Influence of acceleration over the hydroelectrolytic homeostasis in audiogenic seizure-prone rats compared to normoexcitable rats.

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.

Influence of increased sodium intake on cerebral excitability.

The purpose of the study has been to observe the influence of an increased dietary sodium intake over cerebral excitability in rats. Research was conducted on two lots of animals: the first lot (PSA) was maintained under the influence of an increased intake of sodium given in the form of physiologic solution, instead of water. That regimen was started during gestation and continued after birth for another 12-14 months before the rats were sacrified. The second lot was given distilled water (DWA) in an identical manner. In other respects, the diet was similar for both lots We compared the following parameters: a) Electrophysiological (electrocorticogram); b) Hydroelectrolytic balance; c) Sodium concentration capacity of the kidney; d) Mineral-corticoid response; e) Motor and motivational behaviour. The data we obtained point to: 1. A shifting of the ECG frequency spectrum towards higher frequency in rats that consumed NaCl in excess. 2. PSA consume significantly more saline solution than DWA, therefore liquid consumption is also greater. Renal elimination of water, Na and K is significantly greater is PSA compared to DWA. Moreover, DWA conserve sodium while PSA conserve water, the respective values being different in a considerable degree in the two lots. 3. The value of the (urinary Na/urinary K) ratio is double in PSA compared to DWA, pointing to a decrease in mineral-corticoid secretion. 5. The animals that have chronically consumed a hypersaline diet show a significantly greater motor agitation compared to the DWA. When free to choose from among physiological solution, water and glucose solution, PSA show no preference for sodium: this points to the absence of obtained motivation for the saline solution The data support the idea that a chronically increased content of dietary NaCl stimulates cerebral excitability.

On some electrolytic and water metabolism modifications in rats susceptible to audiogenic convulsions.

Following our research in the relationship between mechanisms of blood transportation of sodium and cerebral excitability, we studied adult rats (males-180-230 gm), divided into two groups according to their level of excitability to noise: 1. Rats susceptible to audiogenic convulsions and, 2. Rats with normal response to acoustic stimulation. In the two groups we determined the following parameters: 1. mechanisms of blood transportation of sodium; 2. general free motor behaviour; oriented behaviour (to satisfy motivation for sodium or water); nature and intensity of motivation expressed as milliliters of liquid and grams of sodium consumed; 3. influence of the variable sodium intake on the renal elimination of sodium, potassium and water. Also the influence of the variable water intake on the renal elimination of water. Results obtained show that: cerebral hyperexcitability manifested as susceptibility to audiogenic convulsions is associated with several modifications expressed as follows: 1) Sodium transportation in blood serum occurs in a free state in rats susceptible to audiogenic convulsions, while in normal rats it occurs in a state of interaction with serum proteins; 2) In animals susceptible to audiogenic convulsions one can notice significant hypermotricity in the behaviour cage; 3) Hyperexcitable animals consume significantly more sodium chloride solution which they freely choose, in a motivational manner, than animals with a normal excitability; 4) Increased, motivational consumption of sodium chloride is associated with increased renal elimination of sodium in animals susceptible to audiogenic convulsions. Increased renal elimination of sodium is accompanied by increased elimination of water, therefore with the protection of renal concentration mechanisms; 5) If we take the Na/K ratio as an indicator for the function of the corticosuprarenal and represent it as a function of the sodium intake, the data presented show that ratio is greater in animals with cerebral hyperexcitability, which is in concordance with the data presented, also involving the mineralcorticoid hormones in this response, a similar picture to that of loading the body with sodium; 6) The data presented seem to advocate once more for the idea that normal cerebral excitability is compatible with the existence of mechanisms that transport sodium in a state of oligoenergetic interaction with blood proteins.

The influence of auditory and lithium stimulation on blood and brain serotonin in the normal rat and in that susceptible to audiogenic convulsions.

Investigations were carried out in two groups of male rats: a group susceptible to audiogenic convulsions and a control group. The following parameters were determined under basal conditions and 24 and 48 hours after intraperitoneal administration of a single lithium carbonate dose (0.67 mEq/animal), before and after auditory stimulation: serotonin content in the blood and brain tissue (separately from the hypothalamus, rhinencephalon, midbrain and sensory-motor cerebral cortex) by fluorimetry: water-saline retention, renal potassium elimination, the dynamics of renal lithium elimination. The results showed that in the rats prone to audiogenic convulsions, blood serotonin concentrations are twice those in the controls, whereas serotonin levels in the brain are lower than in the controls. The administration of lithium is followed by a decrease in blood serotonin in the animals with audiogenic convulsions but does not influence the serotonin content in the brain. Acoustic stimulation does not influence the behaviour of the controls but induces convulsions in the animals sensitive to noise. After auditory stimulation under basal conditions or 48 hours after the administration of lithium a decrease takes place in cerebral serotonin and an increase in blood serotonin in the controls whereas in the rats sensitive to noise, cerebral serotonin increases and blood serotonin decreases on stimulation under basal conditions due to the convulsions and metabolic alterations induced by the latter. These findings suggest the existence of different mechanisms for the transport of serotonin in the blood of rats prone to audiogenic convulsions. These mechanisms may be influenced either by acid catabolites resulting from convulsive activity or by the administration of lithium. The latter may induce persistent alterations in the blood transporter, as appears to result from the observation at 48 hours after the administration of lithium.

EEG automatic processing method.

This is a description of researches carried out in man and experimentally in rats. The results - obtained in 44 children aged between 12 and 14 yr. - of the electric signal processed as a F/A ratio were compared to the transport mechanisms of the blood sodium. We found that the normal brain excitability level was consistent only with the blood sodium transport through interaction with the proteins. The lack of such interaction was accompanied by an increased excitability on eeg recordings and by behaviour disturbances. The researches carried out in rats had in view the brain excitability level in two groups of animals aged 6-8 months, which drank from their birth either physiological salt (group 1) or distilled water (group 2). In this species, in spite of direct visible modifications in eeg recordings by sensorial stimulation, the processing as F/A ratio did not show any differences, and this made necessary the use of computers to process rightly the data; the respective digitization and memorising methods are described, too.

Experimental researches regarding the metabolic changes determined by the prolonged exposure to light or by keeping in darkness.

The authors conducted complex investigations in the domain of the intermediary metabolism under experimental conditions on 24 dogs grouped into three lots: lot A, twelve dogs, exposed for six months to the action of continuous light; lot B, six dogs, maintained in darkness; lot C, six dogs, maintained for the same period in the animal house, getting the same food as the other two lots, which are the control lot. We determined some biochemical, hematological, enzymatical parameters, before the beginning of the experiment, and after 24 hours, 48 hours, 7, 14 and 21 days, one, two, three, six months. Then the animals were sacrificed, and fragments from the aorta, coronary vessels, myocardium, brain, adrenals, pancreas and liver were examined both on the optical and on the electronic microscope and we analysed some fats from the vascular tissues. The net decrease of proteinemia with lot A was registered, concomitantly with a net decrease of serumalbumins, of the alpha 1-globulins and of the gamma-globulins, and with a rise of the alpha 2- and beta-globulins. The values of glycemia increased with lot A, and less with lot B. The thrombocytes decreased obviously with lot A, and less with lot B. GPT decreased with lot A, and GOT increased. The serum Zn decreased slowly with lot A, and more irregularly but more obviously with lot B. The serum Cu increased with lot A, and decreased with lot B. Alterations on the level of arterioles from the brain, aorta, myocardium and pancreas were evidenced, as well as electronmicroscopical alterations of the arteriolar walls and of the cellular organelles. The lipids from the brain, aorta and myocardium increased with both of the experimental lots and so did the cerebrosides, lecithins and the sphyngomyelin.

The influence of malathion on the brain serotonin and reproductive function in rats.

By researches carried out in adult female rats we followed the effect of chronic administration of malathion on the serotonin level from hypothalamus, rhynencephalon, mesencephalon and cerebral cortex and on the hypophysio-ovarian system. The obtained results showed that malathion produces: 1) the increase of cerebral serotonin level through the active phases of the gonadal cycle (proestrus + oestrus); 2) the increase of the percent incidence of the gonadal active phases; 3) the decrease of the LH synthesis through the oestral cycle; 4) the increase of the FSH release during the active phases and the decrease of the LH release in the inactive phases of the ovarian cycle. The data show that malathion influences the reproductive function both by its cellular toxic action and by affecting the encephalic regulatory serotoninergic, besides acetylcholinergic, mechanism of the reproductive functions.