PMID- 8538180
OWN - NLM
STAT- MEDLINE
DCOM- 19960208
LR  - 20131121
IS  - 0022-4804 (Print)
IS  - 0022-4804 (Linking)
VI  - 59
IP  - 6
DP  - 1995 Dec
TI  - Role of endogenous nitric oxide in ischemia-reperfusion injury in rat liver.
PG  - 772-9
AB  - Evidence has accumulated that oxygen-derived free radicals contribute to the 
      cellular damage induced by ischemia-reperfusion. It has been suggested that 
      nitric oxide (NO) may act as a protective factor in ischemia-reperfusion injury 
      since NO increases blood flow and may scavenge oxyradicals. Nevertheless, 
      controversy exists as to the role of NO. This study was designed to clarify the 
      role of endogenous NO in ischemia-reperfusion-induced liver injury in rats in 
      vivo. Wistar rats weighing 250-300 g were divided into three groups: (1) 
      untreated group (Control); (2) NG-nitro-L-arginine, a specific inhibitor of NO 
      production (L-NNA); and (3) L-arginine-pretreated L-NNA group (AR+L-NNA). 
      Occlusion of all vessels to the median and left hepatic lobes (60 min) was 
      followed by reperfusion for 1 or 24 hr. L-NNA was administered before ischemia as 
      a 10 mg/kg bolus. L-Arginine was given just before L-NNA administration as a 100 
      mg/kg bolus. Administration of L-NNA resulted in endothelial cell injury 
      characterized by the elevation of serum hyaluronic acid as well as the reduction 
      of hepatic tissue blood flow, and the recovery of hepatic adenosine triphosphate 
      was depressed compared with the control after both 1 and 24 hr of reperfusion. 
      Furthermore, the leakages of various liver enzymes and lipid peroxide were also 
      increased, associated with histological damage. This effect of L-NNA was 
      completely abolished by pretreatment with L-arginine. These results suggest that 
      endogenous NO provides a protective effect against ischemia-reperfusion injury in 
      rat liver.
FAU - Kobayashi, H
AU  - Kobayashi H
AD  - Department of Surgery II, Nagoya University School of Medicine, Japan.
FAU - Nonami, T
AU  - Nonami T
FAU - Kurokawa, T
AU  - Kurokawa T
FAU - Takeuchi, Y
AU  - Takeuchi Y
FAU - Harada, A
AU  - Harada A
FAU - Nakao, A
AU  - Nakao A
FAU - Takagi, H
AU  - Takagi H
LA  - eng
PT  - Journal Article
PL  - United States
TA  - J Surg Res
JT  - The Journal of surgical research
JID - 0376340
RN  - 0 (Adenine Nucleotides)
RN  - 0 (Lipid Peroxides)
RN  - 2149-70-4 (Nitroarginine)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - 9004-61-9 (Hyaluronic Acid)
RN  - 94ZLA3W45F (Arginine)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase)
SB  - IM
MH  - Adenine Nucleotides/metabolism
MH  - Animals
MH  - Arginine/analogs & derivatives/pharmacology
MH  - Hyaluronic Acid/metabolism
MH  - Lipid Peroxides/metabolism
MH  - Liver/*blood supply/cytology/enzymology/metabolism
MH  - Male
MH  - Nitric Oxide/*physiology
MH  - Nitric Oxide Synthase/antagonists & inhibitors
MH  - Nitroarginine
MH  - Osmolar Concentration
MH  - Rats
MH  - Rats, Wistar
MH  - Reperfusion Injury/pathology/*physiopathology
EDAT- 1995/12/01 00:00
MHDA- 1995/12/01 00:01
CRDT- 1995/12/01 00:00
PHST- 1995/12/01 00:00 [pubmed]
PHST- 1995/12/01 00:01 [medline]
PHST- 1995/12/01 00:00 [entrez]
AID - S0022-4804(85)71238-3 [pii]
AID - 10.1006/jsre.1995.1238 [doi]
PST - ppublish
SO  - J Surg Res. 1995 Dec;59(6):772-9. doi: 10.1006/jsre.1995.1238.