Remote ischaemic preconditioning of the hind limb reduces experimental liver warm ischaemia–reperfusion injury

2006 ◽  
Vol 93 (6) ◽  
pp. 762-768 ◽  
Author(s):  
S. Kanoria ◽  
R. Jalan ◽  
N. A. Davies ◽  
A. M. Seifalian ◽  
R. Williams ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Hind Limb ◽  
Ischaemic Preconditioning ◽  
Ischaemia Reperfusion Injury ◽  
Ischaemia Reperfusion ◽  
Warm Ischaemia ◽  
Remote Ischaemic Preconditioning ◽  
Experimental Liver

Nitric oxide is an essential mediator of the protective effects of remote ischaemic preconditioning in a mouse model of liver ischaemia/reperfusion injury

2011 ◽  
Vol 121 (6) ◽  
pp. 257-266 ◽  
Author(s):  
Mahmoud Abu-Amara ◽  
Shi Yu Yang ◽  
Alberto Quaglia ◽  
Peter Rowley ◽  
Achala De Mel ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Reperfusion Injury ◽  
Protective Effects ◽  
Ischaemic Preconditioning ◽  
Ischaemia Reperfusion Injury ◽  
Hepatic Microcirculation ◽  
Ischaemia Reperfusion ◽  
Liver Transaminases ◽  
Remote Ischaemic Preconditioning

NO (nitric oxide) may protect the liver from IR (ischaemia/reperfusion) injury. RIPC (remote ischaemic preconditioning) also protects against liver IR injury; however, the molecular mediator(s) of RIPC are currently unknown. The aim of the present study was to assess the role of NO in hindlimb RIPC-induced protection against liver IR injury. Mice were allocated to the following groups: sham group; RIPC group (six cycles of 4×4 min IR of hindlimb); IR group [40 min lobar (70%) hepatic ischaemia and 2-h reperfusion]; RIPC+IR group (RIPC followed by IR group procedures); and C-PTIO [2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide potassium salt]+RIPC+IR group [C-PTIO (a direct NO scavenger) was administered, followed by the RIPC+IR group procedure]. Hepatic MBF (microcirculatory blood flow) was measured throughout the experiment. Circulating NOx (nitrite and nitrate) levels, plasma liver transaminases, hepatic histopathological and TEM (transmission electron microscopy) studies were performed at the end of the experiment. NOx concentrations were significantly elevated (P<0.05) in the RIPC and RIPC+IR groups. Compared with liver IR alone, RIPC+IR preserved hepatic MBF during liver reperfusion (P<0.05). In contrast, C-PTIO+RIPC+IR reduced MBF compared with RIPC+IR (P<0.05). RIPC+IR reduced plasma transaminases (P<0.05), and histopathological and ultrastructural features of injury compared with IR alone. The protective effects of RIPC+IR in reducing liver IR injury were abrogated in the group that received antecedent C-PTIO (C-PTIO+RIPC+IR). In conclusion, NO is an essential mediator of the protection afforded by hindlimb RIPC against liver IR injury. The mechanisms underlying this protection involve preservation of the sinusoidal structure and maintenance of blood flow through the hepatic microcirculation.

scholarly journals Modulation of microcirculatory changes in the late phase of hepatic ischaemia–reperfusion injury by remote ischaemic preconditioning

HPB ◽  
2012 ◽  
Vol 14 (2) ◽  
pp. 87-97 ◽  
Author(s):  
Niteen Tapuria ◽  
Sameer Junnarkar ◽  
Mahmoud Abu-Amara ◽  
Barry Fuller ◽  
Alexander M. Seifalian ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Late Phase ◽  
Ischaemic Preconditioning ◽  
Ischaemia Reperfusion Injury ◽  
Ischaemia Reperfusion ◽  
Remote Ischaemic Preconditioning

Bradykinin does not mediate remote ischaemic preconditioning or ischaemia-reperfusion injury in vivo in man

Heart ◽  
2011 ◽  
Vol 97 (22) ◽  
pp. 1857-1861 ◽  
Author(s):  
C. M. Pedersen ◽  
M. R. Schmidt ◽  
G. Barnes ◽  
H. E. Botker ◽  
R. K. Kharbanda ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischaemic Preconditioning ◽  
Ischaemia Reperfusion Injury ◽  
Ischaemia Reperfusion ◽  
Remote Ischaemic Preconditioning
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