In vivo quantification of autofluorescence dynamics during renal ischemia and reperfusion under dual UV excitation

2007 ◽  
Author(s):  
Rajesh N. Raman ◽  
Christopher D. Pivetti ◽  
Dennis L. Matthews ◽  
Christoph Troppmann ◽  
Stavros G. Demos
Keyword(s):  
Renal Ischemia ◽  
Ischemia And Reperfusion ◽  
Uv Excitation

In vivo spectroscopic monitoring of renal ischemia and reperfusion in a rat model

2006 ◽  
Author(s):  
Rajesh N. Raman ◽  
Christopher D. Pivetti ◽  
Dennis L. Matthews ◽  
Christoph Troppmann ◽  
Stavros G. Demos
Keyword(s):  
Rat Model ◽  
Renal Ischemia ◽  
Ischemia And Reperfusion ◽  
Spectroscopic Monitoring

A1 adenosine receptor knockout mice exhibit increased renal injury following ischemia and reperfusion

2004 ◽  
Vol 286 (2) ◽  
pp. F298-F306 ◽  
Author(s):  
H. Thomas Lee ◽  
Hua Xu ◽  
Samih H. Nasr ◽  
Jurgen Schnermann ◽  
Charles W. Emala
Keyword(s):  
Renal Function ◽  
Knockout Mice ◽  
Adenosine Receptor ◽  
Renal Injury ◽  
Renal Ischemia ◽  
Myeloperoxidase Activity ◽  
Ischemia And Reperfusion ◽  
Wild Type Littermate ◽  
Renal Histology

Controversy exists regarding the effect of A1 adenosine receptor (AR) activation in the kidney during ischemia and reperfusion (I/R) injury. We sought to further characterize the role of A1 ARs in modulating renal function after I/R renal injury using both pharmacological and gene deletion approaches in mice. A1 AR knockout mice (A1KO) or their wild-type littermate controls (A1WT) were subjected to 30 min of renal ischemia. Some A1WT mice were subjected to 30 min of renal ischemia with or without pretreatment with 1,3-dipropyl-8-cyclopentylxanthine (DPCPX) or 2-chrolo-cyclopentyladenosine (CCPA), selective A1 AR antagonist and agonist, respectively. Plasma creatinine and renal histology were compared 24 h after renal injury. A1KO mice exhibited significantly higher creatinines and worsened renal histology compared with A1WT controls following renal I/R injury. A1WT mice pretreated with the A1 AR antagonist or agonist demonstrated significantly worsened or improved renal function, respectively, after I/R injury. In addition, A1WT mice pretreated with DPCPX or CCPA showed significantly increased or reduced markers of renal inflammation, respectively (renal myeloperoxidase activity, renal tubular neutrophil infiltration, ICAM-1, TNF-α, and IL-1β mRNA expression), while demonstrating no differences in indicators of apoptosis. In conclusion, we demonstrate that endogenous or exogenous preischemic activation of A1 ARs protects against renal I/R injury in vivo via mechanisms leading to decreased necrosis and inflammation.

scholarly journals Tyrosine and Tryptophan vibrational bands as markers of kidney injury: a renocardiac syndrome induced by renal ischemia and reperfusion study

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Gabrielle Nepomuceno ◽  
Carolina Victoria Cruz Junho ◽  
Marcela Sorelli Carneiro-Ramos ◽  
Herculano da Silva Martinho
Keyword(s):  
Raman Spectroscopy ◽  
Kidney Injury ◽  
Cardiorenal Syndrome ◽  
Renal Ischemia ◽  
Ischemia And Reperfusion ◽  
Collagen Iii ◽  
Ft Raman Spectroscopy ◽  
Ft Raman

AbstractRenal injury caused by renal ischemia and reperfusion strongly influences heart morphology, electrophysiology, and redox unbalance. The so-called cardiorenal syndrome is an important class of dysfunction since heart and kidneys are responsible for hemodynamic stability and organ perfusion through a complex network. In the present work we investigate the vibrational spectral features probed by Fourier-Transform Raman (FT-Raman) spectroscopy due to physiological alterations induced by renal ischemic reperfusion aiming to detect molecular markers related to progression of acute to chronic kidney injury and mortality predictors as well. C57BL/6J mice were subjected to unilateral occlusion of the renal pedicle for 60 min and reperfusion for 5, 8, and 15 days. Biopsies of heart and kidney tissues were analyzed. Our findings indicated that cysteine/cystine, fatty acids, methyl groups of Collagen, α-form of proteins, Tyrosine, and Tryptophan were modulated during renal ischemia and reperfusion process. These changes are consistent with fibroblast growth factors and Collagen III contents changes. Interestingly, Tyrosine and Tryptophan, precursor molecules for the formation of uremic toxins such as indoxyl sulfate and p-cresyl sulfate were also modulated. They are markers of kidney injury and their increase is strongly correlated to cardiovascular mortality. Regarding this aspect, we notice that monitoring the Tyrosine and Tryptophan bands at 1558, 1616, and 1625 cm−1 is a viable and and advantageous way to predict fatality in cardiovascular diseases both “in vivo” or “in vitro”, using the real-time, multiplexing, and minimally invasive advantages of FT-Raman spectroscopy.

scholarly journals Quantification of in vivo autofluorescence dynamics during renal ischemia and reperfusion under 355 nm excitation

2008 ◽  
Vol 16 (7) ◽  
pp. 4930 ◽  
Author(s):  
Rajesh N. Raman ◽  
Christopher D. Pivetti ◽  
Dennis L. Matthews ◽  
Christoph Troppmann ◽  
Stavros G. Demos
Keyword(s):  
Renal Ischemia ◽  
Ischemia And Reperfusion

31P NMR Evaluation of in Vivo Renal Ischemia and Reperfusion Injury in Rabbits and Dogs

1987 ◽  
Vol 508 (1 Physiological) ◽  
pp. 417-419 ◽  
Author(s):  
LOUIS F. MARTIN ◽  
DAVI D M. FEHR ◽  
ANASTASIUS O. PETER ◽  
JOSEPH B. SANFORD ◽  
IDA N. GORMAN ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
31P Nmr ◽  
Renal Ischemia ◽  
Ischemia And Reperfusion ◽  
Ischemia And Reperfusion Injury

Leukocyte Adhesion to the Coronary Microvasculature During Ischemia and Reperfusion in an In Vivo Canine Model

Circulation ◽  
1996 ◽  
Vol 93 (10) ◽  
pp. 1784-1787 ◽  
Author(s):  
Frank M. Sheridan ◽  
Paul G. Cole ◽  
David Ramage
Keyword(s):  
Leukocyte Adhesion ◽  
Canine Model ◽  
Ischemia And Reperfusion

In Vivo MRI Visualization of Acute Myocardial Ischemia and Reperfusion in Ferrets by the Persistent Action of the Contrast Agent Gd(BME-DTTA)

Circulation ◽  
1995 ◽  
Vol 92 (12) ◽  
pp. 3549-3559 ◽  
Author(s):  
Tamás Simor ◽  
Wen-Jang Chu ◽  
Lynne Johnson ◽  
Andras Safranko ◽  
Mark Doyle ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Contrast Agent ◽  
Acute Myocardial Ischemia ◽  
Ischemia And Reperfusion ◽  
Myocardial Ischemia And Reperfusion

Ethane production as a measure of lipid peroxidation after renal ischemia

1986 ◽  
Vol 251 (5) ◽  
pp. F839-F843 ◽  
Author(s):  
M. S. Paller ◽  
R. P. Hebbel
Keyword(s):  
Lipid Peroxidation ◽  
Free Radicals ◽  
Superoxide Radical ◽  
Oxygen Free Radicals ◽  
Tissue Injury ◽  
Renal Ischemia ◽  
Radical Scavenger ◽  
Base Line ◽  
Ethane Production

After renal ischemia, oxygen free radicals are formed and produce tissue injury, in large part, through peroxidation of polyunsaturated fatty acids. We used an in vivo method to monitor lipid peroxidation after renal ischemia, the measurement of ethane in expired gas, to determine the time course of lipid peroxidation and the effect of several agents to limit lipid peroxidation after renal ischemia. In anesthetized rats there was no significant increase in ethane production during 60 min of renal ischemia. During the first 10 min of renal reperfusion, there was a prompt increase in ethane production from 2.9 +/- 1.3 to 6.3 +/- 1.9 pmol/min (P less than 0.05). Ethane production was significantly increased during the first 50 min of reperfusion and then rapidly tapered to base-line levels. Preischemic administration of allopurinol to prevent superoxide radical generation or the superoxide radical scavenger superoxide dismutase prevented the increase in ethane production during postischemic reperfusion. These studies confirm that there is increase lipid peroxidation following renal ischemia that can be prevented by agents which limit the formation or accumulation of oxygen free radicals. This in vivo method for measuring lipid peroxidation could also be employed to study the effects of ischemia on lipid peroxidation in other organs, as well as to monitor lipid peroxidation in other forms of injury.

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