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. Author manuscript; available in PMC: 2019 Sep 1.
Published in final edited form as: Nitric Oxide. 2018 Jul 27;79:57–67. doi: 10.1016/j.niox.2018.07.005

Figure 5.

Figure 5.

A) Fall in rectal temperature of LPS-treated rats, demonstrating successful infection. B) Marked increases in NOx in plasma and (C) whole blood of LPS-treated rats as determined by the various purge vessel reagents. D) Effect of LPS treatment on NOx levels in liver homogenates as determined by different purge vessel reagents. E) Demonstration of how the Ac/Asc assay quantitatively releases NO from heme-NO (0.1 to 10 mM HbNO) but not DNICs. The small peak observed for DNICs is < 10% of the signal produced from an equivalent concentration of DNICs in triiodide and is scavengable by acidified sulfanilamide. The heme-NO peak in the Ac/Asc assay is qualitatively different from nitrite due to slower NO-release. F) NOx signal from the liver tissue homogenates in the Ac/Asc assay following detection of a signal in the PBS/FeCN assay. Since the Ac/Asc assay is not expected to detect DNIC, the NOx signal from the liver tissue homogenates in Ac/Asc is qualitatively similar to that of the heme-NO than nitrite, and the NOx levels in Ac/Asc are similar to the NOx levels measured by PBS/FeCN, most of the NO released from liver tissue in the FeNO assay is more likely from heme-NO as opposed to DNICs. N.D. = not detected, N.M. = not measurable.