A remission spectroscopy system for in vivomonitoring of hemoglobin oxygen saturation in murine hepatic sinusoids, in early systemic inflammation

Wunder Christian, Brock, Krug Alfons, Roewer Norbert, Eichelbrönner, Eichelbrönner Otto

Description

During the early stages of systemic inflammation, the liver integrity is compromised by microcirculatory disturbances and subsequent hepatocellular injury. Little is known about the relationship between the hemoglobin oxygen saturation (HbsO 2 ) in sinusoids and the hepatocellular mitochondrial redox state, in early systemic inflammation. In a murine model of early systemic inflammation, we have explored the association between the sinusoidal HbsO 2 detected with a remission spectroscopy system and 1.) the NAD(P)H autofluorescence (an indicator of the intracellular mitochondrial redox state) and 2.) the markers of hepatocellular injury. Results Animals submitted to 1 hour bilateral hindlimb ischemia (I) and 3 hours of reperfusion (R) (3.0 h I/R) exhibited lower HbsO 2 values when compared with sham. Six hours I/R (1 hour bilateral hindlimb ischemia and 6 hours of reperfusion) and the continuous infusion of endothelin-1 (ET-1) further aggravated the hypoxia in HbsO 2 . The detected NAD(P)H autofluorescence correlated with the detected HbsO 2 values and showed the same developing. Three hours I/R resulted in elevated NAD(P)H autofluorescence compared with sham animals. Animals after 6.0 h I/R and continuous infusion of ET-1 revealed higher NAD(P)H autofluorescence compared with 3.0 h I/R animals. Overall the analysed HbsO 2 values correlated with all markers of hepatocellular injury. Conclusion During the early stages of systemic inflammation, there is a significant decrease in hepatic sinusoidal HbsO 2 . In parallel, we detected an increasing NAD(P)H autofluorescence representing an intracellular inadequate oxygen supply. Both changes are accompanied by increasing markers of liver cell injury. Therefore, remission spectroscopy in combination with NAD(P)H autofluorescence provides information on the oxygen distribution, the metabolic state and the mitochondrial redox potential, within the mouse liver.

Informations

• Publié par: biomed
• Publié le: 01 janvier 2005
• Nombre de lectures: 1
• Langue: English

Extrait

Comparative Hepatology

BioMedCentral

Open Access Research A remission spectroscopy system forin vivomonitoring of hemoglobin oxygen saturation in murine hepatic sinusoids, in early systemic inflammation 1 3 2 1 Christian Wunder* , Robert W Brock , Alfons Krug , Norbert Roewer and 1 Otto Eichelbrönner

1 Address: Klinik und Poliklinik für Anästhesiologie, JuliusMaximiliansUniversität Würzburg, Zentrum für Operative Medizin, Oberdürrbacher 2 3 Strasse 6, 97080 Würzburg, Germany, LEA Medizintechnik GmbH, 35394 Giessen, Germany and Department of Pharmacology & Toxicology, University of Arkansas for Medical Sciences, 722057199 Little Rock, USA Email: Christian Wunder*  [e-mail]wuerzburg.de; Robert W Brock  [e-mail]; Alfons Krug  [e-mail]; Norbert Roewer  [e-mail]wuerzburg.de; Otto Eichelbrönner  [e-mail]wuerzburg.de * Corresponding author

Published: 12 January 2005 Received: 20 October 2004 Accepted: 12 January 2005 Comparative Hepatology2005,4:1 doi:10.1186/1476-5926-4-1 This article is available from: http://www.comparative-hepatology.com/content/4/1/1 © 2005 Wunder et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract Background:During the early stages of systemic inflammation, the liver integrity is compromised by microcirculatory disturbances and subsequent hepatocellular injury. Little is known about the relationship between the hemoglobin oxygen saturation (HbsO ) in sinusoids and the 2 hepatocellular mitochondrial redox state, in early systemic inflammation. In a murine model of early systemic inflammation, we have explored the association between the sinusoidal HbsO detected 2 with a remission spectroscopy system and 1.) the NAD(P)H autofluorescence (an indicator of the intracellular mitochondrial redox state) and 2.) the markers of hepatocellular injury. Results:Animals submitted to 1 hour bilateral hindlimb ischemia (I) and 3 hours of reperfusion (R) (3.0 h I/R) exhibited lower HbsO values when compared with sham. Six hours I/R (1 hour bilateral 2 hindlimb ischemia and 6 hours of reperfusion) and the continuous infusion of endothelin-1 (ET-1) further aggravated the hypoxia in HbsO . The detected NAD(P)H autofluorescence correlated 2 with the detected HbsO values and showed the same developing. Three hours I/R resulted in 2 elevated NAD(P)H autofluorescence compared with sham animals. Animals after 6.0 h I/R and continuous infusion of ET-1 revealed higher NAD(P)H autofluorescence compared with 3.0 h I/R animals. Overall the analysed HbsO values correlated with all markers of hepatocellular injury. 2 Conclusion:During the early stages of systemic inflammation, there is a significant decrease in hepatic sinusoidal HbsO . In parallel, we detected an increasing NAD(P)H autofluorescence 2 representing an intracellular inadequate oxygen supply. Both changes are accompanied by increasing markers of liver cell injury. Therefore, remission spectroscopy in combination with NAD(P)H autofluorescence provides information on the oxygen distribution, the metabolic state and the mitochondrial redox potential, within the mouse liver.

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