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Results for “Lithium Compounds”

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At least 1,207 records · Page 67Linked to original sources
PubMed2001

[Measurement of waveguide depth in proton-exchanged LiNbO3 by infrared absorption spectroscopy].

A novel method for determining proton-exchanged LiNbO3 waveguide depth by infrared absorption spectroscopy was proposed. The method overcomes the shortcoming that the conventional prism-coupling + IWKB technique is only applicable to the multimode waveguides. For the commonly used single-mode waveguides, however, it is helpless. The experimental results indicated that this method has good accuracy.

Absorptiometry, Photon↗
PubMed1992

[An experimental model of apneusis and periodic respiration].

In experiments on sodium pentobarbital (40 mg/kg, i. p.) anesthetized mongrel cats of either sex weighting from 2.0 to 4.0 kg, it was stated, that sodium or lithium hydroxybutyrate (HOB) (200 mg/kg, i. v.) effectively slowed down breathing with inspiratory holdings. Thus 3-5 minutes after HOB administration, eupneic pattern of respiration was changed firstly to inspiratory apneustic one (100% of cats), and then to periodic one (80% of cats). This pattern persisted for 60-90 minutes, and after that the respiratory pattern usually changed its direction to the opposite one. In these conditions alterations of arterial blood composition (pH, pO2, pCO2, SO2) and hemodynamic variables (heart rate, arterial pressure) can not be considered as the cause of apneustic pattern of respiration. It is suggested, that HOB can be used for simulating such terminal respiratory patterns as apneustic and periodic ones.

Animals↗
PubMed1992

[Effects of lithium hydroxybutyrate on circadian rhythm of rest-activity and sleep structure in experimental animals].

Lithium hydroxybutyrate (10 mg/kg, 10 days) influences circadian temperature and activity rhythms of rats in "open field" and sleep structure according to the time of preparation of the injection (8.30 or 19.30). It was stated that lithium hydroxybutyrate modified circadian rhythms and sleep structure less after morning injections into the rats, while evening administration destabilized circadian rhythms, increased slow-sleep and decreased REM sleep duration.

Animals↗
PubMedDate not supplied

[The lithium oxybutyrate correction of disorders in higher nervous activity in the progeny of alcoholized male rats].

In experiments on rats it was shown that alcohol administered intragastrically in a dose of 8 g/kg for 4 weeks produced long-term disturbances of CNS function in the offspring similar to those observed under clinical conditions. Early postnatal administration of lithium oxybutyrate (from the 8th through the 14th day of life) was found to prevent the development of the disturbances.

Aging↗
PubMed1986

[Effect of lithium oxybutyrate on the serotonin and 5-hydroxyindoleacetic acid content in the brain of rabbits].

Single administration of lithium hydroxybutyrate (10 mg/kg) to rabbits decreased serotonin and 5-hydroxyindoleacetic acid (5-HIAA) content in the caudate nucleus. The drug administration for 8 days is accompanied by mediator accumulation in the cortex, caudate nucleus, tonsils, hypothalamus, thalamus, and midbrain with parallel reduction in 5-HIAA level in these structures. 15 days of lithium hydroxybutyrate administration lead to the increase of serotonin and 5-HIAA concentration, while 28 days of administration reduced the content of mediator and its metabolite.

Animals↗
PubMed1985

Effects of low extracellular sodium on cytosolic ionized calcium. Na+-Ca2+ exchange as a major calcium influx pathway in kidney cells.

The effects of extracellular Na+ (Na+o) on cytosolic ionized calcium (Ca2+i) and on calcium and sodium fluxes were measured in monkey kidney cells (LLC-MK2). Ca2+i was measured with aequorin and the ion fluxes with 45Ca and 22Na. Na+-free media rapidly increased Ca2+i from 60 to a maximum of about 700 nM in 2-3 min. After the peak, Ca2+i declined and reached a plateau of about twice the resting Ca2+i. The peak Ca2+i was inversely proportional to Na+o and directly proportional to the extracellular calcium concentration (Ca2+o). On the other hand, a pH of 6.8 reduced and Ca2+o substitution with Sr2+ completely blocked the Ca2+i response to low Na+o. A Na+-free medium stimulated calcium efflux from the cells 4-5-fold, a response which was abolished in the absence of extracellular Ca2+. Na+-free media also stimulated calcium influx and sodium efflux. The cell calcium content, however, was not increased. These results indicate that removal of extracellular Na+ increases Ca2+i by stimulating calcium influx and not by inhibiting calcium efflux; the increased calcium influx takes place on the Na+-Ca2+ antiporter operating in the reverse mode in exchange for sodium efflux. The increased calcium efflux occurs as a consequence of the rise in Ca2+i and presumably takes place on the (Ca2+-Mg2+) ATPase-dependent calcium pump.

Animals↗
PubMed1985

[Combined action of lithium salts and serotonin on the caudate nucleus].

Intracaudate injections of lithium hydroxybutyrate (5 micrograms) produce a serotonin-like effect on the power characteristics of the caudatogram frequency ranges. However, when injected in a single dose, the drug is a serotonin antagonist at the level of the caudate nucleus. On the contrary, being administered for a long time, the drug potentiates the action of the mediator.

Animals↗
PubMed1985

[Effect of lithium salts on neuropathological syndromes of spinal origin].

Experiments on noninbred rats were made to study the influence of lithium hydroxybutyrate on two patterns of spinal cord pathology: the generalized myoclonus and painful syndrome of spinal origin. The syndromes were induced by generators of pathologically enhanced excitation in the ventral and dorsal horns of the spinal cord. The effects of lithium chloride and sodium hydroxybutyrate were examined to compare the influence of lithium (cation) and hydroxybutyrate (anion) components to elucidate the role of each of the components. Lithium hydroxybutyrate appeared more effective, since it inhibited the generator of pathologically enhanced excitation in the appropriate structures, provoking the anticonvulsant effect in myoclonus and suppressing the painful syndrome.

Animals↗
PubMed1981

[Effect of lithium preparations on cardiac arrhythmias resulting from ligation of the common carotid arteries].

In experiments on cats with dissected vagus and aortal nerves under chloralose-urethane anesthesia, ventricular disorders of the cardiac rhythm were induced by ligation of the common carotid arteries. Appearance of arrhythmias was preceded by an increase in the sympathetic activity (recorded from the inferior cardiac or renal nerve) accompanied by a rise of the arterial blood pressure and of the heart rate. Intravenous injection of lithium chloride or hydroxybutyrate resulted in lowering of the sympathetic activity, arterial blood pressure, and heart rate, and led to the recovery of the sinus rhythm.

Animals↗
PubMed1982

[Influence of lithium hydroxybutyrate on the electroencephalographic effects of fenamin].

Lithium hydroxybutyrate (10 mg/kg) prevents the amphetamine-induced EEG arousal and amplitude frequency alterations in the motor and visual cortex, posterior hypothalamus, midbrain reticular formation, and caudate nucleus but potentiates the action of the psychostimulant on the EEG of the hippocamp and amygdala. The response to the light flickering rhythm in the visual cortex remains within initial upon concurrent administration of both the drugs.

Amphetamine↗
PubMedDate not supplied

[Toxic effect of lithium salts on the pregnant rat and on the prenatal development of the fetus].

A study was made of toxic effect of lithium carbonate and lithium hydroxybutyrate in doses of 160 and 500 mg/kg (1/4 LD50) respectively on pregnant rats and development of fetuses. The doses of both the drugs contained an equal amount of lithium (30 mg/kg). It was established that toxicity of the drugs in pregnancy rises almost two-fold as compared to that seen in non-pregnant animals. At the same time the toxic action of lithium hydroxybutyrate was more powerful than that of lithium carbonate. However, the latter drug was found to have a greater embryotoxicity. Apparently, the differences in toxicity and embryotoxicity of the lithium salts are to a definite measure determined by anionic component of salts.

Animals↗
PubMed1984

[Comparative study of several preparations in different models of cerebral hypoxia].

The antihypoxic effects of gutimine, piracetam, sodium hydroxybutyrate and lithium hydroxybityrate were studied on different models of brain hypoxia. All the drugs under study produced a remarkable antihypoxic effect in experimental asphyxic hypoxia, increasing brain resistance to oxygen deficiency and rapidly restituting brain function. Drug pretreatment of the animals with carotid artery occlusion raised the number of animals which survived 24 h after the operation. GABA salts appeared the most effective. Sodium hydroxybutyrate increased the lifespan of rats under histotoxic hypoxia.

Animals↗
PubMed1983

[Effect of lithium hydroxybutyrate on the serotonin content of the brain in intact rabbits and during hyperactivity of the central serotoninergic systems].

Chronic administration of lithium hydroxybutyrate (10 mg/kg) to rats reduces the content of serotonin in the caudate nucleus, suppresses the growth of its level in all the subcortical brain structures. After 5-hydroxytryptophan administration it perverses the serotonin-positive action of dorsal raphe nucleus electric stimulation.

Animals↗
PubMedDate not supplied

[Effect of lithium oxybutyrate on the bioelectrical activity of the cortex and subcortical structures of the rabbit brain].

Intravenous administration of 10 mg/kg of lithium hydroxybutyrate to rabbits exerts a depressant effect on spontaneous bioelectrical activity of the cortex and subcortical structures of the brain, with this effect distributing from the cortex to the subcortex. The drug reduces the electrical excitation of the motor cortex, caudate nucleus, thalamus, posterior hypothalamus and reticular formation of the midbrain. The convulsive threshold of the amygdaloid complex decreases. No substantial changes were detected in hypocampal electrical excitability. By its depressant effect lithium hydroxybutyrate compares very favourably with lithium chloride.

Animals↗