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These results indicated the existence of a sodium-related mechanism of T3 uptake into mouse thymocytes that does not operate for T4 uptake. sodium related mechanism of T3 uptake.doc

In patients with hyperthyroidism, short term daily therapy with sodium ipodate plus P and PTU produces a greater reduction of free T3 index values than that caused by P and PTU alone. sodium ipodate improves hyperT.doc

The number of erythrocyte Na,K-ATPase pump units has been found to be reduced in some populations of obese humans, but the effect of dietary factors upon the status of the erythrocyte pump has not been delineated. We have measured the number of Na,K-ATPase pump units by [3H]ouabain binding and the activity of the pump by ouabain-inhibitable 86rubidium uptake in response to nutritional maneuvers in several patient groups. There was no consistent change in the number or activity of Na,K-ATPase units in response to 1) an acute 600-cal meal, 2) a 3-day fast or refeeding after a fast in normal weight or obese subjects, 3) 2 weeks of hypocaloric (600 cal) feeding in obese subjects. Individuals with anorexia nervosa were also not significantly different from age- and sex-matched control subjects with respect to the erythrocyte Na,K pump. It is concluded that the circulating erythrocyte does not regulate the number or activity of Na,K pump units in response to short or medium term nutritional maneuvers. Differences between obese and thin populations with respect to the Na,K pump are not likely to be secondary to nutritional differences between the two groups. sodium.potassium pumps reduced in obesity.doc

Research on potential therapeutic agents for organophosphate toxicity has traditionally been directed toward blocking the action of acetylcholine on its muscarinic receptors or on reactivating the inhibited catalytic enzyme. Here, we used a whole-animal lethality paradigm to study another potential antidotal mechanism: pharmacological disruption of the sodium channel conductance associated with agonist action on cholinergic receptors. Mice were injected with several drugs which have in common the ability to block sodium-channels. Drugs tested were ketamine, phenobarbital, lidocaine, morphine, prednisolone, and lithium. All mice were injected with DFP (7.6 mg/kg) plus atropine; the treatment groups were simultaneously injected with the test drug, while controls received an equal volume of physiological saline. All the test drugs, at one or more doses, revealed protection, not only in terms of prolonging symptom onset but also in terms of mortality. The reduction in mortality was quantitatively similar for each drug. Although the various drugs could have protected by many different, coincidental mechanisms, a more parsimonious explanation is that the effect could have been due to one property which all had in common; namely, sodium-channel blockade. sodium channel blockers and organophosphate toxicity.doc