Marked Difference in Tumor Necrosis Factor-α Expression in Warm Ischemia– and Cold Ischemia–Reperfusion of the Rat Liver

Cryobiology ◽  
2000 ◽  
Vol 41 (4) ◽  
pp. 301-314 ◽  
Author(s):  
Martina Lutterová ◽  
Zoltán Szatmáry ◽  
Marián Kukan ◽  
Daniel Kuba ◽  
Katarı́na Vajdová
2014 ◽  
Vol 20 (8) ◽  
pp. 904-911 ◽  
Author(s):  
Xianwa Niu ◽  
Wen Hua Huang ◽  
Bastiaan De Boer ◽  
Luc Delriviere ◽  
Ling Jun Mou ◽  
...  

1998 ◽  
Vol 85 (6) ◽  
pp. 2005-2011 ◽  
Author(s):  
Pavel L. Khimenko ◽  
G. J. Bagby ◽  
J. Fuseler ◽  
Aubrey E. Taylor

The effects of both recombinant rat tumor necrosis factor-α (TNF-α) and an anti-TNF-α antibody were studied in isolated buffer-perfused rat lungs subjected to either 45 min of nonventilated [ischemia-reperfusion (I/R)] or air-ventilated (V˙/R) ischemia followed by 90 min of reperfusion and ventilation. In the I/R group, the vascular permeability, as measured by the filtration coefficient ( K fc), increased three- and fivefold above baseline after 30 and 90 min of reperfusion, respectively ( P < 0.001). Over the same time intervals, the K fc for theV˙/R group increased five- and tenfold above baseline values, respectively ( P < 0.001). TNF-α measured in the perfusates of both ischemic models significantly increased after 30 min of reperfusion. Recombinant rat TNF-α (50,000 U), placed into perfusate after baseline measurements, produced no measurable change in microvascular permeability in control lungs perfused over the same time period (135 min), but I/R injury was significantly enhanced in the presence of TNF-α. An anti-TNF-α antibody (10 mg/rat) injected intraperitoneally into rats 2 h before the lung was isolated prevented the microvascular damage in lungs exposed to both I/R and V˙/R ( P < 0.001). These results indicate that TNF-α is an essential component at the cascade of events that cause lung endothelial injury in short-term I/R andV˙/R models of lung ischemia.


Vascular ◽  
2014 ◽  
Vol 23 (1) ◽  
pp. 21-30 ◽  
Author(s):  
Volkan Aksu ◽  
Volkan Yüksel ◽  
Serchat Chousein ◽  
Ebru Taştekin ◽  
Şahin İşcan ◽  
...  

Purpose We aimed to examine the effects of sildenafil and n-acetylcystein on ischemia/reperfusion injury in femoral artery endothelium and gastrocnemius muscle. Basic methods 32 rats of Sprague-Dawley breed were randomly divided into four groups (n = 8). Median laparotomy was performed, then a 120-minute ischemia was created by microvascular clamping of infrarenal aorta, followed by the release of clamping. In sildenafil group, 1 mg/kg of sildenafil infusion and in the n-acetylcystein group, 100 mg/kg of n-acetylcystein infusion was administered after release of clamps. Blood samples and tissue samples of femoral artery and gastrocnemius muscle were extracted for a histopathological evaluation. Principal findings Serum levels of malondialdehyde in ischemia/reperfusion group (6.16 ± 0.79) were higher compared to the control group (4.69 ± 0.33), whereas a significant decrease was detected in sildenafil (5.17 ± 0.50) and n-acetylcystein (4.96 ± 0.49) groups. Femoral artery tissue sections of the control group, mean tumor necrosis factor alpha and hypoxy-induced factor-1 alpha immunoreactivity were found to be negative. In the ischemia/reperfusion group, mean tumor necrosis factor α immunoreactivity was intense and mean hypoxy-induced factor-1 alpha immunoreactivity was 51–75%. In the ischemia/reperfusion + Sildenafil and ischemia/reperfusion + NAS groups, mean tumor necrosis factor α immunoreactivity was slight and mean hypoxy-induced factor-1 alpha immunoreactivity was 26–50%. Conclusions In conclusion, sildenafil and n-acetylcystein may reduce femoral artery endothelium and gastrocnemius muscle injury following lower extremity ischemia/reperfusion.


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