MR arthrography: impact of steroids, local anesthetics, and iodinated contrast material on gadolinium signal intensity in phantoms at 1.5 and 3.0 T.

PURPOSE: To determine if gadolinium signal intensity at direct magnetic resonance (MR) arthrography is affected by the addition of steroids, anesthetics, or iodinated contrast material. MATERIALS AND METHODS: This study did not require approval by the institutional review board because no patients or patient data were involved. An in vitro study was performed to evaluate various concentrations of three gadolinium contrast agents (gadopentetate dimeglumine, gadobenate dimeglumine, and gadofosveset trisodium) diluted in either saline or iodinated contrast material (50% and full-strength iohexol 300). Three steroids (betamethasone, triamcinolone, and methylprednisolone) and three local anesthetics (lidocaine, ropivacaine, and bupivacaine) were added to solutions in clinical doses. T1-weighted fat-suppressed MR imaging sequences were performed in phantoms at 1.5 and 3.0 T. Signal intensities were measured. All experiments were repeated in full for a total of three replications each. The data were analyzed by using two-way factorial analysis of variance. RESULTS: Dilution of gadolinium into iohexol reduced the signal intensity in all samples compared with dilution in saline alone. Peak signal intensities were at 0.625 and 1.25 mmol/L of gadolinium in iohexol at both magnet strengths. At 1.5 T, the addition of steroids and anesthetics to the saline solutions had no impact on the signal intensity curves, with the peak signal intensity at gadolinium concentrations of 2.5 and 1.25 mmol/L. At 3.0 T, the addition of steroids and anesthetics had minimal effect on signal intensity curves, with the peak signal intensity at 1.25 mmol/L of gadolinium. CONCLUSION: The addition of steroids and/or anesthetics to gadolinium solutions for MR arthrography does not substantially impact signal intensity. When gadolinium is diluted into a 50% or greater strength of iohexol, the signal intensity curve shifts so that the maximum signal intensity is obtained with lower gadolinium concentrations (0.625-1.25 mmol/L).

Evidence against the involvement of oxidative stress in fatty acid inhibition of insulin secretion.

Prolonged exposure to elevated levels of fatty acids adversely affects pancreatic beta-cell function. Here we investigated 1) whether ceramide synthesis, which we reported to mediate fatty acid inhibition of insulin gene expression, also inhibits insulin secretion and 2) whether fatty acid inhibition of insulin secretion involves the generation of reactive oxygen species (ROS), nitric oxide (NO), or prostaglandin E(2) (PGE(2)). A 72-h culture of islets in the presence of palmitate or oleate resulted in a marked decrease in glucose-induced insulin release assessed in 1-h static incubations. This effect was reproduced by exogenous diacylglycerol, but not by a cell-permeable analog of ceramide. Culture in the presence of fatty acids was not associated with an increase in intracellular peroxide or NO levels, neither was insulin secretion restored by antioxidants or an inhibitor of NO production. Exposure to fatty acids led to an increase in PGE(2) release, but an inhibitor of cyclooxygenase 2 was unable to prevent fatty acid inhibition of insulin secretion. These results indicate that fatty acid inhibition of insulin secretion 1) is not mediated by de novo ceramide synthesis, ROS, NO, or PGE(2), and 2) is likely to be caused by the generation of signals or metabolites downstream of diacylglycerol.