Application of BOLD MRI and DTI for the evaluation of renal effect related to viscosity of iodinated contrast agent in a rat model.

PURPOSE: To evaluate the effects of viscosity of contrast agent (CA) on intrarenal oxygenation and diffusion as measured by blood oxygenation level-dependent (BOLD) magnetic resonance imaging (MRI) and diffusion tensor imaging (DTI) in a rat model. MATERIALS AND METHODS: Radiocontrast iodixanol formulated in three viscosities were designated 270, 320, and 350 (mg iodine/mL). Sixty-three male Wistar rats were divided into four groups. Saline and iodixanol (4 g iodine/kg) were administered. MR images were acquired on a 3.0T scanner at baseline and at 1 hour, 24 hours, 48 hours, and 72 hours postinjection of solutions. BOLD-MRI was performed with a multiple gradient-recalled-echo sequence. The changes in R2*, apparent diffusion coefficient (ADC), fractional anisotropy (FA), histology, and hypoxia-inducible factor-1α (HIF-1α) immunoexpression were evaluated. The R2*, ADC, and FA values were normalized to baseline to calculate ΔR2*, ΔADC, and ΔFA. RESULTS: Compared with baseline levels, distinct elevation of ΔR2* (P < 0.05) and obvious decrease in ΔADC (P < 0.01) and ΔFA (P < 0.05) were observed in all the anatomical compartments at 1 hour after administration of CA. The absolute values in ΔR2*, ΔADC, and ΔFA increased with increases in CA viscosity, and differed significantly between the CA groups in renal cortex (CO), outer stripe of outer medulla (OSOM), and inner stripe of outer medulla (ISOM) (all P < 0.05). A significant positive correlation was observed between ΔR2* and HIF-1α expression (P < 0.001, r = 0.75). Significant negative correlations were observed between ΔADC, ΔFA, and pathologies in CO, OSOM, ISOM (all P < 0.001, r = -0.68-0.87; all P < 0.001, r = -0.60-0.66). CONCLUSION: The effect of CA viscosity on intrarenal oxygenation and diffusion was viscosity-dependent, and was identified using BOLD-MRI and DTI. LEVEL OF EVIDENCE: 1 Technical Efficacy: Stage 3 J. Magn. Reson. Imaging 2017;46:1320-1331.

Effects of iodinated contrast agents on renal oxygenation level determined by blood oxygenation level dependent magnetic resonance imaging in rabbit models of type 1 and type 2 diabetic nephropathy.

BACKGROUND: To evaluate the effects of contrast agents containing increasing concentrations of iodine on the renal oxygenation level determined by blood oxygenation level dependent (BOLD) magnetic resonance imaging (MRI) in a rabbit model of diabetic nephropathy. METHODS: BOLD-MRI was performed using saline or iodinated (I) contrast agents (200, 240, 300, 350 and 400 mg I/mL) at 1, 24, 48, and 72 h after experimentally inducing type 2 diabetic nephropathy in rabbits. Differences in renal oxygenation levels between type 1 and type 2 diabetic nephropathy were also assessed by BOLD-MRI after injecting 400 mg I/mL of contrast agent. RESULTS: Contrast agents increased the R2* values of the renal cortex, outer medulla, and inner medulla to the maximum levels at 24 h. The R2* values then decreased to their lowest levels at 72 h. The R2* was highest following injection of 400 mg I/mL, especially in the outer medulla. The R2* values were not significantly different between types 1 and 2 diabetic nephropathy. CONCLUSIONS: Iodinated contrast agents had the greatest influence on renal outer medulla oxygenation level at 24 h in type 2 diabetic nephropathy, with the greatest effects observed at the 400 mg I/mL dose level. There were no differences in BOLD-MRI values between type 1 and type 2 diabetic nephropathy after administering the contrast agent at 400 mg I/mL.

Clinical application and diagnostic value of noninvasive spinal angiography in spinal vascular malformations.

OBJECTIVE: The purpose of this study was to explore the value of computed tomographic (CT) spinal angiography with 256-slice CT and fast dynamic contrast-enhanced 3-dimensional magnetic resonance angiography (MRA) at 3.0 T in the diagnosis of spinal vascular malformations. METHODS: Seventeen patients who presented with suspected spinal vascular diseases by initial magnetic resonance and clinical findings all underwent CT spinal angiography. Among these, 10 patients underwent MRA, 15 patients underwent digital subtraction angiography (DSA) within 3 to 5 days, and 8 patients finally underwent surgical treatment. RESULTS: Computed tomographic angiography examination clearly showed the abnormal vascular lesions in 16 of the 17 patients, including 7 patients with the diagnosis of spinal dural arteriovenous fistula, 7 patients with perimedullary arteriovenous fistula, and 2 patients with spinal arteriovenous malformations. The results were consistent with the diagnosis of DSA or surgery. One patient was poorly diagnosed. The fistulas could be seen in 12 patients; feeding arteries were correctly displayed in 12 patients. The fistulas and feeding arteries were accurately shown in 7 of 10 patients by MRA; DSA results were also negative in the other 3 patients. CONCLUSIONS: Spinal angiography with 256-slice CT and contrast-enhanced MRA at 3.0 T can clearly show the extent of spinal vascular malformations, feeding arteries, and fistulas. They are safe, noninvasive, as well as rapid and can shorten the time of DSA diagnosis and treatment.

Calcium signal-initiated early activation of NF-kappaB in neurons is a neuroprotective event in response to kainic acid-induced excitotoxicity.

We demonstrate that activation of nuclear factor kappaB (NF-kappaB) in neurons is neuroprotective in response to kainic acid (KA)-induced excitotoxicity. Combination of Western blotting, immunocytochemistry, and electrophoresis mobility shift assay showed that KA exposure induced a fast but transient nuclear translocation of the NF-kappaB p65 subunit and increased DNA-binding activity of NF-kappaB in primary cultured cortical neurons. The transient NF-kappaB activity was associated with upregulation of antiapoptotic Bcl-xL and XIAP gene products revealed by real-time PCR. Knockdown of p65 decreased neuronal viability and antiapoptotic gene expression. In addition, we showed that KA-stimulated DNA-binding activity of NF-kappaB was associated with reactive oxygen species and calcium signals, using AMPA/KA receptor antagonist, calcium chelator, and antioxidant. These results suggest that the fast and transient activation of NF-kappaB initiated by calcium signals is one of the important proximal events in response to KA-induced excitotoxicity, which has neuroprotective effect against KA-induced apoptosis.

Stabilization of mitochondrial function by tetramethylpyrazine protects against kainate-induced oxidative lesions in the rat hippocampus.

Mitochondria are critical regulators of cell death, a key feature of neurodegeneration. Reactive oxygen species (ROS) are crucial to Ca(2+)-mediated effects of glutamate receptor activation leading to neuronal degeneration. Tetramethylpyrazine (TMP) is a principal ingredient of Ligusticum wallichi Franchat (a Chinese herb), used for treatment of cardiovascular and cerebrovascular ischemic diseases. However, its protection against oxidative brain injury associated with excessive activation of glutamate receptors is unknown. In this study, we demonstrate TMP neuroprotection against kainate-induced excitotoxicity in vitro and in vivo. We found that TMP could partly alleviate kainate-induced status epilepticus in rats and prevented and rescued neuronal loss in the hippocampal CA3 but not the CA1 region. The partial prevention and rescue of neuronal loss by TMP were attributable to the preservation of the structural and functional integrity of mitochondria, evidenced by maintaining the mitochondrial membrane potential, ATP production, and complex I and III activities. Stabilization of mitochondrial function was linked to the observation that TMP could function as a reductant/antioxidant to quench ROS, block lipid peroxidation, and protect enzymatic antioxidants such as glutathione peroxidase and glutathione reductase. These results suggest that TMP may protect against oxidative brain injury by stabilization of mitochondrial function through quenching of ROS.

Preliminary evaluation of magnetic resonance fresh blood imaging for diagnosis of Budd-Chiari syndrome.

BACKGROUND: Budd-Chiari syndrome (BCS) is a rare disease with portal hypertension caused by the blockage of the hepatic vein and/or the inferior vena cava (IVC). Angiography is the "golden standard" for diagnosis, but it is an invasive examination. To assess the diagnostic value of a fresh blood imaging (FBI) relative to BCS, we used a magnetic resonance angiography (MRA) with an FBI sequence for a preoperative evaluation of the BCS patients in this study. METHODS: Fifty patients who were suspected of having BCS after they had been checked by a B-ultrasound were studied. 2D and 3D FBI were performed on a 1.5T superconductive MR scanner. Original images were rebuilt using a maximal intensity projection (MIP) method on the console. Two doctors reviewed all images before they learned of the angiography results. We then compared the diagnoses obtained from the FBI and angiography results to evaluate the diagnostic value of the FBI. RESULTS: Forty-one patients were diagnosed as BCS and 9 as non-BCS based on an angiography. The FBI correctly diagnosed 38 patients, incorrectly diagnosed 1 patient, and missed diagnosis in 3 patients. Thus, the diagnostic sensitivity of the FBI is 93% (38/41), the specificity is 89% (8/9) and the accuracy is 92% (46/50). The FBI images of the 13 membranous stenoses of the IVC showed a sudden stenosis of the post-liver segment of the IVC. The Images of the 5 patients with a membranous obstruction of the IVC showed IVC thickening and an absence of blood signals in the post-hepatic segment of the IVC. The images of the 4 patients with the segmental thrombosis of the IVC showed abnormal and intermittent signals in the IVC. The images of the 6 patients with a simple hepatic vein obstruction showed obstructive hepatic veins. The images of the 6 patients with the stenosis of both the IVC and the hepatic veins showed the stenosis of the IVC, the thickening of the hepatic veins and the formation of a compensatory circulation within the liver. Lastly, the images of the 7 patients showed a combination of the IVC thrombosis with stenosis or with the obstruction of one or two hepatic veins. CONCLUSIONS: An FBI can show a membranous stenosis, and an obstruction and thrombosis of the IVC. In addition, it can also demonstrate the thickening of the flexural hepatic vein and the development of intra-hepatic compensatory branches with slow blood flow. Thus, it can guide the puncturing and opening of the hepatic vein involved in an interventional therapy for BCS patients.