Ischemia reperfusion phenomena during aortic surgery

Author(s):  
Ihor Huk
2016 ◽  
Vol 311 (3) ◽  
pp. F567-F575 ◽  
Author(s):  
Saskia J. H. Brinkmann ◽  
Nikki Buijs ◽  
Mechteld A. R. Vermeulen ◽  
Efraim Oosterink ◽  
Henk Schierbeek ◽  
...  

Postoperative renal failure is a common complication after open repair of an abdominal aortic aneurysm. The amino acid arginine is formed in the kidneys from its precursor citrulline, and citrulline is formed from glutamine in the intestines. Arginine enhances the function of the immune and cardiovascular systems, which is important for recovery after surgery. We hypothesized that renal arginine production is diminished after ischemia-reperfusion injury caused by clamping of the aorta during open abdominal aortic surgery and that parenteral glutamine supplementation might compensate for this impaired arginine synthesis. This open-label clinical trial randomized patients who underwent clamping of the aorta during open abdominal aortic surgery to receive a perioperative supplement of intravenous alanyl-glutamine (0.5 g·kg−1·day−1; group A, n = 5) or no supplement ( group B, n = 5). One day after surgery, stable isotopes and tracer methods were used to analyze the metabolism and conversion of glutamine, citrulline, and arginine. Whole body plasma flux of glutamine, citrulline, and arginine was significantly higher in group A than in group B (glutamine: 391 ± 34 vs. 258 ± 19 μmol·kg−1·h−1, citrulline: 5.7 ± 0.4 vs. 2.8 ± 0.4 μmol·kg−1·h−1, and arginine: 50 ± 4 vs. 26 ± 2 μmol·kg−1·h−1, P < 0.01), as was the synthesis of citrulline from glutamine (4.8 ± 0.7 vs. 1.6 ± 0.3 μmol·kg−1·h−1), citrulline from arginine (2.3 ± 0.3 vs. 0.96 ± 0.1 μmol·kg−1·h−1), and arginine from glutamine (7.7 ± 0.4 vs. 2.8 ± 0.2 μmol·kg−1·h−1), respectively ( P < 0.001 for all). In conclusion, the production of citrulline and arginine is severely reduced after clamping during aortic surgery. This study shows that an intravenous supplement of glutamine increases the production of citrulline and arginine and compensates for the inhibitory effect of ischemia-reperfusion injury.


2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Ping Zhu ◽  
Jia-xin Li ◽  
Masayuki Fujino ◽  
Jian Zhuang ◽  
Xiao-Kang Li

During aortic surgery, interruption of spinal cord blood flow might cause spinal cord ischemia-reperfusion injury (IRI). The incidence of spinal cord IRI after aortic surgery is up to 28%, and patients with spinal cord IRI might suffer from postoperative paraplegia or paraparesis. Spinal cord IRI includes two phases. The immediate spinal cord injury is related to acute ischemia. And the delayed spinal cord injury involves both ischemic cellular death and reperfusion injury. Inflammation is a subsequent event of spinal cord ischemia and possibly a major contributor to spinal cord IRI. However, the development of inflammatory mediators is incompletely demonstrated. And treatments available for inflammation in spinal cord IRI are insufficient. Improved understanding about spinal cord IRI and the development of inflammatory cells and cytokines in this process will provide novel therapeutic strategies for spinal cord IRI. Inflammatory cytokines (e.g., TNF-αand IL-1) may play an important role in spinal cord IRI. For treatment of several intractable autoimmune diseases (e.g., rheumatoid arthritis), where inflammatory cytokines are involved in disease progression, anti-inflammatory cytokine antagonist is now available. Hence, there is great potential of anti-inflammatory cytokine antagonist for therapeutic use of spinal cord IRI. We here review the mediators and several possibilities of treatment in spinal cord IRI.


2021 ◽  
Vol 36 (4) ◽  
pp. 1361-1369
Author(s):  
Eda Balcı ◽  
Zeliha A. Demir ◽  
Hülya Yiğit Özay ◽  
Kübra Vardar ◽  
Gülsüm Karduz ◽  
...  

Medicina ◽  
2019 ◽  
Vol 55 (5) ◽  
pp. 187
Author(s):  
Onur M. Yaman ◽  
Ibrahim Guner ◽  
Gulcan Guntas ◽  
Osman Fuat Sonmez ◽  
Gamze Tanriverdi ◽  
...  

Background and objectives: Ischemia–reperfusion (IR) caused by infrarenal abdominal aorta cross-clamping is an important factor in the development of ischemia–reperfusion injury in various distant organs. Materials and Methods: We investigated potential antioxidant/anti-inflammatory effects of thymosin beta 4 (Tβ4) in a rat model of abdominal aortic surgery-induced IR. Tβ4 (10 mg/kg, intravenous (i.v.)) was administered to rats with IR (90-min ischemia, 180-min reperfusion) at two different periods. One group received Tβ4 1 h before ischemia, and the other received 15 min before the reperfusion period. Results: Results were compared to control and non-Tβ4-treated rats with IR. Serum, bronchoalveolar lavage fluid and lung tissue levels of oxidant parameters were higher, while antioxidant levels were lower in the IR group compared to control. IR also increased inflammatory cytokine levels. Tβ4 reverted these parameters in both Tβ4-treated groups compared to the untreated IR group. Conclusions: Since there is no statistical difference between the prescribed results of both Tβ4-treated groups, our study demonstrates that Tβ4 reduced lung oxidative stress and inflammation following IR and prevented lung tissue injury regardless of timing of administration.


2009 ◽  
Vol 157 (1) ◽  
pp. 48-54 ◽  
Author(s):  
Alexander D. Cornet ◽  
Sandra D.K. Kingma ◽  
Ronald J. Trof ◽  
Willem Wisselink ◽  
A.B. Johan Groeneveld

2021 ◽  
Vol 12 ◽  
Author(s):  
Xiao Ling ◽  
Jun Lu ◽  
Jun Yang ◽  
Hanjun Qin ◽  
Xingqi Zhao ◽  
...  

Paralysis or paraplegia caused by transient or permanent spinal cord ischemia–reperfusion injury (SCIRI) remains one of the most devastating post-operative complications after thoracoabdominal aortic surgery, even though perioperative strategies and surgical techniques continue to improve. Uncovering the molecular and cellular pathophysiological processes in SCIRI has become a top priority. Recently, the expression, function, and mechanism of non-coding RNAs (ncRNAs) in various diseases have drawn wide attention. Non-coding RNAs contain a variety of biological functions but do not code for proteins. Previous studies have shown that ncRNAs play a critical role in SCIRI. However, the character of ncRNAs in attenuating SCIRI has not been systematically summarized. This review article will be the first time to assemble the knowledge of ncRNAs regulating apoptosis, inflammation, autophagy, and oxidative stress to attenuate SCIRI. A better understanding of the functional significance of ncRNAs following SCIRI could help us to identify novel therapeutic targets and develop potential therapeutic strategies. All the current research about the function of nRNAs in SCIRI will be summarized one by one in this review.


2014 ◽  
Vol 189 (1) ◽  
pp. 96-105 ◽  
Author(s):  
Ibrahim Guner ◽  
Muhittin O. Yaman ◽  
Ugur Aksu ◽  
Duygu Uzun ◽  
Hayriye Erman ◽  
...  

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Feng Sun ◽  
Haiwei Zhang ◽  
Jianhui Shi ◽  
Tianwen Huang ◽  
Yansong Wang

Spinal cord ischemia/reperfusion (SCI/R) injury is a devastating complication usually occurring after thoracoabdominal aortic surgery. However, it remains unsatisfactory for its intervention by using pharmacological strategies. Oxidative stress is a main pharmacological process involved in SCI/R, which will elicit downstream programmed cell death such as the novel defined necroptosis. Astragalin is a bioactive natural flavonoid with a wide spectrum of pharmacological activities. Herein, we firstly evaluated the effect of astragalin to oxidative stress as well as the possible downstream necroptosis after SCI/R in mice. Our results demonstrated that astragalin improves the ethological score and histopathological deterioration of SCI/R mice. Astragalin mitigates oxidative stress and ameliorates inflammation after SCI/R. Astragalin blocks necroptosis induced by SCI/R. That is, the amelioration of astragalin to the motoneuron injury and histopathological changes. Indicators of oxidative stress, inflammation, and necroptosis after SCI/R were significantly blocked. Summarily, we firstly illustrated the protection of astragalin against SCI/R through its blockage to the necroptosis at downstream of oxidative stress.


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