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Introduction: Acquisition of a deeper understanding of microvascular function across physiological and pathological conditions can be complicated by poor accessibility of the vascular networks and the necessary sophistication or intrusiveness of the equipment needed to acquire meaningful data. Laser Doppler fluximetry (LDF) provides a mechanism wherein investigators can readily acquire large amounts of data with minor inconvenience for the subject. However, beyond fairly basic analyses of erythrocyte perfusion (fluximetry) data within the cutaneous microcirculation (i.e., perfusion at rest and following imposed challenges), a deeper understanding of microvascular perfusion requires a more sophisticated approach that can be challenging for many investigators. Methods: This manuscript provides investigators with clear guidance for data acquisition from human subjects for full analysis of fluximetry data, including levels of perfusion, single- and multiscale Lempel-Ziv complexity (LZC) and sample entropy (SampEn), and wavelet-based analyses for the major physiological components of the signal. Representative data and responses are presented from a recruited cohort of healthy volunteers, and computer codes for full data analysis (MATLAB) are provided to facilitate efforts by interested investigators. Conclusion: It is anticipated that these materials can reduce the challenge to investigators integrating these approaches into their research programs and facilitate translational research in cardiovascular science. [ABSTRACT FROM AUTHOR]

We examined whether the formation or the release of the vasodilators adenosine, prostacyclin (PGI[sub 2] ) and potassium (K[sup +] ) increase in skeletal muscle interstitium in response to nitric oxide synthase (NOS) inhibition. Five subjects performed one-legged knee extensor exercise at 30 W without (controls) and with prior N[sup G] -nitro-L-arginine methyl ester (L-NAME) infusion (4 mg/kg, intravenously). Samples from the interstitial fluid were obtained at rest, during exercise and after exercise with the microdialysis technique. Interstitial adenosine in controls increased (p < 0.05) from 0.11 ± 0.03 μmol/l at rest to 0.48 ± 0.06 μmol/l during exercise. Interstitial adenosine during exercise in L-NAME was similar (p > 0.05) to controls. The 6-keto-prostaglandin F1α concentration in controls was 1.17 ± 0.20 ng/ml at rest and increased (p < 0.05) to 1.97 ± 0.30 ng/ml during exercise and was further elevated (p < 0.05) to 2.76 ± 0.38 ng/ml after exercise and these concentrations were not different (p > 0.05) in L-NAME. The interstitial K[sup +] concentration in controls increased (p < 0.05) from 4.1 ± 0.1 mmol/l at rest to 9.5 ± 0.5 mmol/l during exercise. The interstitial K[sup +] concentration during exercise (6.7 ± 0.4 mmol/l) was lower (p < 0.05) in L-NAME than in controls. The present findings demonstrate that the muscle interstitial concentrations of adenosine, PGI[sub 2] and K[sup +] during exercise are not increased with systemic NOS inhibition. Thus, the lack of effect of NOS inhibition on the rate of blood flow to contracting human skeletal muscle does not appear to be due to compensatory formation or release of adenosine, PGI[sub 2] and K[sup +] in the muscle interstitium. The present study also supports a role for PGI[sub 2] in the regulation of blood flow during exercise.Copyright © 2000 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]