The Role of Tissue Factor in Renal Ischemic Reperfusion Injury of the Rat

2002 ◽  
Vol 102 (2) ◽  
pp. 102-109 ◽  
Author(s):  
Hidetaka Ushigome ◽  
Hajime Sano ◽  
Masahiko Okamoto ◽  
Yayoi Kadotani ◽  
Kenji Nakamura ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Tissue Factor ◽  
Ischemic Reperfusion Injury ◽  
Ischemic Reperfusion ◽  
Renal Ischemic Reperfusion Injury

scholarly journals Role of IL-1 in renal ischemic reperfusion injury.

1998 ◽  
Vol 9 (4) ◽  
pp. 614-619 ◽  
Author(s):  
M Haq ◽  
J Norman ◽  
S R Saba ◽  
G Ramirez ◽  
H Rabb
Keyword(s):  
Renal Function ◽  
Reperfusion Injury ◽  
Interleukin 1 ◽  
Organ Injury ◽  
Central Component ◽  
Ischemic Reperfusion Injury ◽  
Ischemic Reperfusion ◽  
And Control ◽  
Renal Ischemic Reperfusion Injury

Interleukin-1 (IL-1) is a central component of many acute inflammatory processes. Blocking IL-1 receptor (IL-1R) with IL-1R antagonist (IL-1Ra) has attenuated ischemic reperfusion injury in brain, heart, and liver models. However, the role of IL-1 in renal ischemic reperfusion injury (IRI) is not known. Therefore, the role of IL-1 in renal IRI was evaluated using the complementary approaches of IL-1R blockade in wild-type mice in addition to the study of renal IRI in IL-1R knockout (KO) mice. Ischemia was induced by bilateral renal pedicle clamping for 30 min. IL-1Ra was administered at 10 mg/kg every 4 h, high doses that have been protective in previous organ injury models in mice. IL-1R KO animals, previously characterized as insensitive to IL-1, had the absence of IL-1R1 confirmed by DNA blots. IL-1Ra, IL-1R KO, and control groups had similar elevations of blood urea nitrogen (114 +/- 13, 133 +/- 11, and 120 +/- 11 mg/dl) and serum creatinine (1.7 +/- 0.3, 2.1 +/- 0.2, and 1.6 +/- 0.3 mg/dl) 24 h after ischemia. Furthermore, acute tubular necrosis scores were also similar in IL-1Ra-treated mice (3.0 +/- 0.3), IL-1R KO mice (2.7 +/- 0.3), and control mice (3.1 +/- 0.2). However, both IL-1Ra and IL-1R KO groups, compared with control animals, developed significantly less infiltration of polymorphonuclear leukocytes per 10 high-power fields in postischemic renal tissue (1111 +/- 228 and 967 +/- 198 versus 1820 +/- 190, P < 0.05). In contrast to the comparable renal functions at 24 h, recovery of renal function was significantly accelerated in the IL-1R KO group compared with control at both 48 (P < 0.05) and 72 (P < 0.05) h. Recovery in the IL-1Ra group was similar to that in the control animals. These data demonstrate that IL-1 is unlikely to be beneficial in the recovery of renal function after ischemia and may play a deleterious role.

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