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Abstract
A red-green-blue camera-based imaging method is proposed for estimating spatial maps of concentrations of oxyhemoglobin (CHbO), deoxyhemoglobin (CHbR), total hemoglobin (CHbT), tissue oxygen saturation (StO2), and scattering power (b) in liver tissue. Hemodynamic responses to hepatic ischemia-reperfusion of in vivo rat liver tissues induced by portal triad occlusion were evaluated. Upon portal triad occlusion, this method yielded images of decreased CHbO, CHbT, StO2, and b, and increased CHbR followed by a progressive increase in CHbO and StO2 during reperfusion. Time courses of the changes in CHbO, CHbR, CHbT, and StO2 over different regions of interest (ROIs) revealed that ischemia results in an abrupt significant (P<0.05) reduction in CHbO, CHbT, and StO2 with a simultaneous increase in CHbR compared to the baseline level, indicative of the hemodynamic responses during hepatic ischemia-reperfusion. Upon reperfusion, there was a gradual increase in CHbO and StO2, and decrease in CHbR. The change in average scattering power b implies the presence of morphological alterations in the cellular and subcellular structures induced by ischemia or anoxia. This study shows the potential of monitoring spatiotemporal changes in hemodynamic parameters and morphological changes in studies of hepatic pathophysiology.
Highlights
Ischemia and subsequent reperfusion of liver tissue may occur in a number of clinical settings, such as those associated with low-flow states, or temporary occlusion of the supplying blood vessels during liver transplantation, and to a large extent in liver resection surgery
We studied hepatic hemodynamic responses to ischemia-reperfusion to investigate the time course and spatial distribution of chromophore concentrations and tissue oxygenation
The results of hepatic ischemia-reperfusion revealed spatial changes in hepatic hemodynamics, an increase in deoxyhemoglobin concentration, decreases in oxyhemoglobin concentration and tissue oxygen saturation during ischemia, which subsequently recovered on reperfusion
Summary
Ischemia and subsequent reperfusion of liver tissue may occur in a number of clinical settings, such as those associated with low-flow states, or temporary occlusion of the supplying blood vessels during liver transplantation, and to a large extent in liver resection surgery. Ischemia-reperfusion damage to donor liver tissue is thought to be a vital component that may play a role in the decline of posttransplant graft function and rejection. Normothermic ischemia-reperfusion causes up to 10% of early graft rejections [2]. Hepatocellular damage caused by ischemia-reperfusion correlates with the extent of microcirculatory reperfusion failure after portal-triad cross-clamping [3]. The resulting hepatic ischemia, along with subsequent reperfusion, causes ischemia-reperfusion injury and structural changes in hepatic tissue of varying extents, which will alter the scattering properties of light
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