Ions In Cerebrospinal Fluid Research Articles

Metal ions in cerebrospinal fluid: Associations with anxiety, depression, and insomnia among cigarette smokers.

The study aimed to investigate the relationship between cerebrospinal fluid (CSF) metal ions and anxiety, depression, and insomnia among cigarette smokers. We measured CSF levels of various metal ions from 178 Chinese male subjects. Apart from sociodemographic and clinical characteristics data, the Fagerstrom Test for Nicotine Dependence (FTND), Beck Depression Inventory (BDI), Self-Rating Anxiety Scale (SAS), and Pittsburgh Sleep Quality Index (PSQI) were applied. BDI and PSQI scores (all p < 0.001) were significantly higher in active smokers than nonsmokers. Active smokers have significantly higher CSF levels of magnesium, zinc, iron, lead, lithium, and aluminum (all p ≤ 0.002). Some metal ions, including zinc, iron, lead, and aluminum, were found to have a significant correlation with BDI scores, whereas metal ions, including zinc and lead, were found to have a significant correlation with PSQI scores in the general group. More interesting, mediation analysis showed that aluminum mediated the relationship between smoking and depression. Cigarette smoking was indeed associated with depression and insomnia. Active smokers had significantly higher CSF levels of magnesium, zinc, iron, lead, lithium, and aluminum. Furthermore, CSF aluminum played a mediating role in the relationship between smoking and depression, which further confirmed its neurotoxicity.

Association of Cigarette Smoking With Male Cognitive Impairment and Metal Ions in Cerebrospinal Fluid

Objective: Cigarette smoking might accelerate cognitive impairment; however, this has never been investigated using human cerebrospinal fluid (CSF). We conducted this study to investigate the association between cigarette smoking and cognitive impairment through metal ions in CSF.Methods: We obtained 5-ml CSF samples from routine lumbar puncture procedures in patients undergoing anterior cruciate ligament reconstruction before surgery in China. A total of 180 Chinese males were recruited (80 active smokers and 100 non-smokers). We measured specific cigarette-related neurotoxic metal ions in CSF, including iron, copper, zinc, lead, aluminum, and manganese. Sociodemographic data and history of smoking were obtained. The Montreal Cognitive Assessment (MoCA) was applied.Results: Active smokers had fewer years of education (11.83 ± 3.13 vs. 13.17 ± 2.60, p = 0.01), and higher age (33.70 ± 10.20 vs. 29.76 ± 9.58, p = 0.01) and body mass index (25.84 ± 3.52 vs. 24.98 ± 4.06, p =0.03) than non-smokers. Compared to non-smokers, active smokers had significantly higher CSF levels of iron, zinc, lead, and aluminum and lower MoCA scores (all p < 0.05). Average daily numbers of cigarettes smoked negatively correlated with the MoCA scores (r = −0.244, p = 0.048). In young smokers, CSF manganese levels negatively correlated with MoCA scores (r = −0.373, p = 0.009).Conclusions and Relevance: Cigarette smoking might be associated with male cognitive impairment, as shown by lower MoCA scores and higher levels of CSF iron, zinc, lead, and aluminum in active smokers. This might be early evidence of cigarette smoking accelerating male cognitive impairment.

Neuroprotection: Biodegradable Spheres Protect Traumatically Injured Spinal Cord by Alleviating the Glutamate-Induced Excitotoxicity (Adv. Mater. 14/2018)

New treatment strategies for spinal‐cord injury are being actively pursued. In article number 1706032, Helder A. Santos, Guoyong Yin, Jin Fan, and co‐workers show that intrathecally injected biodegradable polymeric microspheres, acetalated dextran, can protect traumatically injured spinal cord. The neuroprotective feature of acetalated dextran microspheres is achieved by sequestering the excessive glutamate and calcium ions in cerebrospinal fluid, and consequently attenuating the glutamateinduced excitotoxicity.

Biodegradable Spheres Protect Traumatically Injured Spinal Cord by Alleviating the Glutamate-Induced Excitotoxicity.

New treatment strategies for spinal cord injury with good therapeutic efficacy are actively pursued. Here, acetalated dextran (AcDX), a biodegradable polymer obtained by modifying vicinal diols of dextran, is demonstrated to protect the traumatically injured spinal cord. To facilitate its administration, AcDX is formulated into microspheres (≈7.2 µm in diameter) by the droplet microfluidic technique. Intrathecally injected AcDX microspheres effectively reduce the traumatic lesion volume and inflammatory response in the injured spinal cord, protect the spinal cord neurons from apoptosis, and ultimately, recover the locomotor function of injured rats. The neuroprotective feature of AcDX microspheres is achieved by sequestering glutamate and calcium ions in cerebrospinal fluid. The scavenging of glutamate and calcium ion reduces the influx of calcium ions into neurons and inhibits the formation of reactive oxygen species. Consequently, AcDX microspheres attenuate the expression of proapoptotic proteins, Calpain, and Bax, and enhance the expression of antiapoptotic protein Bcl-2. Overall, AcDX microspheres protect traumatically injured spinal cord by alleviating the glutamate-induced excitotoxicity. This study opens an exciting perspective toward the application of neuroprotective AcDX for the treatment of severe neurological diseases.

Sequential Determination of Inorganic Cations and Anions in Cerebrospinal Fluid by Microchip Electrophoresis

Analysis of inorganic ions in cerebrospinal fluid (CSF) is used mainly in the diagnostics of central nervous system diseases, such as Alzheimer’s disease or multiple sclerosis. A new analytical method for fast determination of inorganic cations (ammonium, calcium, magnesium, sodium and potassium) and anions (chloride, sulfate, nitrite and nitrate) in CSF on an electrophoretic microchip was developed in this context. Zone electrophoresis (ZE) separations were performed on the microchip with coupled channels (CC) and contact conductivity detection. Two different propionate background electrolytes were used for the sequential determination of cations at pH 3.1 and anions at pH 4.3. ZE was used for the determination of cationic constituents while ZE–ZE approach was employed for the determination of chloride in the first separation channel on the CC microchip and other anionic micro-constituents in the second channel. LOD values were in the range of 0.003–0.012 mg L−1 and 0.019–0.047 mg L−1 for cations and anions, respectively. Repeatability of migration time was up to 1.2 % for both cations and anions. Repeatability of peak area ranged from 0.3 to 5.6 % for cations and from 0.6 to 6.0 % for anions. Recovery of both cations and anions was in the range 90–106 %. CSF samples were only diluted appropriately without other sample pretreatment prior to analysis. Developed sequential method is suitable for fast determination of the studied cations and anions in CSF with total analysis time <15 min.

Acetazolamide and cerebrospinal fluid ions in drugs with normal acid-base balance

The purpose of these experiments was to study the effects of acetazolamide, a carbonic anhydrase inhibitor, on cisternal cerebrosphinal fluid (CSF) ions during normal acid-base balance. We measured blood and CSF acid-base variables in two groups (n = 6 in each) of anesthetized, paralyzed and mechanically ventilated dogs with bilateral ligation of renal pedicles. After baseline samples were obtained, acetazolamide was administered intravenously within 10 min (group II); group I received equal volume (20 ml) of half-normal saline. During the next 6 h, in both groups arterial blood acid-base variables and plasma strong ions remained relatively normal. In group I, mean values for cisternal CSF P CO 2 were 45.3 and 49.3 mm Hg at 0 and 6 h; respective values for CSF [HCO 3 −] were 24.1 and 22.7 mEq/L. In group II, corresponding values for P CO 2 and [HCO 3 −] were 46.4 and 51.9 mm Hg, adn 23.8 and 23.7 mEq/L. respectively. Comparing the two groups, related mean values were not significantly different from each other. Futhermore, acetazolamide had no significant effect of CSF Na +, K + and Cl − concentrations. Based on the results of this study and those reported previously, we conclude that under normal acid-base balance, acetazolamide does not change ionic composition of cisternal CSF, choroidal CSF or brain extracellular fluid.

Effects of acetazolamide on cerebrospinal fluid ions in metabolic alkalosis in dogs.

We hypothesized that inhibition of carbonic anhydrase in the central nervous system by acetazolamide should limit the rise in cisternal cerebrospinal fluid (CSF) [HCO3-] observed in metabolic alkalosis. To test this hypothesis, isosmotic isonatremic metabolic alkalosis was produced in two groups of anesthetized, paralyzed, and mechanically ventilated dogs (8 in each group). Group II animals received 50 mg/kg of acetazolamide intravenously 1 h before induction of metabolic alkalosis of 5-h duration. Renal effects of acetazolamide were eliminated by ligation of renal pedicles. In both groups cisternal CSF [Na+] remained relatively constant during metabolic alkalosis. In group I CSF [Cl-] decreased 3.6 and 8.2 meq/l, respectively, 2.5 and 5 h after induction of metabolic alkalosis. Respective increments in CSF [HCO3-] were 3.4 and 6.0 meq/l. In acetazolamide-treated dogs, during metabolic alkalosis, increments in CSF [HCO3-] (4.8 and 7.2 meq/l, respectively, at 2.5 and 5 h) and decrements in CSF [Cl-] (9.1 and 13.3 meq/l) were greater than those observed in group I. We conclude that, in dogs with metabolic alkalosis and bilateral ligation of renal pedicles, acetazolamide impairs CSF regulation of HCO3- and Cl- ions; acetazolamide not only failed to impede HCO3- rise but actually appeared to increase it. The mechanisms for these observations are discussed.

Plasma ADH increase and thirst suppression elicited by preoptic heating in the dog.

Plasma ADH increase and thirst suppression elicited by preoptic heating in the dog.

The effect of chelation of calcium ions in cerebrospinal fluid on the osmotic thirst in dogs.

The osmotic reactivity of the thirst mechanism was examined in conscious dogs implanted chronically with cannulas in the lateral ventricle and with thermistors in the anterior hypothalamus. The experiments were performed under control conditions and after chelation of calcium ions of the cerebrospinal fluid by infusion of sodium edetate (Na2 EDTA) into the ventricle.In seven out of nine experiments infusion of Na2 EDTA caused an increase in deep body temperature of 1.70 «; 0.35°C and marked elevation of the thirst threshold to the osmotic stimulus. The threshold cellular dehydration causing drinking increased from 2.54 ± 0.63% of intracellular water (ICW) to 6.80 ± 1.57 of ICW. In two experiments, in which infusion of Na2 EDTA did not increase deep body temperature, water intake was enhanced.The possible mechanism of these effects is discussed.

Transfer of Potassium Between Blood, Cerebrospinal Fluid and Brain Tissue

Anesthetized dogs were injected with radioactive potassium. After intravenous injection the appearance of the ions in cerebrospinal fluid was a summation of two exponentials with the maximum at about 30 minutes. The ratio of radioactivities of brain tissue to cerebrospinal fluid was stabilized at 120 minutes, whereas the ratio of cerebrospinal fluid to plasma reached this state after 30 minutes. After intracisternal injection the disappearance of K42 from cerebrospinal fluid was described by two exponentials. The activity in the plasma reached a maximum at 10–15 minutes and thereafter paralleled the disappearance curve from cerebrospinal fluid. Brain tissues did not reach equilibrium. These data have been compared with those obtained using radioactive sodium and bromide and discussed in relation to cerebrospinal fluid formation.