Controlled reperfusion reduces hemorheological alterations in a porcine infrarenal aortic-clamping ischemia-reperfusion model

2016 ◽  
Vol 63 (3) ◽  
pp. 235-243 ◽  
Author(s):  
P. Kenyeres ◽  
L. Sinay ◽  
G. Jancso ◽  
M. Rabai ◽  
A. Toth ◽  
...  
2021 ◽  
Vol 29 (3) ◽  
pp. 320-329
Author(s):  
Tünay Kurtoğlu ◽  
Selim Durmaz ◽  
Ömer Faruk Rahman ◽  
Nesibe Kahraman Çetin ◽  
Mustafa Yılmaz ◽  
...  

Background: This study aims to investigate the effects of 2-aminoethoxydiphenyl borate (2-APB) on aortic clamping-induced lung and kidney tissue oxidation, tissue inflammation, and histological damage in a rat model. Methods: A total of 28 adult female Wistar albino rats were randomly allocated to four equal groups: Control group, ischemia-reperfusion group, dimethyl sulfoxide group, and 2-APB group. Animals in the control group underwent median laparotomy. In the remaining groups, supra-celiac aorta was clamped for 45 min and, then, reperfusion was constituted for 60 min. The 2-APB (2 mg/kg) was administered before clamping. The remaining groups received saline (ischemia-reperfusion group) or dimethyl sulfoxide (dimethyl sulfoxide group). Kidney and lung tissue samples were harvested at the end of reperfusion. Results: Aortic occlusion caused increased tissue total oxidant status and reduced total antioxidant status and glutathione levels in the ischemia-reperfusion and dimethyl sulfoxide groups. Tissue interleukin-1 beta and tumor necrosis factor-alpha levels, nuclear factor kappa beta activation, and histological damage severity scores were also higher in these groups. The 2-APB treatment eliminated the increase in total oxidant status and the decrease in total antioxidant status and glutathione levels. It also caused a decrease in the interleukin-1 beta levels, although it did not significantly alter the tumor necrosis factor-alpha levels, nuclear factor kappa beta immunoreactivity, and histological damage scores. Conclusion: Borate exerted a beneficial antioxidant effect as evidenced by reduced oxidative stress; however, it did not inhibit nuclear factor kappa beta activation and prevent histological damage in supra-celiac aortic clamping-induced kidney and lung injury in rats.


2008 ◽  
Vol 23 (1) ◽  
pp. 44-48 ◽  
Author(s):  
S. Fehmi Katircioglu ◽  
Mustafa Seren ◽  
A. Ihsan Parlar ◽  
Nilufer N. Turan ◽  
Yasemin Manavbasi ◽  
...  

2006 ◽  
Vol 34 (5) ◽  
pp. 1415-1419 ◽  
Author(s):  
Olivier Collange ◽  
Fabienne Tamion ◽  
Stephane Chanel ◽  
Guy Hue ◽  
Vincent Richard ◽  
...  

2003 ◽  
Vol 41 (6) ◽  
pp. 328
Author(s):  
James E. Davies ◽  
Steven P. Goldberg ◽  
Stanley B. Digerness ◽  
Cheryl R. Killingsworth ◽  
Charles R. Katholi ◽  
...  

2003 ◽  
Vol 76 (4) ◽  
pp. 1252-1258 ◽  
Author(s):  
James E. Davies ◽  
Stanley B. Digerness ◽  
Steven P. Goldberg ◽  
Cheryl R. Killingsworth ◽  
Charles R. Katholi ◽  
...  

2015 ◽  
Vol 93 (4) ◽  
pp. 269-274 ◽  
Author(s):  
Omer Erkan Yapca ◽  
Serkan Kumbasar ◽  
Suleyman Salman ◽  
Oguzhan Yarali ◽  
Ebru Sener ◽  
...  

High numbers of proinflammatory cells (PMNLs), which are carried by the blood to ischemic tissue during reperfusion, are considered responsible for inducing the inflammatory response that occurs in ischemia–reperfusion (I/R) injury. Our objective was to determine the controlled reperfusion (CR) interval duration (CRID) that would minimize the injury caused by the PMNLs that infiltrate ischemic tissue. Animal groups were divided into the following groups: Sham group, ovarian I/R group (OIR), and ovarian ischemia controlled-reperfusion groups OICR-1, OICR-2, OICR-3, OICR-4, OICR-5, OICR-6, which had their ovarian artery opened and then closed for 10, 8, 6, 4, 2, or 1 s, respectively. The results show that the COX-2 activity and the gene expression decreased while the COX-1 activity and the gene expression were found to be increased in parallel to the shortening of the period in CRID. From the histopathological examinations, the findings of hemorrhage, edema, congested vascular structures, degenerated cells, and migration and adhesion of PMNLs were scaled as follows: Sham group < OICR-6 < OICR-5 < OICR-4 < OICR-3 < OICR-2 < OICR-1. The results from the histopathological assessments were consistent with the molecular and biochemical findings. In conclusion, our findings suggest that increased COX-2 activity plays a role in I/R injury of the rat ovary, and that controlled reperfusion for 3, 2, or 1 s following 2 h of ischemia may attenuate the effects of I/R injury.


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