Ischemia/Reperfusion of Unilateral Kidney Exaggerates Aging-Induced Damage to the Heart and Contralateral Kidney

Kato, Junichiro; Nakayama, Masaaki; Zhu, Wan Jun; Yokoo, Takashi; Ito, Sadayoshi

doi:10.1159/000362555

Cited by 10 publications

(13 citation statements)

References 27 publications

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“…Finally, our data might be explained by crucial interactions between CsA, age, and oxidative stress [15,47]. Indeed, increased oxidative stress is well known to participate in mitochondrial dysfunction [10,35] and CsA significantly increased ROS production in both ischemic and no ischemic hindlimbs.…”

Section: Effects Of Cyclosporinementioning

confidence: 64%

Skeletal muscle ischemia–reperfusion injury and cyclosporine A in the aging rat

Pottecher

Kindo

Chamaraux-Tran

et al. 2016

Fundamemntal Clinical Pharma

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Old patients exhibit muscle impairments and increased perioperative risk during vascular surgery procedures. Although aging generally impairs protective mechanisms, data are lacking concerning skeletal muscle in elderly. We tested whether cyclosporine A (CsA), which protects skeletal muscle from ischemia-reperfusion (IR) in young rats, might reduce skeletal muscle mitochondrial dysfunction and oxidative stress in aging rats submitted to hindlimb IR. Wistar rats aged 71-73 weeks were randomized to IR (3 h unilateral tourniquet application and 2 h reperfusion) or IR + CsA (10 mg/kg cyclosporine IV before reperfusion). Maximal oxidative capacity (VM ax ), acceptor control ratio (ACR), and relative contribution of the mitochondrial respiratory chain complexes II, III, IV (VS ucc ), and IV (VTMPD /Asc ), together with calcium retention capacity (CRC) a marker of apoptosis, and tissue reactive oxygen species (ROS) production were determined in gastrocnemius muscles from both hindlimbs. Compared to the nonischemic hindlimb, IR significantly reduced mitochondrial coupling, VMax (from 7.34 ± 1.50 to 2.87 ± 1.22 μMO2 /min/g; P < 0.05; -70%), and VS ucc (from 6.14 ± 1.07 to 3.82 ± 0.83 μMO2 /min/g; P < 0.05; -42%) but not VTMPD /Asc . IR also decreased the CRC from 15.58 ± 3.85 to 6.19 ± 0.86 μMCa(2+) /min/g; P < 0.05; -42%). These alterations were not corrected by CsA (-77%, -49%, and -32% after IR for VM ax, VS ucc , and CRC, respectively). Further, CsA significantly increased ROS production in both hindlimbs (P < 0.05; +73%). In old rats, hindlimb IR impairs skeletal muscle mitochondrial function and increases oxidative stress. Cyclosporine A did not show protective effects.

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Section: Effects Of Cyclosporinementioning

confidence: 64%

Skeletal muscle ischemia–reperfusion injury and cyclosporine A in the aging rat

Pottecher

Kindo

Chamaraux-Tran

et al. 2016

Fundamemntal Clinical Pharma

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“…According to our results, the number of ED‐1‐positive cells in the contralateral kidney was increased even in the sham group, which indicated that oxidative stress in kidneys was already increased before I/R. In addition, aging is a well‐known risk factor for oxidative stress and is a possible factor in DOI . Taken together, the basic condition of oxidative stress in individual distant organs might be associated with the pathogenesis of DOI following I/R.…”

Section: Discussionmentioning

confidence: 52%

“…5 These harmful aspects of renal I/R are not limited to the ischaemic kidney itself, but elicit distant organ injury (DOI) in the contralateral kidney, heart, lung, liver and brain, and they are accompanied by inflammation. [6][7][8][9][10][11][12][13][14] Statins, 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors, are commonly used to lower serum cholesterol levels, and they are effective for primary and secondary prevention of cardiovascular diseases. 15,16 Statins possess strong anti-inflammatory and anti-oxidative capabilities that are independent of their direct lipidlowering properties.…”

mentioning

confidence: 99%

Rosuvastatin pretreatment suppresses distant organ injury following unilateral renal ischemia‐reperfusion in hypertensive Dahl salt‐sensitive rats

et al. 2018

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“…The rat model used in the present study is a wellestablished in vivo model of acute kidney injury 18,25 and is supported by a recent systematic review and meta-analysis. 2 Cross-clamping of the renal pedicle for 45 minutes produces significant but not fatal ischemic injury.…”

Section: Discussionmentioning

confidence: 86%

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Khalid

Jenkins²,

Pino-Chavez³

et al. 2015

Exp Clin Transplant

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Objectives: We evaluated a continuous, immediate, localized ischemic preconditioning regimen in a rat model of ischemia-reperfusion injury and assessed whether it attenuated injury at the histologic and molecular levels. Materials and Methods: Fifteen adult male Lewis rats received sham operation, left unilateral warm ischemia (45 minutes of cross-clamping of the renal pedicle; ischemia-reperfusion injury group), or 15 minutes of ischemia followed by a 20-minute reperfusion period, 45 minutes of ischemiareperfusion injury, and subsequent reperfusion (ischemic preconditioning/ischemia-reperfusion injury group). Kidney tissue was retrieved 48 hours later, sectioned, stained with hematoxylin and eosin, and examined. We used RNA extraction and real-time quantitative polymerase chain reaction analysis to assess acute kidney injury markers, cytokines, and microRNA-21. Results: Forty-five minutes of unilateral ischemiareperfusion injury caused marked changes in histology at 48 hours, characterized by endothelial loss, tubulointerstitial damage (inflammation, cast formation), tubular cell necrosis, and glomerular capsule thickening. The ischemia-reperfusion injury and ischemic preconditioning/ischemia-reperfusion injury groups showed no measurable differences in histology. Expression of the acute kidney injury markers was significantly increased in the ischemiareperfusion injury versus Sham group; however, no difference was found between the ischemiareperfusion injury and ischemic preconditioning/ -ischemia-reperfusion injury groups. Similarly, expression of interleukin 17, interleukin 18, and tumor necrosis factor α was significantly increased in the ischemia-reperfusion injury versus Sham group. No significant difference was found between the ischemia-reperfusion injury and ischemic preconditioning/ischemia-reperfusion injury groups for interleukin 17 and interleukin 18; however, tumor necrosis factor α expression was significantly increased in the ischemic preconditioning/ischemiareperfusion injury versus ischemia-reperfusion injury group. Conclusions: In our ischemic preconditioning model, tumor necrosis factor α expression was increased without altering the sequelae of ischemia-reperfusion injury. The long-term consequences of this augmented early inflammatory response and whether these consequences are altered by variations in ischemic preconditioning or a subsequent injury require further study.

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Ischemia/Reperfusion of Unilateral Kidney Exaggerates Aging-Induced Damage to the Heart and Contralateral Kidney

Cited by 10 publications

References 27 publications

Skeletal muscle ischemia–reperfusion injury and cyclosporine A in the aging rat

Skeletal muscle ischemia–reperfusion injury and cyclosporine A in the aging rat

Rosuvastatin pretreatment suppresses distant organ injury following unilateral renal ischemia‐reperfusion in hypertensive Dahl salt‐sensitive rats

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