-Whitney U-test. The data were analyzed by a software program (Stat ViewTM; Abacus Concepts, Berkeley, CA). A P value < 0.05 was considered statistically significant in all tests.
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Results
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There were no differences in hemodynamic, acid-base, and blood gas variables before the induction of ventricular fibrillation or during CPR. One vasopressin-placebo animal, but no vasopressin-dopamine animal, required a repeated dose of 0.4 U/kg vasopressin to restore spontaneous circulation. Heart rate, mean arterial pressure, cardiac index, and systemic vascular resistance were comparable in both groups during the entire postresuscitation phase. Compared with prearrest values (1105 ± 265 mL/min), the superior mesenteric artery blood flow value was significantly (P < 0.05) lower 120 min (825 ± 110 mL/min) and 240 min (860 ± 135 mL/min) after ROSC in the vasopressin-placebo group. During the entire postresuscitation phase, average mean ± STD superior mesenteric artery blood flow was significantly (P = 0.002) higher in the dopamine group compared with the placebo group (1185 ± 130 vs 740 ± 235 mL/min). In the vasopressin-dopamine group, SMAR was significantly (P < 0.05) lower 30, 180, 240, and 360 min after ROSC, compared with the vasopressin-placebo group (Table 1). Average mean ± STD renal blood flow was 255 ± 40 mL/min in the dopamine group and 250 ± 85 mL/min in the placebo group (not significant) (Figures 1 and 2).
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Figure 1. Mean ± SD superior mesenteric artery blood flow prearrest, during cardiopulmonary resuscitation (CPR), and in the postresuscitation phase after the administration of 0.4 U/kg vasopressin combined with a continuous infusion of either 4 µg · kg-1 · min-1 (•) or saline placebo ( ). BL = baseline values at prearrest, BLS = basic life support, ALS = advanced life support, DA = drug administration, ROSC = return of spontaneous circulation. Time is shown in minutes. P = 0.002 versus placebo for area under the curve.
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Figure 2. Mean ± SD renal artery blood flow prearrest, during cardiopulmonary resuscitation (CPR), and in the postresuscitation phase after the administration of 0.4 U/kg vasopressin combined with a continuous infusion of either 4 µg · kg-1 · min-1 (•) or saline placebo (). BL = baseline values at prearrest, BLS = basic life support, ALS = advanced life support, DA = drug administration, ROSC = return of spontaneous circulation. Time is shown in minutes.
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In the postresuscitation phase, neither urinary output nor calculated renal function indices differed significantly between groups, and they were comparable to normal baseline values obtained from the literature (17) (Table 2). The calculated GFR was higher in the postresuscitation phase when vasopressin was combined with dopamine (P = 0.1 at 60 min and P = 0.08 at 360 min). Calculated FeNa was increased in both groups 60 min after ROSC, with a continuous increase in the vasopressin-placebo group but not in the vasopressin-dopamine group.
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Table 2. Urine Output, Calculated Glomerular Filtration Rate, Fractional Excretion of Sodium, Fractional Excretion of Potassium, Osmolar Clearance, and Relationship Between Osmolarity in Urine and Plasma
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At necropsy, all catheters were found in correct positions, and no damage to the rib cage or evidence of gut necrosis was found in any animal.
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Discussion
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Results from these experiments demonstrate that the continuous infusion of small-dose dopamine significantly decreased calculated SMAR and, subsequently, increased mesenteric perfusion after successful CPR with vasopressin. Accordingly, impaired superior mesenteric artery blood flow was restored with dopamine to prearrest levels within 60 minutes. Animals not receiving dopamine never achieved mesenteric artery blood flow values in the postresuscitation phase >75% of baseline. In contrast to the vasodilation observed in the intestinal vessels, renal blood flow and urine output were not influenced by dopamine during or after CPR. However, there was a trend toward higher calculated GFRs when small-dose dopamine infusion was compared with saline placebo.
It is likely that the observed impaired intestinal perfusion was caused by some degree of reperfusion injury. In this regard, oxygen-derived free radicals produced during intestinal ischemia may contribute to the pathomechanisms causing a prolonged reduction in superior mesenteric artery blood flow (14). We further speculate that vasopressin administered during CPR plays an important role in the altered distribution pattern of blood flow during the postresuscitation phase. Vasopressin plasma levels after successful resuscitation with a vasopressin bolus dose of either 0.4 or 0.8 U/kg remain increased for at least 30–60 minutes in the postresuscitation phase, with values of 45–170 pg/mL (18,19). Compared with the normal range of plasma arginine vasopressin concentration, which is 0.5–1.9 pg/mL (17), it is likely that vasopressin-sensitive vascular beds (i.e., the skeletal muscle, mesenteric and iliac circulation) are affected for >60 minutes by a single bolus dose of vasopressin administered during CPR (20).
An ongoing discussion about the possible risks and benefits of using dopamine to treat hypotension is fueled by conflicting laboratory investigations, which revealed intestinal vasoconstriction (21), as well as direct vasodilation (22,23). Furthermore, mucosal oxygen supply and uptake were found to be impaired in dogs (22) but improved in pigs receiving a dopamine infusion, thus preserving splanchnic oxygen reserve capacity (23). However, the administration of a small-dose dopamine infusion in critically ill patients is still used; and, in organs with vascular dopamine receptors (such as renal and splanchnic blood vessels), activation by small-dose dopamine is thought to result in vasodilation, with a subsequently improved regional perfusion (24). In the present model, we administered 4 µg · kg-1 · min-1 dopamine continuously after three minutes of CPR throughout the entire experiment, a dose that is considered to act predominantly on DA1 and DA2 receptors (8). As indicated by decreased SMAR values, our data suggest that increased blood flow toward the gut is due to dopamine-mediated vasodilation of the intestinal vasculature. Moreover, we found the cardiac index not to be significantly influenced by the dopamine infusion, and mean arterial pressure was only slightly increased.
Although intestinal blood flow was not impaired below a critical level of 25% in our study, there is evidence that prolonged CPR or an antecedent intestinal ischemia may cause a critically impaired splanchnic blood flow if repetitive doses of vasopressin are required. In this regard, severe hypoperfusion of the gut may subsequently increase intestinal mucosal permeability, thus potentiating bacterial translocation and sepsis in the postresuscitation phase (14). Based on our results, small-dose dopamine may prevent intestinal hypoperfusion during the recovery phase after successful resuscitation.
Renal artery perfusion was not influenced by dopamine in our experiment; baseline blood flow values were achieved within 90 minutes after ROSC in both groups. This is in close agreement with the findings of other investigations unrelated to CPR, which have been unable to demonstrate any direct renovascular effect of dopamine (11,25). Although small-dose dopamine was reported to counteract the vasoconstricting effects of norepinephrine on the renal vasculature in both healthy volunteers (9) and animals (26), we found no renal vasodilation; RAR was only slightly decreased. It is recognized that renal artery blood flow is the blood flow least affected by vasopressin (20). Accordingly, as renal vascular tone seems not to be influenced by endogenous catecholamines or exogenous vasopressin, renal perfusion may not be enhanced by small-dose dopamine.
Besides a possible increase in renal blood flow, the postulated mechanisms of dopamine action on renal function include: 1) an increased GFR and filtration fraction; 2) an altered renal cortical blood flow distribution favoring perfusion of the inner cortex; and 3) a direct tubular effect enhancing sodium and potassium excretion (24,27). Vasopressin itself is reported to mediate a 65% increase in FeNa in rats (28), although the mechanism of this effect is unknown. Accordingly, we are not able to explain the pharmacological interactions between vasopressin and dopamine receptors in the kidney. The FeNa decreased when dopamine was infused. Nevertheless, the calculated GFR values were higher in the dopamine group, and urine output was slightly improved in the late postresuscitation phase of our experiment, thus indicating a possible favorable effect of dopamine on renal blood flow distribution.
Continuous measurement of organ blood flow with transit time ultrasound transducers was validated (29) and is an established method in CPR research (15). Using this technique, alterations of superior mesenteric and renal artery blood flows can be monitored continuously during a prolonged observation time. Compared with other techniques to measure blood flow during low-flow states, such as colored or radionuclide microspheres, this method is very accurate. Thus, our data closely reflect the hemodynamic effects of vasopressin and dopamine on splanchnic vessels during CPR and in the early postresuscitation phase.
Some limitations of our study should be noted. First, we did not obtain oxygen extraction ratios of the small intestine and kidney; therefore, we are not able to provide information about the effects of dopamine on mucosal oxygen consumption. Second, to implant ultrasound flow probes, a laparotomy and adequate anesthesia were required; both may interfere with the physiological stress response. Third, right renal blood flow was not monitored because we found an accessory right renal artery in most animals during surgery. Because of this anatomic variance, most investigators obtain renal blood flow values solely from the left kidney when using an ultrasound flowprobe-based technique (30). Fourth, in a clinical scenario, longer cardiac arrest or CPR times, as well as preexisting diseases such as atherosclerosis, may render more pronounced alterations in blood flow or renal function after CPR with vasopressin more likely. Fifth, different vasopressin receptors in pigs (lysine vasopressin) and humans (arginine vasopressin) may result in a different hemodynamic response to exogenously administered arginine vasopressin and, subsequently, to the incoherent effects of dopamine. Finally, this study lacks dose-response data. Therefore, we are only able to report the results of small-dose dopamine administered during and after CPR. In the small-dose range, we observed no adverse effects after dopamine delivery. Furthermore, we are not able to discriminate whether the observed effects of small-dose dopamine are caused by an attenuation of the pathomechanisms underlying the reperfusion injury of the intestine or by the counterregulation of vasopressin-mediated prolonged vasoconstriction of mesenteric vessels.
In conclusion, the continuous infusion of small-dose dopamine caused selective vasodilation of intestinal vessels and resulted in a significant increase in mesenteric, but not renal artery, blood flow after successful resuscitation with vasopressin. This regional specificity of small-dose dopamine administration after cardiac arrest and vasopressin treatment during resuscitation suggests that activation of intestinal arterial dopamine receptors may be of clinical value when mesenteric ischemia or acute renal failure is suspected, anticipated, or even confirmed.
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Acknowledgments
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Supported, in part, by Solvay Pharma, Klosterneuburg, Austria; the Department of Anaesthesia and Intensive Care Medicine, a Dean’s grant for medical school graduates, The Leopold-Franzens-University of Innsbruck, Austria; and the Austrian National Bank Science Project 7280.
We greatly appreciate the extensive expertise of Günther Klima, MD, PhD, in animal care.
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Footnotes
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Presented as an abstract to the 72nd scientific session of the American Heart Association, Atlanta, GA, November 1999.
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Accepted for publication August 30, 1999.
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Abstract
Introduction
