Toxic effects of a high dose of non-ionic iodinated contrast media on renal glomerular and aortic endothelial cells in aged rats in vivo

Zhao, Yuhai; Tao, Zhiwen; Xu, Zhihui; Zeng, Tao; Chen, Bo; Wang, Liansheng; Li, Chunjian; Chen, Leilei; Jia, Qingzhe; Jia, En-Zhi; Zhu, Tongyu; Yang, Zhaohui

doi:10.1016/j.toxlet.2011.02.011

Cited by 41 publications

(23 citation statements)

References 36 publications

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“…The increase in SCr and BUN following exposure of rats to CM and glycerol has been reported earlier [17, 18]. Our histopathological studies also confirm significant tubular vacuolar transformation, interstitial edema, and tubular degeneration in this nephropathy model.…”

Section: Discussionsupporting

confidence: 90%

Simvastatin Attenuates Contrast-Induced Nephropathy through Modulation of Oxidative Stress, Proinflammatory Myeloperoxidase, and Nitric Oxide

Al-Otaibi

Elaiwi

Tariq

et al. 2012

Oxidative Medicine and Cellular Longevity

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Contrast media- (CM-) induced nephropathy is a serious complication of radiodiagnostic procedures. Available data suggests that the development of prophylaxis strategies is limited by poor understanding of pathophysiology of CM-induced nephropathy. Present study was designed to determine the role of oxidative stress, myeloperoxidase, and nitric oxide in the pathogenesis of iohexol model of nephropathy and its modification with simvastatin (SSTN). Adult Sprague Dawley rats were divided into seven groups. After 24 h of water deprivation, all the rats except in control and SSTN-only groups were injected (10 ml/kg) with 25% glycerol. After 30 min, SSTN (15, 30, and 60 mg/kg) was administered orally, daily for 4 days. Twenty-four hours after the glycerol injection, iohexol was infused (8 ml/kg) through femoral vein over a period of 2 min. All the animals were sacrificed on day 5 and blood and kidneys were collected for biochemical and histological studies. The results showed that SSTN dose dependently attenuated CM-induced rise of creatinine, urea, and structural abnormalities suggesting its nephroprotective effect. A significant increase in oxidative stress (increased lipid hydroperoxides and reduced glutathione levels) and myeloperoxidase (MPO) and decreased nitric oxide in CM group were reversed by SSTN. These findings support the use of SSTN to combat CM-induced nephrotoxicity.

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Section: Discussionsupporting

confidence: 90%

Simvastatin Attenuates Contrast-Induced Nephropathy through Modulation of Oxidative Stress, Proinflammatory Myeloperoxidase, and Nitric Oxide

Al-Otaibi

Elaiwi

Tariq

et al. 2012

Oxidative Medicine and Cellular Longevity

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“…Tissue vascular density was determined as the ratio between CD31-positive areas and DAPI-positive regions [20]. The VEGF fluorescence intensity was semiquantified by the ratio of the fluorescence intensity to per muscle fiber which was calculated using the Image-Pro Plus software [21,22].…”

Section: Rg1 Treatment Protocolmentioning

confidence: 99%

Beneficial effects of ginsenoside-Rg1 on ischemia-induced angiogenesis in diabetic mice

Yang¹,

Chen²,

Tao³

et al. 2012

ABBS

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Neovascularization and the formation of collateral vessels are often impaired in diabetes mellitus (DM) population compared with non-diabetics. Alterations in vascular endothelial growth factor (VEGF) signaling and endothelial nitric oxide synthase (eNOS) dysfunction have been confirmed to play a crucial role in impaired neovascularization in diabetic mice. Accumulating data have suggested that Rg1, a main component of Panax ginseng, has the ability to promote tubulogenesis of human umbilical vein endothelial cells (HUVECs) in vitro, and that the mechanism involves increased expression level of VEGF as well as increased eNOS activation. Thus, we speculated that Rg1 might also have therapeutic effects on the impairment of neovascularization in diabetic individuals. The aim of the present study was to investigate whether Rg1 could improve angiogenesis in ischemic hindlimb of diabetic mice in vivo. Our data demonstrated that Rg1 treatment resulted in improved angiogenesis in the diabetic ischemic hindlimb, and the potential mechanism might involve increased eNOS activation, upregulated VEGF expression, and inhibited apoptosis. Our results suggest that Rg1 may be used as a novel and useful adjunctive drug for the therapy of peripheral arterial disease in DM.

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“…CI-AKI is a serious complication of radio-contrast vascular examination, especially in high-risk subjects with decreased renal function. Zhao et al (2011) assessed the toxic effects of non-ionic CM (iopromide and iodixanol) on glomerular and aortic endothelial cells (ECs) in an in vivo study. The results showed that endothelial nitric oxide synthase (eNOS) expression in the glomerular endothelium decreased 12 h after CM injection.…”

Section: Discussionmentioning

confidence: 99%

A correlation between acute kidney injury and myonecrosis after scheduled percutaneous coronary intervention

Zhang

Meng

Zhao

et al. 2013

J. Zhejiang Univ. Sci. B

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Slight elevations in cardiac troponin I and T are frequently observed after percutaneous coronary intervention (PCI). Contrast-induced acute kidney injury (CI-AKI) is a complex syndrome induced by exposure to intravascular contrast media (CM). Currently, the relationships between the CM, pre-existing kidney insufficiency, CI-AKI, and myonecrosis after elective PCI are unclear. To investigate the relationship between CI-AKI and post-procedural myonecrosis (PMN) after PCI, we analyzed 327 non-ST-segment elevation acute coronary syndrome subjects undertaking elective PCI. The levels of cardiac troponins (cTns), cTnI and cTnT, at baseline and on at least one occasion 18-24 h after PCI were measured. We also recorded serum levels of creatinine (SCr) and the urine albumin:creatinine ratio (ACR) before coronary angiography, and 24-48 h and 48-72 h after contrast administration. A post-procedure increase in cTns was detected in 16.21% (53/327) of subjects with cTns levels >99th to 599th percentile upper reference limit (URL). Twenty-seven patients (8.26%) developed CI-AKI. CI-AKI occurred more often in subjects with PMN than in those without PMN (20.8% versus 5.8%, respectively, P=0.001). Multiple logistic regression analysis revealed that pre-existing microalbuminuria (MA) was an important independent predictor of PMN (OR: 3.31; 95% CI: 1.26-8.65, P=0.01). However, there was no correlation between the incidence of CI-AKI and PMN (OR: 2.38; 95% CI: 0.88-6.46, P=0.09). We conclude that pre-existing MA was not only an important independent predictor of CI-AKI but also of PMN.

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Toxic effects of a high dose of non-ionic iodinated contrast media on renal glomerular and aortic endothelial cells in aged rats in vivo

Cited by 41 publications

References 36 publications

Simvastatin Attenuates Contrast-Induced Nephropathy through Modulation of Oxidative Stress, Proinflammatory Myeloperoxidase, and Nitric Oxide

Simvastatin Attenuates Contrast-Induced Nephropathy through Modulation of Oxidative Stress, Proinflammatory Myeloperoxidase, and Nitric Oxide

Beneficial effects of ginsenoside-Rg1 on ischemia-induced angiogenesis in diabetic mice

A correlation between acute kidney injury and myonecrosis after scheduled percutaneous coronary intervention

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