Abstract:The radiocontrast/hypertonicity-induced DNA fragmentation of MDCK cells is attenuated by taurine but not by NAC. Because both agents are antioxidants, the antioxidant property is not sufficient for the observed cytoprotective effect. Hence, the antiapoptotic effect of taurine has to be attributed to other, yet to be defined mechanisms. Our results suggest that pharmacological doses of taurine may be particularly protective against RCIN.
“…Moreover, their study also indicated that the disturbance of mitochondrial enzyme activity and mitochondrial membrane potential remained relatively unchanged up to 60 h after iopamidol treatment. As reported in another ex vivo experiment, a highly hyperosmolal, ionic radiocontrast agent diatrizoate can induce DNA fragmentation (apoptosis) in MDCK cells (29). Although we could not determine whether inhibition of mitochondrial function or delayed apoptosis in tubule cells is related to the functional changes in our DW-MR images, it is well known that the deficiency of mitochondrial enzyme activity can reduce the activity of adenosine triphosphate enzyme (ATPase), which may limit the ability of water transport function between extra-and intra-cellular.…”
Purpose: To assess the effects of intravenous-injected iodinated contrast medium (CM) on intrarenal water diffusion using noninvasive diffusion-weighted MRI (DW-MRI).
Materials and Methods:Ten New Zealand White rabbits were randomized to receive a 6 mL/kg body weight intravenous injection of clinically used iopamidol-370 (n ¼ 7) or an equivalent amount of 0.9% physiological saline (n ¼ 3). A sequential DW-MRI was performed to estimate the intrarenal apparent diffusion coefficient (ADC) at 24 h before and 1 h, 24 h, 48 h, and 72 h after administration.Results: Iopamidol produced a progressive ADC reduction in inner stripes of the renal outer medulla (IS) by 13.92% (P ¼ 0.05) at 1 h, 17.52% (P ¼ 0.02) at 24 h, 20.23% (P ¼ 0.01) at 48 h and 16.31% (P ¼ 0.04) at 72 h after injection. Cortical ADC was decreased by 14.14% (P ¼ 0.01) at 48 h and 14.12% (P ¼ 0.01) at 72 h after injection. Iopamidol produced slight decrease of ADCs in outer stripes of the outer medulla (OS) and inner medulla (IM) of kidney but without statistical difference. In control group, no significant ADC changes was observed in each anatomic compartment due to saline injection (P > 0.05).
Conclusion:As demonstrated by DW-MRI, intravenous iopamidol injection resulted in a successive reduction of intrarenal water diffusion, particularly in IS of kidney. This MR technique may be used as a noninvasive tool to perform a time course study of the pathogenesis associated with contrast-induced nephropathy (CIN).
“…Moreover, their study also indicated that the disturbance of mitochondrial enzyme activity and mitochondrial membrane potential remained relatively unchanged up to 60 h after iopamidol treatment. As reported in another ex vivo experiment, a highly hyperosmolal, ionic radiocontrast agent diatrizoate can induce DNA fragmentation (apoptosis) in MDCK cells (29). Although we could not determine whether inhibition of mitochondrial function or delayed apoptosis in tubule cells is related to the functional changes in our DW-MR images, it is well known that the deficiency of mitochondrial enzyme activity can reduce the activity of adenosine triphosphate enzyme (ATPase), which may limit the ability of water transport function between extra-and intra-cellular.…”
Purpose: To assess the effects of intravenous-injected iodinated contrast medium (CM) on intrarenal water diffusion using noninvasive diffusion-weighted MRI (DW-MRI).
Materials and Methods:Ten New Zealand White rabbits were randomized to receive a 6 mL/kg body weight intravenous injection of clinically used iopamidol-370 (n ¼ 7) or an equivalent amount of 0.9% physiological saline (n ¼ 3). A sequential DW-MRI was performed to estimate the intrarenal apparent diffusion coefficient (ADC) at 24 h before and 1 h, 24 h, 48 h, and 72 h after administration.Results: Iopamidol produced a progressive ADC reduction in inner stripes of the renal outer medulla (IS) by 13.92% (P ¼ 0.05) at 1 h, 17.52% (P ¼ 0.02) at 24 h, 20.23% (P ¼ 0.01) at 48 h and 16.31% (P ¼ 0.04) at 72 h after injection. Cortical ADC was decreased by 14.14% (P ¼ 0.01) at 48 h and 14.12% (P ¼ 0.01) at 72 h after injection. Iopamidol produced slight decrease of ADCs in outer stripes of the outer medulla (OS) and inner medulla (IM) of kidney but without statistical difference. In control group, no significant ADC changes was observed in each anatomic compartment due to saline injection (P > 0.05).
Conclusion:As demonstrated by DW-MRI, intravenous iopamidol injection resulted in a successive reduction of intrarenal water diffusion, particularly in IS of kidney. This MR technique may be used as a noninvasive tool to perform a time course study of the pathogenesis associated with contrast-induced nephropathy (CIN).
“…Renal damage may also results from direct contrast-induced cytotoxicity or contrast-induced elevations in tissue osmolality (17). In addition, alterations in the metabolism of prostaglandin, nitric oxide, endothelin and adenosine may also play a role in the pathogenesis.…”
ÖZETAmaç: Bu prospektif çalışma renal disfonksiyonlu olgularda koroner anjiyografiyi takiben kontrast nefropati gelişimi üzerine nebivolol'ün potansiyel koruyucu etkisini metoprolol ile karşılaştırmak amacı ile gerçekleştirilmiştir. Yöntemler: Kreatinin seviyeleri 1.2 mg/dl ve üzerinde olan stabil koroner anjina pektoris'li 90 olgu bu prospektif çalışmaya alındı. Hastalar 2 gruba ayrıldı. Birinci gruptaki 55 olgu koroner arter hastalığı ve/veya hipertansiyon endikasyonu ile 5 mg/gün dozda oral nebivolol aldı. İkinci gruptaki 35 olgu ise benzer endikasyonlarla 50 mg/gün dozda metoprolol aldı. Renal koruma amacı ile hastalar %0.9 NaCl ile (1 mL/kg/saat) işlem önce-si 12 saat ve işlem sonrası 24 saat hidrate edildiler. Hastalara ayrıca işlemden 24 saat önce başlamak ve işlem sonrası 48 saat devam etmek üzere 600 mg N-acetylcysteine (NAC) günde 2 doz halinde verildi. Hastalar daha sonra rutin koroner anjiyografiye alındılar. Serum kreatinini işlemden hemen önce, işlemden sonra ve 48. saatte ölçüldü. Kontrast nefropatisi işlemden sonraki 48 saat içerisinde serum kreatinin değerinde bazal ölçüme göre %25 ve daha fazla artış olarak tanımlandı. Çalışma sonunda gruplar arasında sürekli değişkenlerin karşılaştırması için bağım-sız örneklem t-testi, kategorik verilerin karşılaştırılmasında ise Ki-kare testi kullanıldı. Bulgular: Anjiyografi öncesi her iki grupta da serum kreatinin seviyeleri benzerdi. Anjiyografi sonrası serum kreatinin seviyeleri her iki grupta da artış gösterdi. Anjiyografi sonrası kreatinin seviyeleri bakımından nebivolol ve metoprolol grupları arasında istatistik olarak anlamlı bir fark yoktu.
ABSTRACTObjective: This prospective study was designed to evaluate the potential protective effect of nebivolol compared with metoprolol on the development of contrast-induced nephropathy (CIN) following coronary angiography in patients with renal dysfunction. Methods: Ninety patients with stable coronary angina pectoris with renal insufficiency (creatinine value ≥ 1.2 mg/dl) were included for this prospective study. Patients were divided into two groups. Patients in group 1 (n=55) received oral administration of nebivolol 5 mg/daily for coronary artery disease and/or hypertension. Group 2 consisted of 35 patients who received metoprolol 50 mg/daily for the same indications. All patients were hydrated with 0.9% NaCl at a rate of 1 mL/kg/hr for 12 hours before and 24 hours after the procedure. Patients were also given N-acetylcysteine (NAC) 600 mg twice a day, beginning 24 hours before and continuing 48 hours after the procedure. All patients underwent routine coronary angiography. Serum creatinine was assessed just before, immediately after and 48 hours after the procedure. CIN was defined as an increase in serum creatinine concentration of ≥25% within 48 hours after the procedure compared to the patient's baseline value. Tests for significance between groups were conducted using the independent sample t-test for continuous variables and Chi-square test for categorical variables. Results: Baseline serum creatinin...
“…Rats were housed at [23][24][25] C in a 12-h light/dark cycle with free access to standard rat chow and tap water. All animal experiments were performed with the permission from the Medical Ethics Committee of Tianjin Medical University and followed the protocol outlined in the Guide for the Care and Use of Laboratory Animals published by the US National Institutes of Health (NIH Publication No.…”
Background: The risk of contrast-induced acute kidney injury (CIAKI) is significantly increased in patients with diabetes mellitus. This study aimed to investigate molecular mechanisms of contrast media-induced apoptosis in diabetic rat kidneys, especially the involvement of ERK1/2 and JNK signal pathways. Methods: Diabetic Sprague-Dawley rats were induced by intraperitoneal injection of streptozotocin. Ten weeks later the normal and diabetic rats were administered high-osmolar contrast media (HOCM; meglumine diatrizoate) or normal saline (10 mL/kg) injection for 2 consecutive days. At 24 h after the operation, the rats were sacrificed, the blood samples were collected for examining serum creatinine and the kidneys were collected for determining the expression of caspase-3 by immunohistochemistry and the expression of Bcl-2, Bax, upstream signal molecule p-JNK, and p-ERK1/2 by western blotting. Results: The serum creatinine was significantly increased in diabetes + contrast media group (DC group) after operation compared with in the diabetic group (D group; 103.89 ± 9.01 mmol/L vs. 71.52 ± 7.03 mmol/L, p50.05). While creatinine clearance rate (Ccr) was significantly decreased in DC group after operation (1.49 ± 0.33 mL/min vs. 2.60 ± 0.54 mL/min, p50.05). Especially, in the diabetic kidney, the expression of caspase-3 was also significantly increased after intravenous injection of HOCM compared with normal saline. The expression level of upstream signal molecule p-JNK protein was apparently increased, but p-ERK1/2 protein was significantly decreased (both p50.05). Conclusions: The ionic HOCM-induced renal cells apoptosis in diabetic rats through activating the caspase-3 apoptotic pathway, which might be mediated by upstream MAPK (inhibiting p-ERK1/2 expression and promoting p-JNK expression) signal pathways.
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