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We used flameless atomic absorption spectrophotometry to measure concentrations of Fe, Mo, Li, As, and Zn in cerebrospinal fluid (CSF) of patients with malignant brain tumors benign brain tumors, non-brain malignant tumors and control (non-neoplastic disease) patients. Mean (and SD) concentrations (microgram/L) of these elements in the control group were 62.7 (28.7) for Fe, 6.8 (4.8) for Mo, 0.7 (2.0) for Li, 1.3 (0.7) for As, 7 (5.9) for Zn. We could detect Li in less than 53% of controls. Zn concentrations in CSF of patients with astrocytoma (malignant brain tumor), benign brain tumors, or non-brain tumors were significantly (p less than 0.05) less than in control patients; the ratios for mean concentrations of Zn in tumor patients/control patients for the above groups were 0.3, 0.20, and 0.17, respectively. Concentrations of As in CSF of patients with non-brain malignant tumors were significantly (p less than 0.05) higher than in the controls; the ratio for mean CSF concentration of As in patients with non-brain tumors/control patients was 2.9. Differences in the concentrations of Fe, Li, or Mo among the various groups were nonsignificant.

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The role of the choroid plexus in regulating the lithium concentration in c.s.f. was studied by the use of the cat choroid plexus isolated in situ in a chamber. LiCl solution (154 mM) was infused i.v. to produce plasma lithium concentrations between 0 and 7.5 m-equiv/l. Over this range of plasma values the c.s.f./plasma ratio remained at 0.58. The plasma and c.s.f. concentrations were constant after about 90 min. Lithium (1.8 or 4.5 m-equiv/l.) was added to the artificial c.s.f. placed in the chamber at the start of a 30-min collection period. The lithium concentration in the chamber fluid was measured at the end of the collection period with the plasma concentration either 0 or greater than that in the chamber. When the lithium gradient was from chamber fluid to blood there was a net loss of lithium from the chamber and the amount was proportional to the gradient. However, when the gradient was in the opposite direction lithium was added to the chamber but the amount added was related to the plasma lithium concentration rather than to the blood-c.s.f. gradient. Altering the potassium concentration in the chamber fluid changed the rate of potassium transport without a comparable effect on lithium movement out of the chamber. Lithium transport by the potassium transport system does not appear to be a major factor in the loss of lithium from the chamber. The data suggest that lithium is transported actively across the choroid plexus into the c.s.f. by the system that is responsible for c.s.f. secretion. Movement from c.s.f. to blood appears to be accomplished primarily by passive diffusion when the c.s.f. concentration significantly exceeds that in the plasma.

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Rats received 0.15 M LiCl either as a central treatment in the lateral cerebroventricles (2x20 microliter/rat) or as a peripheral treatment in the peritoneal cavity 15 ml/kg). The central treatment produced high lithium concentrations (1-1.2 mmol/kg) in the brain while peripheral treatment produced high lithium levels (1-2 mmol/1) in the blood at convenient times for behavioral tests. The central treatment antagonized amphetamine-induced hyperactivity but failed to affect open field behavior in otherwise untreated rats. In contrast, the peripheral treatment suppressed open field activity in otherwise untreated rats but failed to influence behavioral effects of amphetamine. The findings demonstrate differences between central and peripheral actions of LiCl on behavior in rats and show lithium to have central actions on hyperactivity induced by amphetamine.

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Central and peripheral injections of LiCl were given to rats to see whether conditioned taste aversions are caused by central or peripheral effects of Li. Rats received an IP injection of either 150 mmol/l LiCl or 150 mmol/l NaCl and a bilateral intracerebroventricular (ICV) injection of either 150 mmol/l LiCl, 150 mmol/l NaCl, or artificial cerebrospinal fluid (CSF) after drinking saccharin solution. Subsequent saccharin intake decreased in rats which received the IP LiCl injection, but failed to depend on which ICV injection had been given. The concentration of Li in bain and CSF was higher 0.5, 1.5, and 4 h after the ICV LiCl injection than after the IP LiCl injection, while the reverse was true for the plasma Li level. It is concluded that conditioned taste aversions are mediated by peripheral effects of Li.

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Simultaneous measurement of plasma, RBC, and plasma lithium concentrations took place with 17 inpatients chronically treated with lithium, at various times after the last lithium dose. RBC lithium levels were significantly higher than CSF lithium levels. Specimens drawn 10 or more hours after the last dose showed higher RBC and CSF lithium and lower plasma lithium than specimens drawn 4 or less hours after the last lithium dose. None of the lithium measurements differentiated manic-depressives from schizophrenics or schizoaffectives. Plasma, RBC, and CSF lithium all intercorrelated highly and equally.

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1 Addition of lithium carbonate (55 mmol/kg dry wt.) to the diet of rats for 4 days resulted in ratios between lithium in the brain and serum and between the cerebrospinal fluid (CSF) and serum of approx. 1 and 0.4, respectively. The relationships between the concentrations were linear. 2 After single intraperitoneal injections of lithium chloride (5 mmol/kg body wt.) the concentration of lithium in the CSF was greater than that of the brain for 2 h. 3 Repeated subcutaneous injections of lithium chloride (0.9 mmol/kg body wt.) resulted in steady state ratios corresponding to those observed when lithium was given in the diet. The rate of elimination from the CSF was intermediate between that of the serum and cerebral tissue until a new equilibrium was reached after approx. 24 h. At that time the ratios between lithium in the brain and serum, and in the CSF and serum were increased to approx. 5 and 0.8, respectively. 4 These results are consistent with passive transfer kinetics of lithium in the CSF and elimination of lithium from the cerebral tissue via the CSF. 5 The results may explain some of the phenomena observed in patients during intoxication with lithium.

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The concentration of lithium was determined in plasma, cerebrospinal fluid (CSF) and bile in two groups of 5 and 6 patients after oral administration of lithium carbonate (0.2 mVal/kg b.w.) in each group. In a third group of 7 patients the lithium concentration in the brain and also in the CSF and the plasma was determined in the steady state. The influx into CSF was delayed in contrast to that into plasma and bile. The elimination was biexponential. The mean plasma half-life of lithium carbonate was 21 hours. The concentration ratio between CSF and bile, respectively, and plasma was 0.44 +/- 0.03 and 1.48 +/- 0.36 in steady state. Two percent of the given dose was eliminated with the bile within 24 hours. There was no concentration difference in steady state between that for CSF and both white and grey brain matter. It is suggested that the concentration of lithium in CSF represents the brain concentration.

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Kinetic examinations of lithium concentrations in the aqueous humour and in the liquor in man were carried out. The passage of lithium into both extravascular compartments took place in different manners. Lithium - liquor concentrations seem to be only of a rather limited positive evidence as to the concentrations at the spot of action; the possible causes for this fact are discussed.

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