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

We have previously shown that an intravenous infusion of adenosine and lidocaine (AL) solution protects against death and severe arrhythmias and reduces infarct size in the in vivo rat model of regional ischemia. The aim of this study was to examine the relative changes of myocardial high-energy phosphates (ATP and PCr) and pH in the left ventricle during ischemia–reperfusion using 31P NMR in AL-treated rats (n = 7) and controls (n = 6). The AL solution (A: 305 μg·(kg body mass)–1·min–1; L: 608 μg·(kg body mass)–1·min–1) was administered intravenously 5 min before and during 30 min coronary artery ligation. Two controls died from ventricular fibrillation; no deaths were recorded in AL-treated rats. In controls that survived, ATP fell to 73% ± 29% of baseline by 30 min ischemia and decreased further to 68% ± 28% during reperfusion followed by a sharp recovery at the end of the reperfusion period. AL-treated rats maintained relatively constant ATP throughout ischemia and reperfusion ranging from 95% ± 6% to 121% ± 10% of baseline. Owing to increased variability in controls, these results were not found to be significant. In contrast, control [PCr] was significantly reduced in controls compared with AL-treated rats during ischemia at 10 min (68% ± 7% vs. 99% ± 6%), at 15 min (68% ± 10% vs. 93% ± 2%), and at 20 min (67% ± 15% vs. 103% ± 5%) and during reperfusion at 10 min (56% ± 22% vs. 99% ± 7%), at 15 min (60% ± 10% vs. 98% ± 7%), and at 35 min (63% ± 14% vs. 120% ± 11%) (p < 0.05). Interestingly, changes in intramyocardial pH between each group were not significantly different during ischemia and fell by about 1 pH unit to 6.6. During reperfusion, pH in AL-treated rats recovered to baseline in 5 min but not in controls, which recovered to only around pH 7.1. There was no significant difference in the heart rate, mean arterial pressure, and rate-pressure product between the controls and AL treatment during ischemia and reperfusion. We conclude that AL cardioprotection appears to be associated with the preservation of myocardial high-energy phosphates, downregulation of the heart at the expense of a high acid-load during ischemia, and with a rapid recovery of myocardial pH during reperfusion.

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

AJP Renal Physiology ◽

10.1152/ajprenal.00185.2003 ◽

2004 ◽

Vol 286 (2) ◽

pp. F298-F306 ◽

Cited By ~ 104

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.

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

Scientific Reports ◽

10.1038/s41598-021-93762-z ◽

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.

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

Optics Express ◽

10.1364/oe.16.004930 ◽

2008 ◽

Vol 16 (7) ◽

pp. 4930 ◽

Cited By ~ 9

Author(s):

Rajesh N. Raman ◽

Christopher D. Pivetti ◽

Dennis L. Matthews ◽

Christoph Troppmann ◽

Stavros G. Demos

Keyword(s):

Renal Ischemia ◽

Ischemia And Reperfusion

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

10.1117/12.699744 ◽

2007 ◽

Cited By ~ 1

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

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In Vivo MR Imaging of Magnetically Labeled Mesenchymal Stem Cells in a Rat Model of Renal Ischemia

Korean Journal of Radiology ◽

10.3348/kjr.2009.10.3.277 ◽

2009 ◽

Vol 10 (3) ◽

pp. 277 ◽

Cited By ~ 8

Author(s):

Sung Il Jung ◽

Seung Hyup Kim ◽

Hyo-Cheol Kim ◽

Kyu Ri Son ◽

Se Young Chung ◽

...

Keyword(s):

Stem Cells ◽

Mesenchymal Stem Cells ◽

Mr Imaging ◽

Rat Model ◽

Renal Ischemia

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

Annals of the New York Academy of Sciences ◽

10.1111/j.1749-6632.1987.tb32923.x ◽

1987 ◽

Vol 508 (1 Physiological) ◽

pp. 417-419 ◽

Cited By ~ 1

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

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Influence of acidosis and hypoxia on liver ischemia and reperfusion injury in an in vivo rat model

Journal of Applied Physiology ◽

10.1152/japplphysiol.01112.2001 ◽

2002 ◽

Vol 93 (1) ◽

pp. 319-323 ◽

Cited By ~ 18

Author(s):

Bob H. M. Heijnen ◽

Yasser Elkhaloufi ◽

Irene H. Straatsburg ◽

Thomas M. van Gulik

Keyword(s):

Reperfusion Injury ◽

Rat Model ◽

Respiratory Acidosis ◽

Bile Secretion ◽

Respiratory Support ◽

Ischemia And Reperfusion ◽

Liver Ischemia ◽

Hepatocellular Injury ◽

Ischemia And Reperfusion Injury

The contribution of acidosis to the development of reperfusion injury is controversial. In this study, we examined the effects of respiratory acidosis and hypoxia in a frequently used in vivo liver ischemia and reperfusion (I/R) injury rat model. Rats were anesthetized with intraperitoneal anesthetics and subjected to partial liver ischemia (70%) for 60 min and subsequent reperfusion for 90 min under the following conditions: 1) no acidosis and normoxia, maintained by controlled ventilation; 2) acidosis and normoxia, maintained by passive supply with oxygen; 3) no acidosis and hypoxia, maintained by bicarbonate administration without respiratory support; and 4) acidosis and hypoxia, i.e., without respiratory support or pH correction. Changes in plasma aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels were measured as parameters of hepatocellular injury, and bile secretion was monitored. AST and ALT levels were lowest in the ventilated rats and highest in the bicarbonate-treated rats. No differences in bile secretion were found between groups. Our results suggest that respiratory acidosis significantly enhanced liver I/R injury under normoxic conditions, whereas respiratory acidosis significantly reduced liver I/R injury under hypoxic conditions.

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