Abstract：
:The steatotic liver is characterized by deranged intrahepatic microvasculature that is believed to predispose it to ischemia-reperfusion injury. The aim of this study was to investigate the distorted hepatic hemodynamics and its impact on the redox status of the steatotic liver. Hepatic hemodynamic parameters, hepatic microcirculatory perfusion (HMP), and in vivo reduced nicotinamide adenine dinucleotide (phosphate) [NAD(P)H] autofluorescence, which reflects the mitochondrial redox status and tissue oxygen levels, were measured in obese (n = 7) and lean Zucker rats (n = 7). Portal venous and total hepatic blood flow per unit of liver weight were found to exhibit a 37.9% and 35.9% reduction, respectively, in the steatotic liver compared to the nonsteatotic liver of the lean group (P < 0.0001) as was HMP (obese, 96.1 +/- 18.1 PU; lean, 143.8 +/- 12.0 PU, P < 0.05) that showed a 33.2% decrease in the former. Hepatic arterial resistance, however, was 38.7% lower in the obese rat (83.1 +/- 9.1 mmHg. ml(-1). min) than in the lean rat (135.5 +/- 15.8 mmHg. ml(-1). min) (P < 0.05). NAD(P)H fluorescence intensity was significantly elevated in the steatotic liver (0.16 +/- 0.001 aU) compared with the lean one (0.14 +/- 0.007 aU) (P = 0.014). Our results suggest that, in response to a reduced portal venous blood flow, there is a significant decrease in hepatic arterial resistance that, nevertheless, cannot completely compensate for the drop in overall hepatic perfusion and oxygenation of the microvascular bed in the steatotic liver of the obese Zucker rat.
journal_name
Microvasc Resjournal_title
Microvascular researchauthors
Sun CK,Zhang XY,Wheatley AMdoi
10.1016/s0026-2862(03)00021-9keywords:
subject
Has Abstractpub_date
2003-07-01 00:00:00pages
15-21issue
1eissn
0026-2862issn
1095-9319pii
S0026286203000219journal_volume
66pub_type
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