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J Am Coll Cardiol, 2006; 47:620-625, doi:10.1016/j.jacc.2005.08.071 (Published online 13 January 2006).
© 2006 by the American College of Cardiology Foundation
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Assessment of Renal Flow and Flow Reserve in Humans

Ganesh Manoharan, MBBCh, MD*, Nico H.J. Pijls, MD, PhD{dagger}, Norbert Lameire, MD, PhD{ddagger}, Katia Verhamme, MD, PhD§, Guy R. Heyndrickx, MD, PhD*, Emanuele Barbato, MD*, William Wijns, MD, PhD*, Juraj Madaric, MD*, Xanden Tielbeele, MD{dagger}, Jozef Bartunek, MD, PhD* and Bernard De Bruyne, MD, PhD*,*

* Cardiovascular Centre Aalst, OLV-Clinic, Aalst, Belgium
{dagger} Department of Cardiology, Catharina Hospital Eindhoven, Eindhoven, the Netherlands
{ddagger} Department of Nephrology, University of Ghent, Ghent, Belgium
§ Department of Epidemiology, OLV-Clinic, Aalst, Belgium


Figure 1
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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·kg–1 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.

 

Figure 2
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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.

 

Figure 3
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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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