Signal Processing Methodology to Study the Cutaneous Vasodilator Response to a Local External Pressure Application Detected by Laser Doppler Flowmetry

2004 ◽  
Vol 51 (1) ◽  
pp. 190-192 ◽  
Author(s):  
A. Humeau ◽  
L. Fizanne ◽  
A. Garry ◽  
J.-L. Saumet ◽  
J.-P. L'Huillier
Keyword(s):  
Signal Processing ◽  
Laser Doppler Flowmetry ◽  
External Pressure ◽  
Laser Doppler ◽  
Doppler Flowmetry ◽  
Vasodilator Response ◽  
Pressure Application

Higher-order spectral analysis in laser-Doppler flowmetry signal processing

1999 ◽  
Vol 7 (2-3) ◽  
pp. 85-101 ◽  
Author(s):  
Vassilios Alexopoulos ◽  
Stefanos Kollias ◽  
Philippe Leger ◽  
Henry Boccalon ◽  
Zoltan Csiki
Keyword(s):  
Signal Processing ◽  
Spectral Analysis ◽  
Laser Doppler Flowmetry ◽  
Higher Order ◽  
Laser Doppler ◽  
Doppler Flowmetry

Role of nitric oxide in vasodilator response induced by salbutamol in rat diaphragmatic microcirculation

1997 ◽  
Vol 272 (5) ◽  
pp. H2173-H2179 ◽  
Author(s):  
H. Y. Chang
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Cyclic Amp ◽  
Laser Doppler Flowmetry ◽  
Ringer Solution ◽  
Laser Doppler ◽  
Microvascular Blood Flow ◽  
Doppler Flowmetry ◽  
Vasodilator Response

To determine the contribution of nitric oxide (NO) to the vasodilator response induced by salbutamol in diaphragmatic microcirculation, we studied a diaphragmatic preparation in anesthetized rats. With bicarbonate-buffered Ringer solution continuously suffusing the diaphragm, laser-Doppler flowmetry was used to record microvascular blood flow (QLDF). The drugs were applied to the surface of the diaphragm. Salbutamol (3.2 x 10(-7)-10(-4) M), isoproterenol (3.2 x 10(-8)-3.2 x 10(-6) M), and forskolin (3.2 x 10(-7)-10(-5) M) each elicited a concentration-dependent increase in QLDF. The vasodilator response induced by salbutamol (3.2 x 10(-7), 10(-6), and 3.2 x 10(-6) M) was attenuated by a 15-min suffusion of N omega-nitro-L-arginine (L-NNA, 10(-4) M), and pretreatment with L-arginine (10(-2) M) could restore salbutamol-induced vasodilator responses. Salbutamol-induced vasodilation was also abolished by propranolol (10(-5) M). Similarly, the vasodilator response elicited by isoproterenol (3.2 x 10(-8), 10(-7), and 3.2 x 10(-7) M) and forskolin (3.2 x 10(-7), 10(-6), and 3.2 x 10(-6) M) was inhibited by L-NNA (10(-4) M). In contrast, the vasodilator response induced by adenosine (10(-6), 10(-5), and 10(-4) M) was not affected by L-NNA (10(-4) M). These data indicate that in rat diaphragmatic microcirculation salbutamol-induced vasodilation may be partly mediated by beta-adrenoceptors on the endothelium. Moreover, these data suggest that an elevation of cyclic AMP in the endothelium may cause release of NO.

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