Ischemic Preconditioning Protects the Dog Kidney from Ischemia-Reperfusion Injury

Salehipour, Mehdi; Khezri, Abdolaziz; Monabbati, Ahmad; Jalaeian, Hamed; Kroup, Mohsen; Azizi, Valiallah; Tanideh, Nader

doi:10.1159/000109718

Cited by 12 publications

(4 citation statements)

References 36 publications

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“…2 Ischemic preconditioning is a brief period of ischemia followed by reperfusion, which makes the tissues resistant to injury resulting from prolonged ischemia and reperfusion. The phenomenon of ischemic preconditioning has been recognized as one of the most potent mechanisms to protect against myocardial, 3 cerebral, 4 renal, 5 and retinal ischemic injury. 6 Oxidative stress and calcium accumulation have an important role in the progression of hepatic IR injury and apoptosis.…”

Section: Introductionmentioning

confidence: 99%

Study of the protective effect of ischemic and pharmacological preconditioning on hepatic ischemic reperfusion injury induced in rats

Osman

Kamel

2017

JGH Open

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Background and AimHepatic ischemia reperfusion injury is the main cause of liver failure following liver surgery, so an effective method is needed to prevent or reduce this hepatic injury. The aim of the present study is to investigate the potential effect of ischemic preconditioning versus pharmacological preconditioning with lisinopril or verapamil for protection against hepatic ischemia reperfusion injury induced in rats.MethodsRats were divided into six groups. Group I served as control untreated. Rats of group II were subjected to laparotomy without induction of ischemia reperfusion. Ischemia reperfusion by ligation of the portal trait for 30 min, followed by reperfusion for 2 h, was performed in rats of groups III–VI. Ischemic preconditioning was performed for rats of group IV before induction of ischemia reperfusion. Lisinopril and verapamil was given daily for 3 days before induction of ischemia reperfusion in groups V and VI, respectively. Serum level of liver transaminases and liver malondialdehyde content were measured, and hepatic histopathological examination was assessed.ResultsInduction of ischemia reperfusion resulted in significant elevation of liver transaminases and liver malondialdehyde content associated with significant hepatic histopathological injury that were significantly improved by ischemic preconditioning, lisinopril, or verapamil treatment. Verapamil showed the most significant improvement compared with ischemic preconditioning or lisinopril treatment.ConclusionIschemic preconditioning and pharmacological preconditioning by lisinopril or verapamil can protect against hepatic ischemia reperfusion probably through inhibition of oxidative stress and neutrophil infiltration. The most potent protection is demonstrated by verapamil treatment.

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Section: Introductionmentioning

confidence: 99%

Study of the protective effect of ischemic and pharmacological preconditioning on hepatic ischemic reperfusion injury induced in rats

Osman

Kamel

2017

JGH Open

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“…Ischemic preconditioning (IPC) is known to protect tissue from ischemia and has an effect both locally [1] and systemically [2]. Remote IPC (RIPC) induced by limb ischemia provides systemic protection against prolonged ischemia in the target organ.…”

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confidence: 99%

Remote ischemic preconditioning reduces thrombus formation in the rat

Røpcke

Hjortdal

Toft

et al. 2012

Journal of Thrombosis and Haemostasis

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13 Huang Q, Neuenschwander PF, Rezaie AR, Morrissey JH. Substrate recognition by tissue factor-factor VIIa. Evidence for interaction of residues Lys165 and Lys166 of tissue factor with the 4-carboxyglutamate-rich domain of factor X. J Biol Chem 1996; 271: 21752-7.14 Boettcher JM, Davis-Harrison RL, Clay MC, Nieuwkoop AJ, Ohkubo YZ, Tajkhorshid E, Morrissey JH, Rienstra CM. Atomic view of calcium-induced clustering of phosphatidylserine in mixed lipid bilayers. Biochemistry 2011; 50: 2264-73.Remote ischemic preconditioning reduces thrombus formation in the rat Ischemic preconditioning (IPC) is known to protect tissue from ischemia and has an effect both locally [1] and systemically [2]. Remote IPC (RIPC) induced by limb ischemia provides systemic protection against prolonged ischemia in the target organ. RIPC has been reported to reduce infarct size in patients with ST-elevation myocardial infarction (STEMI) undergoing primary angioplasty [3] and is currently being evaluated in patients with ischemic stroke undergoing thrombolysis (NCT00975962). We hypothesized that the reduction in ischemic damage with RIPC could rely on a direct effect on arterial thrombus formation and embolization, and investigated this in a dynamic in vivo rat model of experimental thrombosis [4].Animals were treated according to Danish law on animal experiments. RIPC was induced using a protocol described previously [5]. At the time of surgery, a tourniquet was placed for 10 minutes on the left hind limb. Photographs demonstrating blue coloring of the left paw documented ischemia.Ten millimeters of the femoral artery on the right hind leg were dissected distal to the inguinal ligament. The artery was fixed in a clamp and an arteriotomy was performed comprising one-third of the vessel circumference. The proximal vessel edge was inverted by two 10-0 Nylon sutures exposing full thickness of the vessel wall to the lumen. After clamp release, a thrombus would build up at the arteriotomy site, and fragments of thrombus were seen to detach and embolize downstream. This model of a thrombogenic anastomosis is well established in rats [6,7] and pigs [8].The right femoral artery was placed in a trans-illuminator projecting a light beam through the vessel [8,9]. Recordings with a digital recorder were performed through the microscope for 30 min after clamp release and were analyzed offline in a blinded fashion. The thrombus area was measured as the number of pixels every minute, using special ImageJ based software. (ImageJ 1.45s, NIH, USA). The area was measured for 20 min while the number of emboli was counted manually every minute for 30 min. The area of the thrombus and number of emboli were displayed versus time in a graph. The area under the curve (AUC) for thrombus formation over time was determined. Two independent investigators analyzed 10 random videos (coefficient of variation was 21% for counting emboli and 8% for area measurement).Data were consistent with a Gaussian distribution, and the unpaired t-test was used for comparison of the two g...

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“…1,4,26 Our finding that IPC does not alter histologic or molecular markers of renal injury in this model should be placed in the context of the current controversy as to whether IPC protects from subsequent renal IRI. Although several investigators have found IPC to be effective in protecting against renal IRI in various animal species, 3,[27][28][29][30] other studies have found no evidence that IPC is protective against renal injury. 4,5,31 A recent meta-analysis by Wever and associates 2 analyzed 58 animal studies and concluded that IPC was associated with significantly improved serum creatinine, blood urea nitrogen, and histologic injury score after IRI.…”

Section: Discussionmentioning

confidence: 99%

Untitled

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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Ischemic Preconditioning Protects the Dog Kidney from Ischemia-Reperfusion Injury

Cited by 12 publications

References 36 publications

Study of the protective effect of ischemic and pharmacological preconditioning on hepatic ischemic reperfusion injury induced in rats

Study of the protective effect of ischemic and pharmacological preconditioning on hepatic ischemic reperfusion injury induced in rats

Remote ischemic preconditioning reduces thrombus formation in the rat

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