An association was found between the source of study support and the published outcome. Though the reason for this association cannot be determined from the data collected, future studies may clarify the importance of this finding for readers concerned with the relationship of funding bodies to the publication of research outcomes.

Utilizing a murine model, we tested the hypothesis that ␣ 2-adrenergic receptor agonists (clonidine and dexmedetomidine) protect against RCN induced with iohexol (a nonionic low-osmolar radiocontrast). C57BL/6 mice were pretreated with saline, clonidine, or dexmedetomidine before induction of RCN. Some mice were pretreated with yohimbine (a selective ␣ 2-receptor antagonist) before saline, clonidine, or dexmedetomidine administration. ␣2-Agonist-treated mice had reduced plasma creatinine, renal tubular necrosis, renal apoptosis, and renal cortical proximal tubule vacuolization 24 h after iohexol injection. Yohimbine reversed the protective effects of clonidine and dexmedetomidine pretreatment. Injection of iohexol resulted in a rapid (ϳ90 min) fall of renal outer medullary blood flow. Clonidine and dexmedetomidine pretreatment significantly attenuated this perfusion decrease without changing systemic blood pressure. To determine whether proximal tubular ␣ 2-adrenergic receptors mediate the cytoprotective effects, we treated cultured human proximal tubule (HK-2) cells and rat pulmonary microvascular endothelial cells with iohexol after vehicle, clonidine, or dexmedetomidine pretreatment. Iohexol caused a direct dose-dependent reduction of HK-2 and rat pulmonary microvascular endothelial cell viability, but ␣ 2-agonists failed to preserve the viability of both cell types. We conclude that ␣ 2-adrenergic receptor agonists protect mice against RCN by preserving outer medullary renal blood flow. As ␣2-agonists are widely utilized during the perioperative period, our findings may have significant clinical relevance to improving outcomes following radiocontrast exposure.acute renal failure; iohexol; clonidine; dexmedetomidine; yohimbine; HK-2 cells; medullary ischemia ARTERIOGRAPHY, ANGIOCARDIOGRAPHY, and contrast-enhanced CT scans account for Ͼ3,000,000 iodinated radiocontrast exposures each year in the United States (15). Renal dysfunction secondary to radiocontrast administration remains prevalent and debilitating (3). Radiocontrast nephropathy (RCN) remains the third most common cause of inpatient acute renal failure, behind ischemia-reperfusion injury and nephrotoxic medication administration (23). The diagnosis of RCN confers a 5.5-fold increase in hospital mortality (18,29), may necessitate hemodialysis (7), and is associated with an increased length of hospital stay and incidence of myocardial infarction (25).Although the pathogenesis of RCN remains incompletely understood, tubular hypoxic injury, due to a reduction of renal medullary blood flow, and direct tubular cytotoxicity play a substantial role (8,12,31). The risk of developing nephropathy after radiocontrast exposure may be as high as 50%, depending on numerous risk factors (21). Preexisting renal dysfunction and dehydration are the most predictive contributors to RCN, whereas volume of contrast exposure, contrast osmolality, congestive heart failure, diabetes, anemia, and advanced age also increase risk (2, 3). Despite the exploration of numerous proph...

Three diabetes surveys carried out at two yearly intervals on 10000 men aged 40 years and over have enabled us to compare four groups of subjects with regard to their serum uric acid level in relation to carbohydrate metabolism. Prediabetics, that is, persons who screened negative at previous surveys and subsequently developed diabetes, had a higher mean uric acid level than normals (p less than 0.001). Their uric acid level was considerably higher than in diabetics, who had a mean value lower than normals (up to p less than 0.001). Men, without diabetes, but having an abnormal GTT were found to have a mean value higher than the normals at each survey.

A study was made of 100 paediatric encounters in which an accompanying parent stated that the child had been given acetaminophen syrup during the preceding 24 hours. In 80% of cases a household teaspoon had been used to determine the amount of medication required. The volumes of these spoons were measured using a syringe. The range was from 1.5 to 5 cm3 with 79% containing 2 to 3 cm3. The mean volume was 2.95 cm3 (SD 0.79) and the median was 2.5 cm3. The mean dose administered was 62% of that recommended when the calculation was made according to age and 64% according to body weight. Much of the underdosing observed was due to parents' assumption that a household teaspoon contains 5 cm3 of acetaminophen syrup and also to a failure to correct for advancing age and increasing weight.