3 Tesla 23Na Magnetic Resonance Imaging During Acute Kidney Injury.

RATIONALE AND OBJECTIVES: Sodium and proton magnetic resonance imaging (23Na/1H-MRI) have shown that muscle and skin can store Na+ without water. In chronic renal failure and in heart failure, Na+ mobilization occurs, but is variable depending on age, dialysis vintage, and other features. Na+ storage depots have not been studied in patients with acute kidney injury (AKI). MATERIALS AND METHODS: We studied 7 patients with AKI (mean age: 51.7 years; range: 25-84) and 14 age-matched and gender-matched healthy controls. All underwent 23Na/1H-MRI at the calf. Patients were studied before and after acute hemodialysis therapy within 5-6 days. The 23Na-MRI produced grayscale images containing Na+ phantoms, which served to quantify Na+ contents. A fat-suppressed inversion recovery sequence was used to quantify H2O content. RESULTS: Plasma Na+ levels did not change. Mean Na+ contents in muscle and skin did not significantly change following four to five cycles of hemodialysis treatment (before therapy: 32.7 ± 6.9 and 44.2 ± 13.5 mmol/L, respectively; after dialysis: 31.7 ± 10.2 and 42.8 ± 11.8 mmol/L, respectively; P > .05). Water content measurements did not differ significantly before and after hemodialysis in muscle and skin (P > .05). Na+ contents in calf muscle and skin of patients before hemodialysis were significantly higher than in healthy subjects (16.6 ± 2.1 and 17.9 ± 3.2) and remained significantly elevated after hemodialysis. CONCLUSIONS: Na+ in muscle and skin accumulates in patients with AKI and, in contrast to patients receiving chronic hemodialysis and those with acute heart failure, is not mobilized with hemodialysis within 5-6 days.

Involvement of drinking and intestinal sodium absorption in hyponatremic effect of atrial natriuretic peptide in seawater eels.

Atrial natriuretic peptide (ANP) decreases plasma Na+ concentration and promtes seawater (SW) adaptation in eels. The hyponatremia may most probably be caused by increased branchial extrusion of Na+, but the mechanism has not been determined yet. The present study examined initially the effects of ANP on branchial Na+ efflux in vivo using isotopic 22Na. However, the efflux rate was not altered by infusion of a hyponatremic dose of ANP (5 pmol.kg(-1).min(-1)). Therefore, we sought to examine whether the ANP-mediated hyponatremia is caused by a decrease in the uptake of Na+ from the environment. Since a decrease in drinking was highly correlated with a degree of hyponatremia, conscious SW eels were infused with dilute SW into the stomach at a normal drinking rate to offset the antidipsogenic effect of ANP. Under this regimen, the hyponatremic effect of ANP was abolished. Then, we examined the site of Na+ absorption in the alimentary tract by measuring the changes in ion composition of intraluminal fluid along the tract. Since Na+ was absorbed at the esophagus and anterior/middle intestine, a sac was prepared at each site and the effects of ANP were examined in situ in conscious SW eels. ANP infusion did not alter Na+ absorption at the esophagus, but it profoundly reduced the absorption at the intestine. Together with our previous finding that ANP does not alter renal Na+ excretion, we propose that ANP reduces plasma Na+ concentration in SW eels by inhibiting drinking and subsequent absorption of Na+ by the intestine.

Calculation of the absorbed dose for the overexposed patients at the JCO criticality accident in Tokai-mura.

The doses for the overexposed patients were estimated by the measurement result of specific activity of 24Na in blood. The present method is almost based on documents of the International Atomic Energy Agency (IAEA) and the Oak Ridge National Laboratory. The neutron energy spectrum obtained using the ANISN code (Multigroup One-Dimensional Discrete Ordinates Transport Code System with Anisotropic Scattering) was assumed. The values in ICRP Publication 74 were applied for the doses in each organ per unit neutron fluence. Gamma-ray dose was indirectly estimated based on (a) the result of environmental monitoring around the accident site and (b) a graph in IAEA manual, which gives the kerma ratio of neutrons and gamma-rays as a function of the critical volume or the atomic ratio of hydrogen to 235U. The estimated neutron doses were 5.4 Gy for patient A. 2.9 Gy for patient B and 0.81 Gy for patient C. The estimated gamma-ray doses were 8.5 or 13 Gy for patient A, 4.5 or 6.9 Gy for patient B, and 1.3 or 2.0 Gy for patient C.

Inhibition of Na,K-ATPase and sodium pump by anticancer ether lipids and protein kinase C inhibitors ET-18-OCH3 and BM 41.440.

The anticancer ether lipid analogs ET-18-OCH3 and BM 41.440 inhibited Na, K-ATPase in the purified rat brain membrane fragments, with a potency comparable to that of their inhibition of protein kinase C. They also inhibited Na,K-ATPase in the crude membrane fraction of HL60 cells. Kinetic analysis indicated that the lipids had a mode of action different from that of ouabain, a classic inhibitor of the ATPase. The lipids also blocked 22Na uptake in the inside-out membrane vesicles of human erythrocytes. It is suggested that Na,K-ATPase might represent an additional site with which certain protein kinase C inhibitors can interact to alter cellular activities.