Assessment of Renal Flow and Flow Reserve in Humans
Ganesh Manoharan, MBBCh, MD*,
Nico H.J. Pijls, MD, PhD ,
Norbert Lameire, MD, PhD ,
Katia Verhamme, MD, PhD ,
Guy R. Heyndrickx, MD, PhD*,
Emanuele Barbato, MD*,
William Wijns, MD, PhD*,
Juraj Madaric, MD*,
Xanden Tielbeele, MD ,
Jozef Bartunek, MD, PhD* and
Bernard De Bruyne, MD, PhD*,*
* Cardiovascular Centre Aalst, OLV-Clinic, Aalst, Belgium
Department of Cardiology, Catharina Hospital Eindhoven, Eindhoven, the Netherlands
Department of Nephrology, University of Ghent, Ghent, Belgium
Department of Epidemiology, OLV-Clinic, Aalst, Belgium

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Figure 1 Example of simultaneous pressure and velocity pressure tracing before, during, and after intrarenal administration of a bolus of 50 µg·kg1 of dopamine (DOPA); immediately after administration of the bolus, a marked decrease in renal artery average peak velocity is observed, followed by an almost two-fold increase in flow velocities without changes in blood pressure nor in heart rate.
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Figure 2 Percent increase in renal artery average peak velocity (APV) after intrarenal administration of various vasodilatory stimuli. Dopa = dopamine; Fenol = fenoldopam; ISDN = isosorbide dinitrate; PAPAV = papaverine; RI = renal vascular resistance index.
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Figure 3 Percentage change in renal artery average peak velocity (upper panel), in mean arterial blood pressure (mid-panel), and in renovascular resistance index (lower panel) during the intravenous infusion of increasing dosages of dopamine. BL = baseline.
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