Low‐Intensity Photobiomodulation Decreases Neuropathic Pain in Paw Ischemia‐Reperfusion and Spared Nervus Ischiadicus Injury Experimental Models

Pain Practice ◽  
2020 ◽  
Vol 20 (4) ◽  
pp. 371-386
Author(s):  
Glauce R. Pigatto ◽  
Maiara H.S. Quinteiro ◽  
Ricardo L. Nunes‐de‐Souza ◽  
Norberto C. Coimbra ◽  
Nivaldo A. Parizotto
Keyword(s):  
Neuropathic Pain ◽  
Ischemia Reperfusion ◽  
Experimental Models ◽  
Low Intensity ◽  
Nervus Ischiadicus

Effects of External Low Intensity Focused Ultrasound on Inflammatory Markers in Neuropathic Pain

2021 ◽  
pp. 135977
Author(s):  
Abigail Hellman ◽  
Alicia Clum ◽  
Teresa Maietta ◽  
Adithya Srikanthan ◽  
Vraj Patel ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Inflammatory Markers ◽  
Focused Ultrasound ◽  
Low Intensity

scholarly journals Ischemia-Reperfusion Injuries Assessment during Pancreas Preservation

2021 ◽  
Vol 22 (10) ◽  
pp. 5172
Author(s):  
Thomas Prudhomme ◽  
John F. Mulvey ◽  
Liam A. J. Young ◽  
Benoit Mesnard ◽  
Maria Letizia Lo Faro ◽  
...  
Keyword(s):  
Ex Vivo ◽  
Ischemia Reperfusion ◽  
Graft Function ◽  
Impedance Analysis ◽  
Experimental Models ◽  
Caspase Activation ◽  
Pancreas Perfusion ◽  
Number Of Factors ◽  
Pancreas Preservation ◽  
Metabolite Concentrations

Maintaining organ viability between donation and transplantation is of critical importance for optimal graft function and survival. To date in pancreas transplantation, static cold storage (SCS) is the most widely practiced method of organ preservation. The first experiments in ex vivo perfusion of the pancreas were performed at the beginning of the 20th century. These perfusions led to organ oedema, hemorrhage, and venous congestion after revascularization. Despite these early hurdles, a number of factors now favor the use of perfusion during preservation: the encouraging results of HMP in kidney transplantation, the development of new perfusion solutions, and the development of organ perfusion machines for the lung, heart, kidneys and liver. This has led to a resurgence of research in machine perfusion for whole organ pancreas preservation. This review highlights the ischemia-reperfusion injuries assessment during ex vivo pancreas perfusion, both for assessment in pre-clinical experimental models as well for future use in the clinic. We evaluated perfusion dynamics, oedema assessment, especially by impedance analysis and MRI, whole organ oxygen consumption, tissue oxygen tension, metabolite concentrations in tissue and perfusate, mitochondrial respiration, cell death, especially by histology, total cell free DNA, caspase activation, and exocrine and endocrine assessment.

scholarly journals Nrf2 at the heart of oxidative stress and cardiac protection

2018 ◽  
Vol 50 (2) ◽  
pp. 77-97 ◽  
Author(s):  
Qin M. Chen ◽  
Anthony J. Maltagliati
Keyword(s):  
Cancer Biology ◽  
Wound Repair ◽  
De Novo ◽  
Gene Knockout ◽  
Ischemia Reperfusion ◽  
Protein Translation ◽  
Experimental Models ◽  
Matrix Remodeling ◽  
Cardiac Protection ◽  
Nrf2 Protein

The NFE2L2 gene encodes the transcription factor Nrf2 best known for regulating the expression of antioxidant and detoxification genes. Gene knockout approaches have demonstrated its universal cytoprotective features. While Nrf2 has been the topic of intensive research in cancer biology since its discovery in 1994, understanding the role of Nrf2 in cardiovascular disease has just begun. The literature concerning Nrf2 in experimental models of atherosclerosis, ischemia, reperfusion, cardiac hypertrophy, heart failure, and diabetes supports its cardiac protective character. In addition to antioxidant and detoxification genes, Nrf2 has been found to regulate genes participating in cell signaling, transcription, anabolic metabolism, autophagy, cell proliferation, extracellular matrix remodeling, and organ development, suggesting that Nrf2 governs damage resistance as well as wound repair and tissue remodeling. A long list of small molecules, most derived from natural products, have been characterized as Nrf2 inducers. These compounds disrupt Keap1-mediated Nrf2 ubquitination, thereby prohibiting proteasomal degradation and allowing Nrf2 protein to accumulate and translocate to the nucleus, where Nrf2 interacts with sMaf to bind to ARE in the promoter of genes. Recently alternative mechanisms driving Nrf2 protein increase have been revealed, including removal of Keap1 by autophagy due to p62/SQSTM1 binding, inhibition of βTrCP or Synoviolin/Hrd1-mediated ubiquitination of Nrf2, and de novo Nrf2 protein translation. We review here a large volume of literature reporting historical and recent discoveries about the function and regulation of Nrf2 gene. Multiple lines of evidence presented here support the potential of dialing up the Nrf2 pathway for cardiac protection in the clinic.

scholarly journals Guidelines for experimental models of myocardial ischemia and infarction

2018 ◽  
Vol 314 (4) ◽  
pp. H812-H838 ◽  
Author(s):  
Merry L. Lindsey ◽  
Roberto Bolli ◽  
John M. Canty ◽  
Xiao-Jun Du ◽  
Nikolaos G. Frangogiannis ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Best Practice ◽  
Ischemia Reperfusion ◽  
Experimental Models ◽  
Myocardial Ischemia And Infarction ◽  
Clinical Scenarios ◽  
Permanent Occlusion ◽  
Myocardial Ischemia Reperfusion ◽  
Underlying Mechanisms ◽  
And Function

Myocardial infarction is a prevalent major cardiovascular event that arises from myocardial ischemia with or without reperfusion, and basic and translational research is needed to better understand its underlying mechanisms and consequences for cardiac structure and function. Ischemia underlies a broad range of clinical scenarios ranging from angina to hibernation to permanent occlusion, and while reperfusion is mandatory for salvage from ischemic injury, reperfusion also inflicts injury on its own. In this consensus statement, we present recommendations for animal models of myocardial ischemia and infarction. With increasing awareness of the need for rigor and reproducibility in designing and performing scientific research to ensure validation of results, the goal of this review is to provide best practice information regarding myocardial ischemia-reperfusion and infarction models. Listen to this article’s corresponding podcast at ajpheart.podbean.com/e/guidelines-for-experimental-models-of-myocardial-ischemia-and-infarction/.

Silencing of sodium/hydrogen exchanger in the heart by direct injection of naked siRNA

2011 ◽  
Vol 111 (2) ◽  
pp. 566-572 ◽  
Author(s):  
Patricio E. Morgan ◽  
María V. Correa ◽  
Irene L. Ennis ◽  
Ariel A. Diez ◽  
Néstor G. Pérez ◽  
...  
Keyword(s):  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Direct Injection ◽  
Experimental Models ◽  
Left Ventricular ◽  
Maximal Velocity ◽  
Mrna Levels ◽  
Small Interference Rna

Cardiac Na+/H+ exchanger (NHE1) hyperactivity is a central factor in cardiac remodeling following hypertension, myocardial infarction, ischemia-reperfusion injury, and heart failure. Treatment of these pathologies by inhibiting NHE1 is challenging because specific drugs that have been beneficial in experimental models were associated with undesired side effects in clinical practice. In the present work, small interference RNA (siRNA) produced in vitro to specifically silence NHE1 (siRNANHE1) was injected once in vivo into the apex of the left ventricular wall of mouse myocardium. After 48 h, left ventricular NHE1 protein expression was reduced in siRNANHE1-injected mice compared with scrambled siRNA by 33.2 ± 3.4% ( n = 5; P < 0.05). Similarly, NHE1 mRNA levels were reduced by 20 ± 2.0% ( n = 4). At 72 h, siRNANHE1 spreading was evident from the decrease in NHE1 expression in three portions of the myocardium (apex, medium, base). NHE1 function was assessed based on maximal velocity of intracellular pH (pHi) recovery (dpHi/d t) after an ammonium prepulse-induced acidic load. Maximal dpHi/d t was reduced to 14% in siRNANHE1-isolated left ventricular papillary muscles compared with scrambled siRNA. In conclusion, only one injection of naked siRNANHE1 successfully reduced NHE1 expression and activity in the left ventricle. As has been previously suggested, extensive NHE1 expression reduction may indicate myocardial spread of siRNA molecules from the injection site through gap junctions, providing a valid technique not only for further research into NHE1 function, but also for consideration as a potential therapeutic strategy.

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