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Published on: April 5, 2011
Influence of acceleration over the hydroelectrolytic homeostasis in audiogenic seizure-prone rats compared to
1D. Danielopolu Institute of Normal and Pathological Physiology, Bucharest.
Abstract:
This research concentrated on the hydroelectrolytic balance response after centrifugation (+5G/30 minutes, five times) in two lots of rats: one lot made up of animals with normal cerebral excitability, and another one of animals prone to audiogenic seizure. Both before and after centrifugation, we determined: water (ml/24 hrs.) and sodium chloride (mEq/24 hrs.) consumption; dependence of sodium, potassium and water elimination on the amount of sodium ingested (mEq/24 hrs.). We also determined the renal capacity of sodium concentration and the mineral-corticoid response based on the urine Na/K ratio and on the determination of plasma renin activity (PRA). Data obtained show that audiogenic seizure-prone rats consume less sodium and water after centrifugation, unlike normoexcitable rats in which there have been no differences in this respect. Exposure to hypergravitation induces in both lots an increase of sodium, potassium and water elimination. Renal elimination of water is greater in the normoexcitable animals than in the seizure-prone ones. By contrast, sodium elimination is greater in the audiogenic seizure-prone animals. Urine sodium concentration is lower in the seizure-prone animals, consistent with the amounts of water eliminated. Their mineral-corticoid response is intensely diminished after centrifugation in comparison to that of the control, normo-excitable animals. PRA is diminished in both lots. Our findings support the assumption that seizure-prone rats are unable to adaptatively respond to acceleration by preserving sodium through the intervention of cortico-surrenal mechanisms. As water is not preserved, it seems that in this category of animals, both during and after centrifugation, it is mostly the hypothalamo-retrohypophyseal mechanisms that come into play. This could be the outcome of disturbances occurring in the mechanisms of blood sodium transport that are deficient in the seizure-prone animals.
