Effect of normothermic perfusion using fructose-1,6-bisphosphate for maintenance of liver function during in situ extended hepatectomy by the total hepatic vascular exclusion technique.
BACKGROUND
Recently, hepatic surgery has made remarkable progress, and it is important to use appropriate liver perfusion. We evaluated the effect of normothermic liver perfusion with the addition of fructose-1, 6-bisphosphate (FBP) and oxygenation to maintain liver parenchymal, non-parenchymal, and Kupffer cell function.


METHODS
The rats were divided into five groups according to the perfusate and continuous perfusion was performed: Control group = 4 degrees C lactate Ringer with 10% glucose (LRG) solution; normothermic group = 25 degrees C LRG solution; normothermic oxygenated group = 25 degrees C oxygenated LRG solution; normothermic FBP group = 25 degrees C LRG solution with addition of 10 mmol/L FBP; normothermic oxygenated FBP group = 25 degrees C oxygenated LRG solution with addition of 10 mmol/L FBP. Parameters under evaluation were oxygen consumption, liver energy level (adenosine triphosphate, total adenine nucleotide), glutathione, lipid peroxide, hyaluronic acid uptake ratio, apoptosis, and histomorphology. Moreover, we studied the effect of FBP and normothermia on Kupffer cells activation in vitro.


RESULTS
Liver energy level was lower in the normothermic group than the control group. But, it was improved by oxidation or addition of FBP, and it was satisfactorily maintained up to 120 min in the group with normothermic oxygenated FBP. Hyaluronic acid uptake was maintained highly at all times as measured in normothermic oxygenated FBP group. The uptake of lipopolysaccharide was significantly higher as a result of adding FBP, compared with that in the control group and the normothermic group. Moreover, the apoptotic index in the liver was decreased in normothermic FBP group compared to control group.


CONCLUSIONS
The normothermic liver perfusion under additional FBP and oxygenation protects both parenchymal and non-parenchymal cells from reperfusion injury.
Uemura
Ryuichiro
R
Second Department of Surgery, Wakayama Medical University, School of Medicine, Wakayama, Japan.
Uchiyama
Kazuhisa
K
Ozawa
Satoru
S
Yamaue
Hiroki
H
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D017209:Apoptosis; D004734:Energy Metabolism / Q000187:drug effects; D005635:Fructosediphosphates / Q000494:pharmacology*; D006498:Hepatectomy / Q000379:methods*; D022781:Hepatocytes / Q000166:cytology / Q000378:metabolism; D020287:In Situ Nick-End Labeling; D007552:Isotonic Solutions / Q000494:pharmacology; D007728:Kupffer Cells / Q000166:cytology / Q000378:metabolism; D015227:Lipid Peroxidation / Q000187:drug effects; D008099:Liver / Q000166:cytology / Q000378:metabolism* / Q000601:surgery*; D008102:Liver Circulation; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects; D010100:Oxygen / Q000494:pharmacology; D010477:Perfusion / Q000379:methods*; D051381:Rats; D017207:Rats, Sprague-Dawley; D020127:Recovery of Function / Q000187:drug effects; D000077325:Ringer's Lactate; D013696:Temperature
D005635:Fructosediphosphates; D007552:Isotonic Solutions; D000077325:Ringer's Lactate; D000255:Adenosine Triphosphate; C029063:fructose-1,6-diphosphate; D010100:Oxygen