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It was demonstrated in experiments on hamsters that lithium oxybutyrate (preliminary or therapeutic injection in a dose of 400 mg/kg) leads to relative normalization of microcirculation and secretory activity of the mast cells. Lithium oxybutyrate can be used for the prevention and treatment of postischemic disorders.
The nature of two novel C27 bile acids present as the taurine conjugates in urine from a patient with Zellweger's syndrome was studied. Bile acids conjugated with taurine were isolated from unconjugated and glycine-conjugated bile acids by means of ion-exchange chromatography. After alkaline hydrolysis of the taurine conjugates, the hydrolysate was acidified and extracted with ether; the extract was again subjected to ion-exchange chromatography to separate neutral from acidic compounds. The neutral fraction, which consisted mainly of two steroidal lactones, was treated with lithium aluminum hydride, and the reduction products were identified as (22R)-5 beta-cholestane-3 alpha,7 alpha,12 alpha,22,26-pentol and (23R)-5 beta-cholestane-3 alpha,7 alpha,12 alpha,23,26-pentol by direct comparison of their gas-liquid chromatographic behaviors and mass spectral data with those of chemically synthesized authentic samples. Thus, the chemical structure of two native bile acids present in urine from a patient with Zellweger's syndrome should be formulated as (22R)-3 alpha,7 alpha,12 alpha,22-tetrahydroxy-5 beta-cholestanoic acid and (23R)-3 alpha,7 alpha,12 alpha,12 alpha,23-tetrahydroxy-5 beta-cholestanoic acid, respectively.
The sensitivity of the vessel smooth muscles to vasopressin and their contractile responses were obviously increased in hypertensive rats, whereas the vasopressin inhibitory effect and tachyphylaxis were decreased. These changes seem to be connected with the prevalence of V1-activating over V2-inhibitory vasopressin receptors in hypertensive rats' vessel smooth muscles. Administration of lithium oxybutyrate for 4 weeks normalized central hemodynamics and decreased the sensitivity to vasopressin. The findings suggest a possible role of the inositol pathway in transmission of hormonal signal (vasopressin) to hypertensive rats' vessel smooth muscles as well as participation of vasopressin in pathogenesis of arterial hypertension and the possibility of using lithium oxybutyrate for its correction.
The possible use of sodium hydroxybutyrate and lithium hydroxybutyrate for the prevention of the decrease in splenic natural killer activity has been studied in CBA mice upon 6-hour immobilization stress. Both agents proved to be effective in preventing stress-induced depression of NK activity. However, a protective effect of lithium hydroxybutyrate was observed at a dose 4 times lower than that of sodium hydroxybutyrate.
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Application of antihypoxant drugs in postoperative period has been investigated. Lithium oxybutyrate was administered to 30 lung cancer patients before and shortly after operation. The results were compared with the data on 26 patients in control. Major characteristics, and, primarily, its antihypoxic protective effect have been evaluated. Lithium oxybutyrate administration is recommended in lung cancer patients during and shortly after surgery.
BACKGROUND: Insufficient data exist on the production of compound A during closed-system sevoflurane administration with newer carbon dioxide absorbents. METHODS: A modified PhysioFlex apparatus (Dräger, Lübeck, Germany) was connected to an artificial test lung (inflow at the top of the bellow approximately/= 160 ml/min CO2; outflow at the Y piece of the lung model approximately/= 200 ml/min, simulating oxygen consumption). Ventilation was set to obtain an end-tidal carbon dioxide partial pressure of approximately 40 mmHg. Various fresh carbon dioxide absorbents were used: Sodasorb (n = 6), Sofnolime (n = 6), and potassium hydroxide (KOH)-free Sodasorb (n = 7), Amsorb (n = 7), and lithium hydroxide (n = 7). After baseline analysis, liquid sevoflurane was injected into the circuit by syringe pump to obtain 2.1% end-tidal concentration for 240 min. At baseline and at regular intervals thereafter, end-tidal carbon dioxide partial pressure, end-tidal sevoflurane concentration, and canister inflow (T degrees(in)) and canister outflow (T degrees(out)) temperatures were measured. To measure compound Ainsp concentration in the inspired gas of the breathing circuit, 2-ml gas samples were taken and analyzed by capillary gas chromatography plus mass spectrometry. RESULTS: The median (minimum-maximum) highest compound Ainsp concentrations over the entire period were, in decreasing order: 38.3 (28.4-44.2)* (Sofnolime), 30.1 (23.9-43.7) (KOH-free Sodasorb), 23.3 (20.0-29.2) (Sodasorb), 1.6 (1.3-2.1)* (lithium hydroxide), and 1.3 (1.1-1.8)* (Amsorb) parts per million (*P < 0.01 vs. Sodasorb). After reaching their peak concentration, a decrease for Sofnolime, KOH-free Sodasorb, and Sodasorb until 240 min was found. The median (minimum-maximum) highest values for T degrees(out) were 39 (38-40), 40 (39-42), 41 (40-42), 46 (44-48)*, and 39 (38-41) degrees C (*P < 0.01 vs. Sodasorb), respectively. CONCLUSIONS: With KOH-free (but sodium hydroxide [NaOH]-containing) soda limes even higher compound A concentrations are recorded than with standard Sodasorb. Only by eliminating KOH as well as NaOH from the absorbent (Amsorb and lithium hydroxide) is no compound A produced.
We have previously described the synthesis of bisphosphonate-containing inhibitors of inositol monophosphatase. In the present study, a more detailed examination of the in vitro and in vivo properties of one of these compounds, L-690,330, is described. L-690,330 is a competitive inhibitor of inositol monophosphatase with a Ki, depending on the source of IMPase, of between 0.2 and 2 microM. Although approximately 1,000-fold more potent in vitro than lithium, in muscarinic ml receptor-transfected Chinese hamster ovary cells prelabelled with [3H]inositol, L-690,330 only produced 40% of the accumulation of [3H]inositol monophosphates achieved by lithium at the same concentration (10 mM), suggesting that the ability of L-690,330 to cross the cell membrane is limited. Nevertheless, under conditions of cholinergic stimulation (100 mg/kg of pilocarpine s.c.), high doses of L-690,330 were able to increase brain inositol(l)phosphate levels in vivo to three- to fourfold control levels. This effect was dose dependent (ED50 = 0.3 mmol/kg s.c.) and was maximal after 1 h. In peripheral tissues, the effects of L-690,330 on inositol(l)phosphate levels mimicked those of lithium both qualitatively and quantitatively. However, in the brain, the effects of L-690,330 were much less than seen with lithium, consistent with the blood-brain barrier restricting access of the polar L-690,330 into the CNS, thereby further limiting entry of compound into cells in the brain. In the future, it may be possible to develop prodrugs of this compound, which circumvent many of the cell permeability problems inherent in bisphosphonate compounds.