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Background: In previous literature, reference values for cerebrospinal fluid (CSF) may be based on patients who were not truly healthy, other species, or outdated information. In the present study, we performed a lumbar puncture in patients requiring spinal anesthesia by a reasonable indication to evaluate CSF parameters in healthy adults., Methods: All patients between the ages of 20 and 70 years scheduled for elective orthopedic or urologic surgery requiring spinal anesthesia were enrolled in this study. We measured electrolytes and gas tension analysis in CSF and whole blood samples in adult humans., Results: A total of 28 patients were included with an average age of 44.2 years. The concentration of Na^+ in blood was slightly lower when compared with that in CSF. There were significantly higher levels of K^+ and Ca^(2+) in the blood when we compared with CSF. Significantly lower levels of Cl^- and Mg^(2+) in the blood were observed when compared with CSF. The glucose level of CSF was about half of that in blood., Conclusions: We provided updated reference values for various solutes in blood and CSF in adults. Analysis of CSF parameters and relevant paired blood samples is highly informative, helping clinicians diagnose a variety of central nervous system diseases.

The choroid plexus (CP) is an extensively vascularized neuroepithelial tissue that projects into the brain ventricles. The restriction of transepithelial transport across the CP establishes the blood-cerebrospinal fluid (CSF) barrier that is fundamental to the homeostatic regulation of the central nervous system microenvironment. However, the molecular mechanisms that control this process remain elusive. Here we show that the genetic ablation of Sox9 in the hindbrain CP results in a hyperpermeable blood-CSF barrier that ultimately upsets the CSF electrolyte balance and alters CSF protein composition. Mechanistically, SOX9 is required for the transcriptional up-regulation of Col9a3 in the CP epithelium. The reduction of Col9a3 expression dramatically recapitulates the blood-CSF barrier defects of Sox9 mutants. Loss of collagen IX severely disrupts the structural integrity of the epithelial basement membrane in the CP, leading to progressive loss of extracellular matrix components. Consequently, this perturbs the polarized microtubule dynamics required for correct orientation of apicobasal polarity and thereby impedes tight junction assembly in the CP epithelium. Our findings reveal a pivotal cascade of SOX9-dependent molecular events that is critical for construction of the blood-CSF barrier., Competing Interests: The authors declare no competing interest., (Copyright © 2021 the Author(s). Published by PNAS.)

The diagnosis of drowning is still a difficult task in forensic science. Biochemical changes in different body fluids have been examined for the identification of drowning. However, none of them alone gives accurate results in the diagnosis of drowning and differentiation of saltwater and freshwater drowning. This study aimed to examine cerebrospinal fluid changes in drowned rabbits. Six groups of rabbits were used including immersed dead rabbits in freshwater or saltwater (as control groups), alive fully conscious rabbits drowned in freshwater and saltwater, and anesthetized rabbits drowned in freshwater and saltwater. Cerebrospinal fluid electrolytes except for potassium levels were significantly higher in rabbits drowned consciously in saltwater than their level in the control group. In rabbit drowned in freshwater, the examined electrolytes decreased significantly. In addition, urea, creatinine, uric acid, glucose, and tumor necrosis factor were different in cases of freshwater and saltwater drowning from those of control rabbits. Electrolytes and biochemical changes of unconscious rabbits drowned in water showed no significant difference from those of control rabbits. Cerebrospinal fluid examination in drowning gives promising results in the diagnosis of drowning. In addition, the differentiation between freshwater and saltwater drowning was possible.

Study Objective: A glucose check is used for investigation of a suspected accidental dural puncture in epidural anesthesia. However, glucose-positive clear fluid is sometimes aspirated from an epidural catheter in cases without clinical evidence of puncture. The goal of the study was to investigate time-dependent changes in the aspirate composition after injection of a local anesthetic into the epidural space., Design: Observational study., Setting: Operating rooms at Hamamatsu University Hospital., Patients: The subjects were 30 patients (ASA I or II) undergoing surgery with combined epidural and general anesthesia., Interventions: After epidural injection of local anesthetics, aspiration through the catheter was performed every 10min until fluid could not be aspirated. pH, Na, K, Cl, Ca and glucose were measured in fluid samples using a blood gas analysis apparatus., Main Results: No patients had pain or clinical signs suggesting dural puncture throughout the perioperative period. Fluid aspiration was possible in 15 patients (50%) after 10min and in 7, 3, 2 and 2 patients after 20, 30, 40 and 50min, respectively. Glucose was detected in each aspirated fluid sample and gradually increased with time to become closer to the level in cerebrospinal fluid (CSF). Each electrolyte also changed to approach the level found in CSF., Conclusions: A glucose check may increase the risk of a false-positive finding for accidental dural puncture with increasing time after local anesthetic injection. Conversely, detection of glucose at the time of epidural catheter placement may provide useful information for detection of accidental dural puncture., (Copyright © 2016 Elsevier Inc. All rights reserved.)

Sulforhodamine 101 (SR101) is widely used for astrocyte identification, though the labeling mechanism remains unknown and the efficacy of labeling in different brain regions is heterogeneous. By combining region-specific isolation of astrocytes followed by transcriptome analysis, two-photon excitation microscopy, and mouse genetics, we identified the thyroid hormone transporter OATP1C1 as the SR101-uptake transporter in hippocampus and cortex.

To clarify whether peripheral inflammation has a remote effect on the central nervous system, the electrolyte disposition between the circulating blood and central nervous system was evaluated in rats with carrageenan-induced acute peripheral inflammation (API). λ-Carrageenan was subcutaneously injected in the hind paw of the rat, and lithium was utilized as a surrogate marker of sodium. When the plasma and cerebrospinal fluid (CSF) concentrations of lithium were examined following lithium being intravenously administered, it was revealed that the CSF concentration of lithium in API rats is reduced compared to that in normal rats, while the plasma concentration profile of lithium in API rats is indistinguishable from that in normal rats. The pharmacokinetic analysis showed that the lithium disposition from the plasma to CSF markedly decreased by 35.8% in API rats compared to that in normal rats. On the other hand, when lithium was immediately administered into the lateral ventricle, its elimination profiles in CSF were not different between normal and API rats. It is therefore probable that the lithium disposition from the plasma to CSF alters in API rats, reflecting the entry process of electrolytes from the circulating blood to brain tissue being suppressed in response to peripheral inflammation.

The altered electrolyte handling of the choroid plexus was investigated in rats with acute renal failure (ARF) using lithium and rubidium as surrogate markers for sodium and potassium, respectively. Firstly, the transport of these two markers from the plasma to cerebrospinal fluid (CSF) was evaluated after they were concurrently injected into the femoral vein. As a result, their disposition from the plasma to CSF was shown to decrease in ARF rats, but the relationship profile between those two markers was not different from that observed in normal rats, indicating that the decreased disposition of lithium and rubidium occurs without affecting the stoichiometric balance. To clarify the mechanisms accounting for the decreased disposition, an inhibition study was then performed. When bumetanide, an inhibitor of the Na(+) /K(+) /2Cl(-) co-transporter, was directly introduced into the cerebroventricle prior to lithium and rubidium being intravenously administered, a marked increase in the markers' disposition was observed. However, such an increased disposition did not occur when bumetanide was injected into the femoral vein. Other inhibitors, such as amiloride for the Na(+) /H(+) exchanger and ouabain for Na(+) /K(+) -ATPase, did not show any effects on marker disposition regardless of the inhibitor being administered into either the cerebroventricle or femoral vein. These findings suggest that the decreased marker disposition in ARF rats is due to an increased efflux process of the choroid plexus mediated by the Na(+) /K(+) /2Cl(-) co-transporter. That is, electrolyte efflux from the CSF to plasma increases, and thereby the electrolyte influx from the plasma to CSF is counteracted., (Copyright © 2010 John Wiley & Sons, Ltd.)

Background and Objective: We investigated cerebrospinal fluid characteristics in patients with and without diabetes mellitus and the influences that changes in these characteristics have on sensory and motor block when spinal anaesthesia is performed., Methods: We included 44 patients in each study group. All received spinal administration of 15 mg of 0.5% isobaric bupivacaine. Blood and cerebrospinal fluid were analysed for glucose, total protein, urea, albumin, immunoglobulin G, sodium, chloride, potassium, calcium, magnesium and osmolarity as well as the performance of the local anaesthetic from establishment until complete regression of sensory and motor block., Results: The cerebrospinal fluid of the two groups differed significantly (P < 0.05) in the levels of total protein, albumin, immunoglobulin G, glucose and osmolarity. Sensory and motor block was established more rapidly in the diabetic group (P < 0.05), and the total duration from maximum block until regression to two dermatomes was greater (P < 0.05), as was the complete regression from sensory and motor block (P < 0.05)., Conclusion: This study shows that diabetes mellitus has an influence on sensory and motor block after the administration of spinal isobaric bupivacaine.

Purpose: To investigate in vitro, the cellular network activity of the hippocampus in Q54 mice that display spontaneous seizures because of a gain-of-function mutation of the Scn2a sodium channel gene., Methods: Extacellular recordings were obtained from CA1 and CA3 pyramidal neurons in hippocampal slices prepared from Q54 transgenic and nontransgenic littermates (WT) under physiologic conditions as well as during periods of orthodromic stimulation of the Schaffer collaterals. Cerebral spinal fluid samples were analyzed and cresyl violet histology of the hippocampus was conducted., Results: Increased spontaneous extracellular activity was found in both CA1 and CA3 regions of Q54 hippocampal slices. Q54 slices also demonstrated significantly greater spontaneous and afterdischarge activity as well as population spike amplitude and duration following tetanic stimulus in comparison to WT slices. Frequency analysis of tetanically stimulated recordings indicated high-frequency components (100 and 200 Hz) unique to Q45 slices. Analysis of cresyl violet histology supports healthy Q54 slices up to 10 weeks, while Q54 cerebral spinal fluid shows elevated osmolarity., Conclusion: Evidence for hyperexcitability and increased synaptic efficacy in Q54 mice was found by observing spontaneous activity as well as evoked activity. Response to tetanic stimulation included unique high-frequency oscillations, and resulted in an increased population spike amplitude and duration. Histological assessment shows equivalent neuronal development in both experimental groups. The data support the hypothesis that modified Scn2a channels in Q54 mice result in network hyperexcitability of the hippocampus necessary for the development and maintenance of temporal lobe seizures.

Objectives: Several works have investigated the role of serum magnesium (Mg) concentrations in traumatic brain injury. However, there is restricted information about cerebrospinal fluid (CSF) levels of Mg in patients with severe head injury (SHI). We assessed the changes of Mg concentrations in CSF and serum in patients with SHI during the first 10 days after the trauma., Methods: Eleven patients with SHI were studied prospectively on days 1-3, 5 and 10 with analysis of CSF and serum levels of Mg and Ca. The control group consisted of nine patients with hydrocephalus., Results: CSF levels of Mg were significantly higher in patients than controls in the corresponding time points except on days 5 and 10 of trauma. The CSF Mg levels tended to decrease and the highest level was found on day 1 after trauma (2.81 +/- 0.65 mg/dl). In the control group, the CSF level of Mg was 1.95 +/- 0.66 mg/dl. No significant difference can be detected between controls and patients regarding serum Mg and Ca levels. In addition, significantly higher values of Ca in the CSF were observed in all time points after trauma in patients with SHI than in the controls. There was no correlation between the CSF and serum levels of Mg and Ca levels., Discussion: Our study demonstrates that in patients with SHI, CSF levels of Mg and Ca are elevated during the whole observation period. Further works should be designed in order to show the role and importance of CSF levels of ionized Mg in outcome of patients with SHI.

Estimation of time since death from sodium and potassium ion concentration levels in CSF (cerebrospinal fluid) was carried out in 100 medico legal autopsies with known time of death in the department of Forensic medicine, Gandhi Medical College in Bhopal region of Central India. CSF was aspirated from lateral ventricles after opening the skull and dura, and concentration of these ions were estimated by flame photometry. Results revealed a significant correlation of sodium and potassium ions in CSF up to 25 h of time since death, with average per hour rise of 1.21 meq/h for potassium and fall of 1.115 meq/h for sodium ions. A useful relationship between sodium potassium ion ratio and PMI (post-mortem interval) was also elicited. The study concludes that changes in CSF electrolyte is a significant parameter to estimate time since death.

Cerebral microdialysis is an invasive technique for neurochemical monitoring that has been established for neuro-critical disorders such as subarachnoid hemorrhage and severe brain injury. We present data on cerebral microdialysis in stroke patients which were obtained in an ongoing study supported by the German Ministry for Education and Research. So far, 50 patients have been included who required critical care due to massive stroke of the middle cerebral artery territory. By correlating the microdialysis results with follow-up CT scans, we could define the neurochemical characteristics of three different brain compartments: (1) noninfarcted brain tissue with normal microdialysis values, (2) brain areas adjacent to the infarct core which were not hypodense in CT scans but caused reversible neurochemical alterations, and (3) the infarct core with massive concentration changes which did not normalize over the measuring period of 3 to 5 days. Microdialysis values averaged over time and correlated with initial PET scans helped to describe neurochemical predictors of a malignant, i.e., life-threatening, space-occupying course of the ischemic stroke. We discuss the value of this method in guiding therapy and predicting clinical outcome in the context of other neurological critical care disorders and describe the pros and cons of cerebral microdialysis as an invasive monitoring technique.

Though diabetes is a disease with vascular complications, little is known about its effects on the blood-brain barrier or the blood-cerebrospinal fluid barrier (BCSFB). The BCSFB is situated at choroid plexuses located in the lateral, third, and fourth ventricles. Choroid plexuses are the primary site of cerebrospinal fluid (CSF) production and express numerous ion transporters. Previous studies have shown a perturbation of ion transport in the periphery and brain during diabetes. In this study, we investigated the effect of diabetes on ion transporters in the choroid plexuses of streptozotocin (STZ)-induced diabetic rats. Diabetes was induced in male Sprague-Dawley rats by intraperitoneal injection of STZ (60 mg/kg in citrate buffer, confirmed by glucose analysis: 601 +/- 22 mg/dl diabetic rats, 181 +/- 46 mg/dl age-matched controls); and at 28 days, rats were killed, choroid plexuses harvested, and protein extracted. Western blot analyses were carried out using antibodies for ion transporters, including Na(+)-K(+)-2Cl(-) cotransporter and the Na(+)-K(+)-ATPase alpha1-subunit. The efflux of the K(+) analog (86)Rb(+) from choroid plexus was also studied. Diabetic rats showed an increase in expression of the Na(+)-K(+)-2Cl(-) cotransporter and the Na(+)-K(+)-ATPase alpha1-subunit, as compared with age-matched controls, a decrease in Na(+)-H(+) exchanger expression, and no change in Na(+)-K(+)-ATPase beta1- or beta2-subunit. The net effect of these changes was a 66% increase in (86)Rb(+) efflux from diabetic choroid plexus compared with controls. These changes in expression may affect choroid plexus ion balance and thus significantly affect CSF production in diabetic rats.

Astragalus lusitanicus is a toxic legume grown in Morocco and in some other Mediterranean countries. In small ruminants, poisoning by this plant is dominated by nervous signs characterized by many cycles of excitement-depression. Macroscopic examination of poisoned animals showed congestive lesions and oedema in the brain and lungs. Microscopic lesions consisted mainly of vacuolar degeneration in neurons, hepatocytes and in spleen and kidney cells. Serum activity of AST and CK as well as blood glucose and urea were increased as a result of poisoning. However, serum activity of alpha-mannosidase was not modified as is the case in locoism. Chemical investigations showed that A. lusitanicus does not contain swainsonine or miserotoxin and its selenium concentration is very low. However, this legume contains indolizidin alkaloids and a first compound was purified and identified.

Fever accompanies subarachnoid hemorrhage (SAH) in the majority of patients. In a previous study, hemoglobin (Hb) was shown to catalyze in vitro, under aerobic conditions, the conversion of arachidonic acid to prostaglandin E2 (PGE2) and prostaglandin F2alpha. The aim of the present work was to assess whether this pathway also operates in vivo and to provide a mechanism to explain post-SAH fever. To this end, PGE2 concentration was determined in cerebrospinal fluid (CSF) of conscious rabbits chronically cannulated in the lateral ventricle and cisterna magna, following intracerebroventricular (i.c.v.) injection of 10 microg or 100 microg of commercial rabbit bicrystallized Hb as a model of SAH. Before i.c.v. injection, Hb solutions were filtered on a polimixin-B column to remove substantially, by over 90%, endotoxin-like substances. Results show that in nine rabbits injection of 10 microg Hb did not significantly modify body temperature or significantly alter CSF PGE2 content. On the contrary, in nine rabbits, injection of 100 microg Hb produced a significant increase in core temperature which was accompanied by a significant increase in CSF PGE2. When data related to these two parameters from the 9 control and 18 Hb-treated rabbits were analyzed as a single group, a linear, positive, and highly significant correlation was found. These findings indicate that, once Hb is released into the subarachnoid space during SAH, it enhances CSF PGE2 content and elicits hyperthermia, thus offering an explanation for the fever that is an aggravating condition in most SAH patients.

A 30-year-old HIV-positive man presented with acute hydrocephalus secondary to tuberculous meningitis, for which an external ventricular drain was inserted. He developed marked natriuresis in the postoperative period, which resulted in acute hyponatraemia (131 to 122 mmol/l) and a contraction of his intravascular volume. A diagnosis of cerebral salt wasting syndrome was made, and he responded to sodium and fluid loading. This case highlights the differentiation of cerebral salt wasting syndrome from the more commonly occurring syndrome of inappropriate anti-diuretic hormone secretion as the aetiology of the hyponatraemia.

Cerebrospinal fluid (CSF) plays an important role in the brain's adaptive response to acute osmotic disturbances. In the present experiments, the effect of 48-h dehydration on CSF formation and absorption rates was studied in conscious adult sheep. Animals had cannulas chronically implanted into the lateral cerebral ventricles and cisterna magna to enable the ventriculocisternal perfusion. A 48-h water deprivation altered neither CSF production nor resistance to CSF absorption. However, in the water-depleted sheep, intraventricular pressure tended to be lower than that found under control conditions. This likely resulted from decreased extracellular fluid volume and a subsequent drop in central venous pressure occurring in dehydrated animals. In conclusion, our findings provide evidence for the maintenance of CSF production during mild dehydration, which may play a role in the regulation of fluid balance in the brain during chronic hyperosmotic stress.

The concentrations of total protein, glucose, cholesterol, triglyceride, urea nitrogen, creatinine, sodium, potassium, chloride, calcium, inorganic phosphorus, copper, magnesium, and iron and the activities of aspartate aminotransferase (AST), alanine aminotransferase, (ALT), alkaline phosphatase (ALP), lactate dehydrogenase (LD), creatine kinase (CK) and amylase were determined in cerebrospinal fluid (CSF) and serum from 21 clinically healthy adult camels. The concentrations of sodium, potassium and chloride in CSF were similar to those of serum; whereas the values for all other constituents were significantly higher (P<0.05) in serum than in CSF.

To evaluate the effects of bacterial meningitis on blood and CSF parameters, an experiment was conducted with five Iranian crossbred male calves. Blood and CSF samples were collected 3 times within a 5-day interval before the administration of bacteria for obtaining control values. Following the injection of E. coli, K12 into the cerebrospinal fluid from the lumbosacral space, samples were collected and clinical signs of meningitis were observed. Blood and CSF samples were obtained from the meningitis group 3 times at 1, 3, and 5 days post injection. The treatment of the infected calves using lincospectin and tetracycline was carried out immediately after the onset of clinical signs. After the treatment, blood and CSF samples were obtained 3 times during a 5-day period. Following the induction of meningitis, the number of WBCs, neutrophils, eosinophils and monocytes significantly increased (P < 0.05). However, the percent of lymphocytes decreased significantly (P < 0.05). The concentrations of glucose, potassium and activity of AST, LDH, CK significantly increased (P < 0.05). In contrast, the concentrations of phosphorous, sodium and magnesium significantly decreased (P < 0.05). Furthermore, following the induction of meningitis, the CSF was slightly xantochromic and turbid. The concentrations of protein, cholesterol, phosphorous, potassium, the activities of AST, LDH, CK, and the cell numbers in the CSF increased significantly (P < 0.05). In contrast, the concentration of glucose and pH in the CSF decreased significantly (P < 0.05). This study showed that bacterial meningitis can have profound effects on blood and CSF parameters which enable one to reach diagnosis.

CSF samples were taken from 50 healthy pigs of both sexes and cytologically and biochemically examined. With the aid of regression calculations it was investigated, whether deep freezing of CSF samples influences the laboratory results. The parameters glucose, urea, creatinine, total protein, magnesium, anorganic phosphate, AST and AP were in good agreement with the values of the original samples exhibiting only slight variations. Minor age relationship was only seen with respect to the two enzymes LDH and HBDH. A linear relationship was found between values in CSF and in serum of the parameters urea, creatinine, sodium and potassium. CSF examination should include cell count, Pandy's test and bacteriological investigation as well as the determination of the levels of the enzymes LDH and HBDH. The activity of the enzymes AST and ALT increases along with the severity of the tissue damage (meningitis). The specific gravity increases similarly to the total protein level in cases of chronic compression of the spinal cord, and Pandy's test becomes positive. However, CSF glucose levels are partly reduced in animals with central nervous symptoms. The levels of the enzymes AP and CK are often increased in central nervous disturbances, but do not admit drawing a conclusion on the degree of damage.

Unlabelled: During acute febrile diseases mild disturbances of water and electrolyte balance occur frequently. It has been suggested that changes in electrolyte balance, in particular hyponatraemia, might predispose a child to convulsions during febrile illness; however, the changes of electrolytes in the CSF are not known. We have studied the effects of fever and convulsions on water and electrolyte balance in CSF and serum by measuring osmolality and electrolyte concentrations in children. The febrile population consisted of 60 children, 36 of whom had seizures during fever. Twenty-one children without convulsions and nine children with epileptic symptoms were nonfebrile controls. We noticed that CSF is subject to changes in osmolality and electrolyte concentration during fever, while convulsions do not exhibit such changes. CSF osmolality and sodium concentrations were lower in febrile children than in nonfebrile controls. The osmolality in febrile children with convulsions was 3.8% (P < 0.01) and without seizures 3.5% (P < 0.01) lower than in nonfebrile nonconvulsive children. The changes in CSF sodium concentration, and to a lesser extent potassium and chloride concentrations, paralleled those of CSF osmolality. A positive correlation was observed between the CSF and serum osmolatities (r = 0.73, P < 0.0001), and sodium concentrations (r = 0.63, P < 0.0001). A negative correlation between the body temperature and both CSF osmolality (r = -0.66, P < 0.0001) and sodium concentration (r = -0.59, P < 0.0001) exhibits also the important regulative role of increased body temperature., Conclusion: Fever is an important factor for disturbances in fluid and electrolyte balance. The alterations in CSF osmolality and sodium concentration do not, however, give an unambiguous explanation for the susceptibility to simple febrile seizures.

A sharp (16.4%) increase of blood serum osmolality very close to the critical values was found in acute period of ischemic stroke, while sodiumemia exceeded the normal levels by 50 mmol/l and more. Meanwhile, the concentrations of Na ions in liquor of such patients was not significantly increased. The levels of Ca, K, Mg ions as well as the osmolality of blood serum and liquor were stable too. The alterations of these parameters were not significantly changed in epileptic patients out of fits. Both the analysis of the reasons of hyperosmia and hypersodiumemia development and the search for the methods of their prophylaxis and correction will be quite important in further investigations.

Acid-base balance and electrolytes concentration in cerebrospinal fluid (CSF) of patients with bacterial and lymphocytic meningitis were assessed. Inflammatory process causing the damage of blood-brain barrier and brains hypoxia leads to statistically significant changes of pH, pO2, bicarbonates and K+ concentrations in CSF of patients with bacterial meningitis, which in lymphocytic meningitis were not observed. Patients with fatal; outcome of bacterial meningitis showed higher CSF's acidosis and lover bicarbonates with higher K+ concentrations, which suggest deeper damage of brain hemostasis regulating mechanisms in those patients.

Cerebrospinal fluid and serum were obtained from 17 adult, healthy llamas (9 males, 1 castrated male, and 7 females). Osmolality; activities of lactate dehydrogenase and creatine kinase; and concentrations of glucose, sodium, chloride, potassium, total protein, and albumin were determined in serum and CSF. Total and differential cell counts were determined in CSF, and electrophoresis of CSF proteins was performed. Total nucleated cell count was low, 0 to 3/microliters, which is lower than that reported for other domestic species and is similar to values in healthy people. Differential leukocyte percentages were disparate depending on the degree of blood contamination. Blood contamination influenced the percentage of neutrophils and eosinophils in CSF. Samples with few erythrocytes had differential leukocyte distribution similar to that of other species: mostly lymphocytes, fewer monocytoid cells, and scant neutrophils. Older llamas had a few eosinophils in the CSF. Total protein, albumin, and gamma-globulin concentrations in llamas were similar to values in cattle and were higher than values in most domestic species. Glucose concentration in CSF was approximately 40% of the value in serum (nonruminant animals and peoply typically have CSF glucose concentration that is approximately 60 to 80% of the serum glucose concentration). Sodium and Cl concentrations in CSF were higher than those in serum, whereas K concentration was lower in CSF, compared with serum. Activities of creatine kinase and lactate dehydrogenase in CSF were markedly lower than those in serum, and the ranges of values in this group of healthy llamas were narrow.

Data on canine cisternal cerebrospinal fluid (CSF) ions in acute respiratory alkalosis are limited and fragmentary. We hypothesized that with the fall in arterial PCO2 (PaCO2) and in the face of normal osmoregulation, CSF [Na+] remains relatively constant and CSF [Na+-Cl-] narrows to account in part for the fall in CSF [HCO3-]. We therefore measured blood and CSF acid-base variables and ions of two groups of pentobarbital-anesthetized, mechanically ventilated dogs (n = 10 in each group). In the control group, PaCO2 was kept constant and changes in serum and CSF ions were minimal. In Group II (acute respiratory alkalosis), both PaCO2 and cisternal CSF PCO2 decreased by 10 mm Hg. Five hours after induction of respiratory alkalosis, mean CSF [HCO3-] decreased significantly by 4.4 +/- 1.2 mEq/L (mean +/- SD). The fall in CSF [HCO3-] was similar to changes in CSF strong ion difference (SID = Na(+)+K(+)+Ca(2+)+Mg(2+)-CL(-)-lactate), which decreased 4.4 +/- 1.9 mEq/L. Concentrations of the four major CSF cations did not change significantly. Cisternal CSF lactate rose significantly by 1.2 +/- 0.9 mEq/L, accounting for 25% of the change in CSF [HCO3-]. The remaining (75%) change in CSF [HCO3-] was accounted for by changes in CSF [Cl-].

NaCl cotransport carrier is known to be involved in transepithelial fluid absorption and secretion in various tissues. Recent studies indicate that Na-K-2Cl cotransport carrier also exists in the choroid plexus cells and that inhibition of the carrier decreases cerebrospinal fluid (CSF) production. In this study, we used large-dose intravenous furosemide, an inhibitor of Na-K-2Cl carrier, to determine the effects on cisternal CSF ionic composition in acute respiratory acidosis. In pentobarbital-anesthetized mechanically ventilated dogs, renal pedicles were ligated to prevent furosemide-induced diuresis. The experimental group (group II, n = 7) received 400 mg/kg of furosemide intravenously, and group I (control group, n = 7) received the vehicle. In group II, serial serum and CSF furosemide concentrations were approximately 10(-3) and 10(-5) mol/l, respectively. During 5 h of acute respiratory acidosis in both groups, the mean arterial PCO2 increased approximately 25 Torr, with comparable changes in CSF PCO2. In both groups, CSF [HCO3-] and [H+] rose approximately 3 meq/l and 20 neq/l, respectively. Changes in CSF [Na+], [K+], [Cl-], and [Na(+)-Cl-] were also similar and were not significantly different from each other when the two groups were compared. These data show that furosemide at the dose that inhibits NaCl cotransport carrier does not significantly alter ionic composition of cisternal CSF.

Sodium/chloride cotransport carrier is known to be involved in transepithelial fluid absorption and secretion in various tissues. Recent studies indicate that Na,K,2Cl cotransport carrier also exists in the choroid plexus cells and inhibition of the carrier alters ionic composition of the choroidal tissue. In this study, we report the effects of large dose intravenous bumetanide, a potent inhibitor of Na,K,2Cl carrier, on cisternal CSF ionic composition in acute respiratory acidosis in pentobarbital-anesthetized mechanically ventilated dogs. Renal pedicles were ligated to prevent bumetanide-induced diuresis. The experimental group (Group II, n = 7) received 50 mg/kg of bumetanide intravenously and Group I (the control group, n = 7) received the vehicle. Analysis of serum and choroidal plexus tissue revealed bumetanide concentration of approximately 10(-5) mol/L in Group II. During 5 h of acute respiratory acidosis in both groups, the mean PaCO2 increased approximately 25 mm Hg, with comparable changes in CSF PCO2. In both groups, CSF [HCO3-] and [H+] increased approximately 3 mEq/L and 20 nEq/L, respectively. Furthermore, changes in CSF [Na+], [K+], [Ca2+], [Mg2+], [Cl-], and [Na(+)-Cl-] were also similar and were not significantly different from each other. These data show that bumetanide, at the dose that inhibits NaCl cotransport carrier, does not significantly affect ionic composition of cisternal CSF.

By studying early postmortem changes in cerebrospinal fluid (CSF) it is possible to draw conclusions as to premortem focal brain cell injury and terminal brain ischemia. Cisternal fluid (CF) from 40 different adult cadavers with no known neurological disorder was analyzed and compared with known in vivo values. They were divided into four groups (n = 10 in each group), CF samples taken 2, 4, 10, and 24 h after death. The enzyme activity of CK and CK-BB (EC 2.7.3.2) increased linearly and statistically significantly 4-24 h postmortem (P < 0.001) the 2 h values being already 10 to 20 times higher than in vivo, LD and its isoenzymes 1 to 3 (EC 1.1.1.27) distinctly 10 to 24 h after death. Glucose and pyruvate concentrations in the CF declined, as did Na+ and Cl-. Lactate and K+ increased over time. The earliest statistically significant changes between different timepoints were seen in lactate, pyruvate and K+ concentrations. The GABA concentration was already more than 170 times at 2 h postmortem, and glutamate more than 20 times higher than in vivo. The concentrations of alanine, glycine, lysine, histidine, isoleucine, phenylalanine, and tyrosine were 2 to 3 times higher at 2 h postmortem than during life. The concentrations of all amino acids and ammonia increased linearly and statistically significantly (P < 0.001) in the CF 4 to 24 h postmortem.

Creatine kinase (CK) and its brain-specific isoenzyme (CK-BB), neuron-specific enolase (NSE), neural cell adhesion molecule (NCAM) and the ions sodium, potassium, chloride and calcium were measured both in CSF and serum and inorganic phosphate in CSF in order to assess their prognostic value in total brain ischemia due to cardiac arrest. The samples were collected at 4, 28 and 76 h after resuscitation. Twenty consecutive patients resuscitated from ventricular fibrillation or asystole were included in the study. Nine of the patients recovered consciousness (recovered) but eleven remained comatose (disabled). The follow-up period was 2 years after which only one patient was still alive. The earliest statistically significant differences between neurologically recovered and disabled patient groups were seen in CSF inorganic phosphate (P = 0.030) already at 4 h and CK-BB (P = 0.046) and NSE (P = 0.020) activity at 28 h. Later, at 76 h after the resuscitation CSF NSE differentiated the groups most clearly (P = 0.014). The values were higher in the disabled patients. A negative correlation between CSF parameters and Glasgow Coma scores was also seen at these timepoints. Statistically significant differences between the groups were seen in both CSF and blood pCO2, pO2, base excess (BE) and actual bicarbonate (HCO3-). CSF or serum NCAM has no prognostic value in anoxic-ischemic coma. The results suggest that in CSF CK-BB and NSE are useful prognostic indicators of hypoxic brain injury when measured 28-76 h after cardiac arrest whereas blood samples have no prognostic value.

Can loop diuretics like ethacrynic acid and furosemide, when administered intravenously, significantly alter ion transport and fluid dynamics in CNS? To shed light on this unresolved issue, we tested the ability of these agents to effect redistribution of Na, K and Cl in adult rat brain. Cl penetration into various CNS regions was assessed as the volume of distribution, i.e., uptake, of 36Cl from blood. Ethacrynic acid and furosemide (50 mg/kg IV) reduced by 20-30% the rate of permeation of 36Cl across the blood-CSF barrier, and they elevated [K] and [Cl] in choroid plexus (CP) by 15-25%. The loop diuretic-induced buildup of K and Cl in CP (lateral and 4th ventricle) was likely a reflection of decreased movement of these ions across the apical membrane into CSF. 36Cl activity in parietal cortex and pons-medulla decreased in treatment with furosemide and ethacrynic acid, due to slowing of Cl transport across blood-brain and/or blood-CSF barriers. Our inhibitory findings in intact rats are consistent with those from previous in vitro experiments demonstrating diminution by loop diuretics of Na, K and Cl transport across isolated CP membranes.

Cerebrospinal fluid and plasma sodium, potassium, chloride, calcium and glucose concentration were measured parallel in 14 pathological newborn babies of gestational age and birthweight of 36.3 +/- 4.3 wks and 2410 +/- 890 g, respectively, at the age of 37.8 +/- 4.4 wks postconceptionally. Whilst potassium, calcium and glucose level is much lower in the cerebrospinal fluid than in the plasma, similar sodium and higher chloride concentration was found in the cerebrospinal fluid. The significant positive correlation between plasma and cerebrospinal fluid glucose and sodium levels proves the lack of a functioning barrier for these compounds. On the other hand, cerebrospinal potassium level varied within a narrow range, independently of the plasma-concentration and the maturity of the studied babies. Pathophysiological implications of the results are further discussed in short.

In order to investigate the effect of saline loading on the atrial natriuretic peptide (ANP) in the central nervous system (CNS), time course measurements of the ANP content in the cerebrospinal fluid (CSF), blood pressure, water and electrolyte balances were carried out after saline loading in rats. Cisternal saline loading (120 ml/day) was found to induce a significant increase in urinary volume and electrolyte excretion, and to cause an initial rise in mean arterial blood pressure (MAP) in WKY rats. The ANP content in the CSF was significantly increased after saline loading, as compared to that in the control period. The ANP in both the plasma and CSF revealed a significant increase over the control values following chronic saline loading. Based on these results, it is suggested that the ANP in the CSF could exert a regulatory effect on the blood pressure and water balance, either by a direct action on the kidney or indirectly via an action on the CNS.

Serum and CSF calcium, magnesium, potassium and sodium were analyzed in 14 patients suffering from subarachnoid haemorrhage and in 10 healthy controls. The calcium and potassium concentrations in serum and CSF were decreased while magnesium unchanged and sodium were unchanged. A deranged electrolyte homeostasis was thus detectable in the CSF following subarachnoid haemorrhage. It could not be established whether symptoms of delayed cerebral ischemia were related to CSF calcium and/or potassium levels.

Concentrations of Na+, K+, Ca2+, and Mg2+ were measured in the cerebrospinal fluid from the lateral ventricles of hungry and satiated sheep. The concentrations of those ions and the ratios between them varied little before and after a meal. Concentrations were, in milliequivalents per litre: Na+, 156.6 +/- 1.5; K+, 2.94 +/- 0.02; Ca2+, 2.37 +/- 0.04; and Mg2+, 2.18 +/- 0.03.

In the present study we investigated if an amiloride inhibitable Na+ -H+ exchange mechanism may also be involved in the regulation of cisternal cerebrospinal fluid (CSF) [HCO3-] during acute respiratory acidosis (ARA). In anesthetized, paralyzed and ventilated dogs either mock CSF (group I, control) or mock CSF containing amiloride (group II) was injected into the cerebral lateral ventricles and ARA was induced by 8-10% CO2 breathing during 4 1/2 hours. During hypercapnia arterial PCO2 and plasma [HCO3-] rose respectively by about 35 mm Hg and 3 mmol/L in both groups. The rise in cisternal CSF PCO2 (about 40 mm Hg) was similar. However, changes in CSF [HCO3-] were significantly different between the two groups; in the control group, mean CSF [HCO3-] rose by 2.4, 4.1 and 4.4 mmol/L respectively, 1 1/2, 3 and 4 1/2 h after induction of ARA. In the amiloride group the respective rise was only 1.1, 2.5 and 2.5 mmol/L. The differences in CSF [HCO3-] could not be ascribed to differences in CSF lactate concentration. We conclude that an amiloride inhibitable Na+ -H+ exchange may play a role in the regulation of CSF [HCO3-] during acute respiratory acidosis in dogs.

The concentrations of Na+, K+, Cl-, Ca++, and Mg++ were measured in the CSF and serum of controls and in those of patients with hydrocephalus. Hydrocephalus was proved with pneumoencephalography. The amounts of Na+, K+, Ca++, and Mg++ were significantly higher in the CSF of patients with hydrocephalus than in the CSF of controls. The changes in the electrolyte concentration gradients seem to indicate that it is not the blood-brain barrier but the brain-CSF barrier which is disturbed in hydrocephalus.

As part of an experiment designed to study the acute and chronic metabolic changes associated with dietary chloride (Cl) restriction and sodium bicarbonate (NaHCO3) supplementation in cows in early lactation, base-line and final experimental CSF specimens were collected to evaluate the relative effects of a nutritional Cl deficiency on serum and CSF electrolyte concentrations. Attention was paid to the comparative alterations in serum and CSF Cl concentrations as an indication of the potential for the choroid plexus active Cl transport mechanism to conserve CSF Cl concentrations in the face of total body Cl depletion. Serum Cl values in cows fed the restricted Cl diets decreased from 96.4 +/- 3.5 mEq/L to 83.4 +/- 4.5 mEq/L in a 2-week trial and from 106.0 +/- 2.8 mEq/L to 75.5 +/- 6.7 mEq/L in an 8-week trial, as an indication of a nutritional Cl deficiency. Healthy cows maintained CSF Cl concentrations approximately 20% higher than the serum values, whereas cows fed a diet containing 0.10% Cl and 0.70% NaHCO3 for 2 weeks maintained CSF Cl values at 134.8% of the serum Cl concentrations, and CSF Cl concentrations in cows given a diet with 0.10% Cl and 0.80% NaHCO3 for 8 weeks increased to 137.2% of the serum Cl values.

Total cerebral ischaemia in rats caused a marked increase in the cisternal CSF potassium concentration but little change in CSF sodium or chloride concentration. The anaesthetic techniques studied (pentobarbitone, halothane/oxygen and nitrous oxide/oxygen/relaxant) did not effect the potassium increase following cerebral ischaemia. We conclude that the mechanism of barbiturate protection following cerebral ischaemia is different from that of hypothermia.

Studies reporting the composition of cerebrospinal fluid obtained from hydrocephalic humans have been critically reviewed. Hydrocephalus-induced alterations in the cerebrospinal fluid concentrations of neurotransmitters and peptide neuromodulators, products of glycolysis and nucleotide metabolism, neural cell-derived proteins and enzymes, and serum-derived proteins have been documented. The data are interpreted with reference to experimental studies. The reported changes suggest that in the hydrocephalic brain there are disturbances of oxidative metabolism and neurotransmission, and perhaps damage to periventricular cells particularly when intracranial pressure is elevated. Although no assays have provided and entirely useful guide to aid decisions regarding shunt therapy, they have provided in vivo information regarding the pathophysiology of hydrocephalus.

During acute respiratory acidosis increments in cisternal cerebrospinal fluid (CSF) [HCO3-] approximate decrements in CSF [Cl-] with CSF [Na+] remaining unchanged; the mechanisms mediating this reciprocal anionic relationship are unclear. In the present study we investigated the effects of DIDS (4,4'-diisothiocyano-disulfonic stilbene), a known inorganic anion exchange blocker, on CSF ionic regulation in acute respiratory acidosis. In two groups of anesthetized paralyzed dogs we injected either mock CSF (group I, n = 8) or mock CSF containing DIDS (group II, n = 9) into the lateral cerebral ventricles. After 45 min, acute respiratory acidosis was induced for 6 h. During acute respiratory acidosis, CSF PCO2 rose in average by 38 mm Hg in both groups; increments in CSF [HCO3-], however, were significantly lower by about 2 mEq/L in DIDS-treated animals than in controls throughout the experimental period. Such differences were not due to changes in CSF lactate concentration which were similar in both groups. Furthermore, CSF [Na+] remained unchanged in both groups. Since disulfonic stilbene derivatives combine selectively with the carrier involved in anion transport and inhibit inorganic anion exchange, the data in the present study suggest that in the central nervous system a DIDS-inhibitable carrier is involved in the rise of CSF [HCO3-] observed during acute respiratory acidosis.

Cerebrospinal fluid (csf) of sheep was obtained by acute lumbar puncture and from chronic cannulations of the lateral cerebral ventricle. The concentrations of ions in the csf including chloride which had previously been reported to be very high, were found to be similar to those of other mammals and were not greatly affected by changes in plasma electrolyte composition associated with adrenalectomy.

We describe the chemical values of the normal cerebro-spinal fluid and any variation during meningitis. We also refere the physical peculiarity and the variations of non-proteins-nitrogen, of enzymes, of glucose and its metabolites, of proteins and cells. On the picture we resume the most significative variation for differential diagnosis among bacterial, viral and tuberculous meningitis.