Effects of Adenosine on Renal Function and Central Hemodynamics After Coronary Artery Bypass Surgery

In the early postoperative period after coronary artery bypass surgery, arterial hypertension commonly occurs which requires intravenous vasodilator therapy. Purine adenosine is a potent vasodilator and when exogenously administered it decreases systemic arterial blood pressure effectively. We evaluated the effects of adenosine on central hemodynamics and renal function when used to control postoperative hypertension after coronary artery bypass grafting (CABG). Two separate series of experiments were performed postoperatively in the Intensive Care Unit (ICU). In the first study (n = 10), postoperative hypertension was controlled in the rewarming phase, with sodium nitroprusside (SNP, 1.7 ± 0.4 μg · kg−1 · min−1) or adenosine (147.2 ± 38.9 μg · kg−1 · min−1) to keep mean arterial systolic pressure at approximately 80 mm Hg. In the second study on a separate group of patients (n = 9), low doses of adenosine (0, 30, 60, 90, and 0 μg · kg−1 · min−1) were infused when the patients were normotensive and rewarmed. Central hemodynamics, urine flow (UF), renal blood flow (RBF), glomerular filtration rate (GFR), and ECG were evaluated during periods of 30 min for each drug in the first study and during each ose of adenosine in the second study. RBF and GFR were determined using standard urinary clearance methods for 51Cr-ethylenediaminetetraacetic acid and p−aminohippuric acid. In the first study, adenosine infusion, compared to SNP, decreased (A -- V)O2, increased central filling pressures and heart rate, and caused a more pronounced ST segment depression. During adenosine administration RBF (−44%), GFR (−52%), and UF (−76%) decreased, while renal vascular resistance and filtration fraction (FF) were unaltered compared to data obtained during SNP infusion. In the second study, mean arterial and diastolic arterial pressure decreased with 14% at 60 and 90 μg · kg−1 · min−1, while central filling pressures were virtually unchanged during adenosine infusion. At 60 and 90 μg · kg−1 · min−1 of adenosine, UF decreased by 72% and 78%, respectively, and GFR by 51% and 60%, respectively. Adenosine also decreased RBF at 90 μg · kg−1 · min−1 by 50% and FF at all infusion rates by 13--30%. A renal hyperemia was noticed after adenosine was discontinued. Adenosine induced a significant depression of the ST segment at 60--90 μg · kg−1 · min−1 compared to control. In conclusion, adenosine when used as intravenous vasodilator after CABG, causes a decrease in RBF, GFR, UF, most likely caused by a pre-glomerular vasoconstriction. Adenosine may also induce myocardial ischemia, detected as a more pronounced ST segment depression when compared to SNP. These undesirable renal and myocardial effects of adenosine are seen already at a dose of 60--90 μg · kg−1 · min−1.