Hepatic Microcirculation in Zucker Fatty Rats

Sato, Nobuhiro; Eguchi, Hiroshi; Matsumura, Tae; Kamada, Takenobu

doi:10.1007/978-1-4684-5188-7_59

Cited by 33 publications

(34 citation statements)

References 6 publications

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“…Moderate steatosis reduced the flow in the HM which previously has been reported with fatty liver [27,28]. The reduction in HM occurs due to sinusoidal compression and a decrease in sinusoidal diameter by the enlarged fatladen hepatocytes [27].…”

Section: Discussionmentioning

confidence: 78%

“…The reduction in HM occurs due to sinusoidal compression and a decrease in sinusoidal diameter by the enlarged fatladen hepatocytes [27]. This change in HM by the enlarged hepatocytes is augmented by an increase in fibroblast numbers with the formation of collagen bundles in the perisinusoidal space which causes further narrowing of the sinusoids [22,24].…”

Section: Discussionmentioning

confidence: 99%

“…Thickening of the sinusoidal wall with membranous formation and proliferation of collagen fibres with 'intrasinusoidal block' decreases the diffusion of protein-bound substances such as ICG into the extravascular space [32,33]. Impairment of ICG excretion could also be explained by reduced transport across the biliary canalicular membrane which is energy-dependent and would be influenced by a reduction in hepatic adenosine triphosphate content [34], secondary to the reduction of regional blood volume and decrease of regional oxygenation [27].…”

Section: Discussionmentioning

confidence: 99%

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Hepatic Indocyanine Green Uptake and Excretion in a Rabbit Model of Steatosis

Seifalian¹,

El-Desoky²,

Davidson³

2001

Eur Surg Res

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Transplantation of a fatty liver is associated with a higher incidence of primary non-function of the graft. Indocyanine green (ICG) has been used for assessing hepatic dysfunction but not for quantifying liver steatosis. New Zealand white rabbits were fed a normal diet (group A) or a high-cholesterol (2%) diet for 4, 8, and 12 weeks in groups B, C, and D, respectively. Laparotomy was performed for liver exposure. Hepatic artery, portal vein, and total blood flow, hepatic microcirculation, portal pressure, liver function parameters, and blood cholesterol levels were measured. The hepatic ICG concentration was measured using near-infrared spectroscopy, and its uptake and excretion rates were calculated. The severity of steatosis was assessed from liver biopsy specimens by a semiquantitative grading system. Cholesterol feeding resulted in mild steatosis after 4 weeks and in moderate steatosis after 8 and 12 weeks. Mild steatosis was associated with insignificant changes in haemodynamic parameters, liver function, and ICG handling as compared with controls. Moderate steatosis caused a significant reduction in portal and total hepatic blood flow and microcirculation with a significant increase in hepatic artery flow and portal pressure. These haemodynamic changes were associated with a significant alteration in liver function tests. With moderate steatosis, ICG uptake and excretion were significantly reduced. The ICG uptake rate significantly correlated with total blood flow and microcirculation. The ICG excretion rate significantly correlated with the changes in bilirubin, liver enzymes, and albumin. Direct ICG quantification by near-infrared spectroscopy could be used to assess the severity of hepatic steatosis by reflecting impaired parenchymal perfusion and liver dysfunction.

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Section: Discussionmentioning

confidence: 78%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Hepatic Indocyanine Green Uptake and Excretion in a Rabbit Model of Steatosis

Seifalian¹,

El-Desoky²,

Davidson³

2001

Eur Surg Res

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“…The reduction in HM associated with steatosis has been reported in other studies with fatty livers [42,43]. The reduction in HM occurs due to sinusoidal compression and decrease in sinusoidal diameter by the enlarged fat-laden hepatocytes [42].…”

Section: Discussionmentioning

confidence: 89%

Effect of ischaemic preconditioning on hepatic oxygenation, microcirculation and function in a rat model of moderate hepatic steatosis

et al. 2004

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IPC (ischaemic preconditioning) may protect the steatotic liver, which is particularly susceptible to I/R (ischaemia/reperfusion) injury. Hepatic steatosis was induced in Sprague-Dawley rats with a high-cholesterol (2%) diet for 12 weeks after which rats were subjected to I/R (ischaemia/reperfusion; 45 min of lobar ischaemia followed by 2 h of reperfusion). Rats were divided into three study groups (n=6 each) receiving: (i) sham laparotomy alone, (ii) I/R, and (iii) IPC (5 min of ischaemia, followed by 10 min of reperfusion) before I/R. Hepatic extra- and intra-cellular oxygenation and HM (hepatic microcirculation) were measured with near-infrared spectroscopy and laser Doppler flowmetry respectively. Plasma liver enzymes and hepatic tissue ATP were measured as markers of liver injury. Histology showed moderate-grade steatosis in the livers. At the end of 2 h of reperfusion, I/R significantly decreased extra- and intra-cellular oxygenation concomitant with a failure of recovery of HM (21.1+/-14.4% of baseline; P<0.001 compared with sham animals). IPC increased intracellular oxygenation (redox state of the copper centre of cytochrome oxidase; P<0.05 compared with rats receiving I/R alone) and flow in HM (70.9+/-17.1% of baseline; P<0.001 compared with rats receiving I/R alone). Hepatocellular injury was significantly reduced with IPC compared with I/R injury alone (alanine aminotransferase, 474.8+/-122.3 compared with 5436.3+/-984.7 units/l respectively; P<0.01; aspartate aminotransferase, 630.8+/-76.9 compared with 3166.3+/-379.6 units/l respectively; P<0.01]. In conclusion, IPC has a hepatoprotective effect against I/R injury in livers with moderate steatosis. These data may have important clinical implications in liver surgery and transplantation.

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“…Haemorheological disorders contribute to decreased organ perfusion, impaired microcirculation, and the occurrence of diabetic complications. Experimental studies on animal models with fatty liver have shown that fatty infiltration reduces hepatic blood flow and parenchymal microcirculation [5,6]. A significant reduction in hepatic microcirculation has been found in liver donors with steatosis compared with that in normal liver donors [7].…”

Section: Introductionmentioning

confidence: 98%

Type 2 diabetic patients with non-alcoholic fatty liver disease exhibit significant haemorheological abnormalities

Wang

Zou

et al. 2011

Front. Med.

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Haemorheological abnormalities have been described in diabetes mellitus, as well as in non-alcoholic fatty liver disease (NAFLD). However, the relationship between the changes in liver fat content and haemorheology is unknown. The current study aims to show the correlation between haemorheological parameters and intrahepatic lipid content (IHLC) in patients with type 2 diabetes. The serum biochemical markers, such as fasting plasma glucose (FPG), haemoglobin A1c (HbA1c), liver enzymes, lipid profiles, and haemorheological properties, were examined. IHLC was quantified using proton magnetic resonance spectroscopy ((1)H-MRS) scanning of the liver. A significant correlation was observed between IHLC and whole blood viscosity at high, middle, and low shear rates. IHLC also positively correlated with haematocrit, the reduced whole blood viscosity at low and middle shear rates, and the erythrocyte aggregation index. Diabetic patients with NAFLD exhibited significant haemorheological abnormalities compared with patients without NAFLD. In summary, haemorheological disorders are linked to non-alcoholic fatty liver in type 2 diabetes.

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Hepatic Microcirculation in Zucker Fatty Rats

Cited by 33 publications

References 6 publications

Hepatic Indocyanine Green Uptake and Excretion in a Rabbit Model of Steatosis

Hepatic Indocyanine Green Uptake and Excretion in a Rabbit Model of Steatosis

Effect of ischaemic preconditioning on hepatic oxygenation, microcirculation and function in a rat model of moderate hepatic steatosis

Type 2 diabetic patients with non-alcoholic fatty liver disease exhibit significant haemorheological abnormalities

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