Neutrophil Mediated Remote Organ Injury after Lower Torso Ischemia and Reperfusion Is Selectin and Complement Dependent

2000 ◽  
Vol 48 (1) ◽  
pp. 32 ◽  
Author(s):  
Constantinos Kyriakides ◽  
William G. Austen ◽  
Yong Wang ◽  
Joanne Favuzza ◽  
Francis D. Moore ◽  
...  
2021 ◽  
Vol 22 (18) ◽  
pp. 9911
Author(s):  
Hannah V. Hayes ◽  
Vivian Wolfe ◽  
Michael O’Connor ◽  
Nick C. Levinsky ◽  
Giovanna Piraino ◽  
...  

Mesenteric ischemia and reperfusion (I/R) injury can ensue from a variety of vascular diseases and represents a major cause of morbidity and mortality in intensive care units. It causes an inflammatory response associated with local gut dysfunction and remote organ injury. Adenosine monophosphate-activated protein kinase (AMPK) is a crucial regulator of metabolic homeostasis. The catalytic α1 subunit is highly expressed in the intestine and vascular system. In loss-of-function studies, we investigated the biological role of AMPKα1 in affecting the gastrointestinal barrier function. Male knock-out (KO) mice with a systemic deficiency of AMPKα1 and wild-type (WT) mice were subjected to a 30 min occlusion of the superior mesenteric artery. Four hours after reperfusion, AMPKα1 KO mice exhibited exaggerated histological gut injury and impairment of intestinal permeability associated with marked tissue lipid peroxidation and a lower apical expression of the junction proteins occludin and E-cadherin when compared to WT mice. Lung injury with neutrophil sequestration was higher in AMPKα1 KO mice than WT mice and paralleled with higher plasma levels of syndecan-1, a biomarker of endothelial injury. Thus, the data demonstrate that AMPKα1 is an important requisite for epithelial and endothelial integrity and has a protective role in remote organ injury after acute ischemic events.


2014 ◽  
Vol 2014 ◽  
pp. 1-13 ◽  
Author(s):  
Constantinos Nastos ◽  
Konstantinos Kalimeris ◽  
Nikolaos Papoutsidakis ◽  
Marios-Konstantinos Tasoulis ◽  
Panagis M. Lykoudis ◽  
...  

Liver ischemia/reperfusion injury has been extensively studied during the last decades and has been implicated in the pathophysiology of many clinical entities following hepatic surgery and transplantation. Apart from its pivotal role in the pathogenesis of the organ’s post reperfusion injury, it has also been proposed as an underlying mechanism responsible for the dysfunction and injury of other organs as well. It seems that liver ischemia and reperfusion represent an event with “global” consequences that influence the function of many remote organs including the lung, kidney, intestine, pancreas, adrenals, and myocardium among others. The molecular and clinical manifestation of these remote organs injury may lead to the multiple organ dysfunction syndrome, frequently encountered in these patients. Remote organ injury seems to be in part the result of the oxidative burst and the inflammatory response following reperfusion. The present paper aims to review the existing literature regarding the proposed mechanisms of remote organ injury after liver ischemia and reperfusion.


1997 ◽  
Vol 41 (6) ◽  
pp. 713-718 ◽  
Author(s):  
H. YAMADA ◽  
I. KUDOH ◽  
H. NISHIZAWA ◽  
K. KANEKO ◽  
H. MIYAZAKI ◽  
...  

2021 ◽  
Vol 28 (9) ◽  
pp. 1671
Author(s):  
Levent Demirtas ◽  
Cebrail Gursul ◽  
Ahmet Gurbuzel ◽  
Ilyas Sayar ◽  
Mehmet Gurbuzel ◽  
...  

2000 ◽  
Vol 93 (6) ◽  
pp. 1407-1412 ◽  
Author(s):  
Ulrike Korth ◽  
Günter Merkel ◽  
Francisco F. Fernandez ◽  
Oliver Jandewerth ◽  
Günes Dogan ◽  
...  

Background Tourniquets are often used as part of orthopedic surgery but may cause local and remote organ injury. The authors hypothesized that the procedures used to induce ischemia (circulatory occlusion or exsanguination) may have differential effects on the metabolic state of the muscle that should be reflected in the interstitial levels of metabolites. Methods Microdialysis probes were implanted in both quadriceps femoris muscles of 18 patients. Interstitial fluid was obtained during tourniquet-induced ischemia and reperfusion and was analyzed for glucose, lactate, choline, and purines by high-performance liquid chromatography. Results At a flow rate of 2 microl/min, the average baseline concentrations in the dialysate were 2.5 mM for glucose, 1.7 mM for lactate, 5.2 microM for choline, and 14.3 microM for hypoxanthine. Circulatory occlusion by tourniquet caused a 40% decrease of the extracellular glucose concentration within 30 min. Concomitantly, the interstitial levels of lactate and hypoxanthine increased in a linear fashion to 206% (lactate) and 241% (hypoxanthine) of basal values. The extracellular concentration of choline was also significantly elevated. After exsanguination, the glucose levels were significantly more reduced (by 65%), and the levels of lactate (to 268%) and hypoxanthine (to 286%) were more increased than after circulatory occlusion alone. Conclusion Our microdialysis results demonstrate that the interstitial concentrations of glucose, lactate, and hypoxanthine, which are indicators of tissue ischemia, change more prominently after exsanguination than after circulatory occlusion alone.


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