Ope score over time following the initiation of fenoldopam. The modified

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Given the mechanism of fenoldopam, early administration of the R promising avenue to reduce cancer burden is always to enable the medication in the treatment and prevention of AKI may be beneficial. RBF is dependent on renal vascular resistance (RVR) and systemic vascular resistance (SVR), such that if RVR increases relative to the SVR, RBF will decrease [44] RBF has been shown to decrease during the first 24 hours of ATN, and the kidney loses its ability to autoregulate, such that during the first 12 to 24 hours of AKI, there is a Still, though its direct relationship between renal perfusion pressure (RPP) and RBF [45-47]. More specifically, it is the renal outer medullary blood flow that is decreased, at least partially, secondary to cellular detachment and luminal occlusion [48]. Prior work has demonstrated that in post-ischemic AKI, nitric oxide synthase (NOS) activity is maximal at baseline and cannot be increased further by other stimuli of NOS activity [4]. Therefore, attempting to increase RBF via nitric oxide-dependent vasodilators may prove unsuccessful [4,49]. Given fenoldopam's nitric oxide independent mechanism of action and its preferential corticomedullary blood flow augmentation and ability to increase oxygenation, it is conceivable that it providesSimmons et al. BMC Anesthesiology 2010, 10:9 http://www.biomedcentral.com/1471-2253/10/Page 5 ofTable 3: s12889-015-2195-2 SCr (mg/dL) by AKIN Stage and TimeAKIN Stage Pre-Fenoldopam Mean (SE) ALL 1 2 3 1.7 (0.1) 1.5 (0.1) 1.7 (0.1) 1.8 (0.1) Median (IQR) 1.7 (1.4-1.9) 1.5 (1.3-1.7) 1.9 (1.7-1.9) 1.7 (1.4-2.0) Mean (SE) 1.6 (0.1) 1.3 (0.1) 1.8 (0.3) 1.8 (0.2) 24 Hours Median (IQR) 1.4 (1.2-1.9) 1.3 (1.0-1.5) 1.5 (1.3-1.9) 1.5 (1.2-2.1) Mean (SE) 1.5 (0.1) 1.2 (0.1) 1.3 (0.1) 1.7 (0.2) 48 Hours Median (IQR) 1.3 (1.0-1.6) 1.1 (0.9-1.4) 1.3 (1.0-1.7) s12889-015-2195-2 1.4 (1.1-2.1)p