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Advances in Urology
Volume 2012 (2012), Article ID 676303, 8 pages
http://dx.doi.org/10.1155/2012/676303
Methodology Report

Monitoring Detrusor Oxygenation and Hemodynamics Noninvasively during Dysfunctional Voiding

1Near Infrared Spectroscopy Research Group, Department of Urology, Faculty of Medicine, University of British Columbia and UBC Hospital Bladder Care Centre, Unit IB—Room F329, 221 Wesbrook Mall, Vancouver, BC, Canada V6T 1Z3
2Stellenbosch Institute for Advanced Study, Wallenberg Research Centre, 10 Marais Street, Stellenbosch 7600, South Africa

Received 21 April 2012; Revised 3 July 2012; Accepted 17 July 2012

Academic Editor: Ferdinando Fusco

Copyright © 2012 Andrew J. Macnab et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

The current literature indicates that lower urinary tract symptoms (LUTSs) related to benign prostatic hyperplasia (BPH) have a heterogeneous pathophysiology. Pressure flow studies (UDSs) remain the gold standard evaluation methodology for such patients. However, as the function of the detrusor muscle depends on its vasculature and perfusion, the underlying causes of LUTS likely include abnormalities of detrusor oxygenation and hemodynamics, and available treatment options include agents thought to act on the detrusor smooth muscle and/or vasculature. Hence, near infrared spectroscopy (NIRS), an established optical methodology for monitoring changes in tissue oxygenation and hemodynamics, has relevance as a means of expanding knowledge related to the pathophysiology of BPH and potential treatment options. This methodological report describes how to conduct simultaneous NIRS monitoring of detrusor oxygenation and hemodynamics during UDS, outlines the clinical implications and practical applications of NIRS, explains the principles of physiologic interpretation of NIRS voiding data, and proposes an exploratory hypothesis that the pathophysiological causes underlying LUTS include detrusor dysfunction due to an abnormal hemodynamic response or the onset of oxygen debt during voiding.