Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: DrugBank:BIOD00035 (CSF)
 30,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this double-blind study dihydrotachysterol (DHT) was given orally to eight psychotic patients; in each case marked increases in psychosis and agitation accompanied increases in serum calcium and phosphorus within two weeks after active drug was substituted for placebo. In the three patients whose psychoses exhibited periodic spontaneous exacerbations, the agitated episodes grew more severe. Serum creatine phosphokinase (CPK) increased in all but one patient. By contrast, when three periodically psychotic patients received synthetic salmon calcitonin (SCT), the severity and frequency of agitated episodes decreased while CSF calcium increased in all three. These data support the hypothesis that the observed abrupt increases in serum calcium and phosphorus might cause the opposite CSF calcium shifts, the behavioral agitation and the increases in serum CPK frequently noted during acute psychosis.
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PMID:Calcium: pacesetting the periodic psychoses. 3 47

The development of the chloride ion, glucose and total protein concentration was investigated in the cerebrospinal fluid of 11- to 21-day-old chick embryos and compared with their development in the blood plasma. Developmental changes in the chloride concentration in the plasma and CSF were very small, but it was always higher in the CSF than in the plasma. The plasma/CSF ratio fell during development, from 0.906 in 11-day-old embryos to 0.778 at the end of incubation. The CSF glucose concentration fell up to the 19th day of incubation, but a significant increase was recorded shortly before hatching. The plasma glucose concentration rose throughout the whole of the investigated period of embryogenesis. Up to the 19th day the P/CSF ratio rose from 1.59 to 4.05 and in 21-day-old embryos fell to 2.47. The developmental increase in the plasma total protein concentration was accompanied by the reverse process in the CSF. During the second half of incubation the P/CSF ratio rose from 1.88 to 7.9 Calculation of total osmolarity from the Na+, K+, Ca2+, Cl- and glucose concentration showed permanent hyperosmolarity of the CSF compared with the plasma. The P/CSF ratio was maintained within limits of 0.94 to 0.98.
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PMID:Some basic chemical components of the cerebrospinal fluid in developing chick embryos. 12 80

The authors demonstrate that, while the intracerebral movement of proteins and other relatively large molecules is restricted by tight junctions of endothelia and epithelia of the brain, calcium ion penetrates these barriers and moves between the blood and CSF cavities by extracellular pathways. Mechanisms underlying CSF formation are considered on the basis of this anatomical continuity of the vascular, extracellular, and CSF compartments of the brain for very small molecules.
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PMID:Experimental intracerebral movement of electron microscopic tracers of various molecular sizes. 16 97

In the unanesthetized rat, Ca++ ions in solutions ranging from 2.6 to 112.0 mM in excess of the normal level in CSF were applied at different sites in the brain and by three separate procedures, Colonic temperature was monitored and in certain experiments, the amount of food pellets and water consumed was measured simultaneously following the administration of excess Ca++ ions. An infusion into the lateral cerebral ventricle of excess calcium in a volume of 5.0 mul produced a concentration-dependent hypothermia, This fall in temperature was not attenuated by a prior intraventricular infusion of mecamylamine and often enhanced by atropine. Depending on the site, a microinjection of excess Ca++ ions in a volume of 0.5 to 1.0 mul directly into the hypothalamus produced hypothermia or feeding. The sites of maximum sensitivity at which excess calcium caused a decline in temperature were clustered in the caudal hypothalamus, whereas those at which calcium elicited feeding were distributed widely in caudo-lateral, medial and rostral hypothalamic areas. Push-pull perfusions at a rate of 20 to 25 mul per min for 10 to 20 min at homologous sites caused similar responses but the cation concentration required to evoke feeding or hypothermia was significantly less than that of either microinjection or intraventricular infusion. These findings demonstrate species continuity in the rat concerning anatomical localization of the postulated set-point mechanism for body temperature. Several different pathways in the feeding system are affected by an alteration in the hypothalamic level of calcium.
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PMID:Feeding and body temperature in the rat: diencephalic localization of changes produced by excess calcium ions. 18 84

Sleep and behavior of the rat were recorded during cerebroventricular infusion of artificial cerebrospinal fluid (aCSF) containing regular or excess concentrations of calcium. Three different types of aCSF were used for control infusions. Depending on the ionic composition, paradoxical sleep (PS) was reduced by 6--52% during a 1-h aCSF infusion period, whereas the total amount of sleep was not altered. The depression of PS by aCSF could be prevented by increasing the concentration of Ca in the infusate by a factor of 2--5 (2.6--9.1 mM). Infusions of high concentrations of Ca (9.1--54.6 mM) caused feeding and wet-dog shakes. A slow-wave cortical EEG pattern prevailed during feeding elicited by either infusion of excess Ca or systemic administration of a small dose of pentobarbital. It is concluded (a) that the ionic composition of the CSF may selectively influence the occurrence of a sleep state, and (b) that Ca-induced feeding may be related to a covert sedative action of this cation.
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PMID:Cerebral ventricular infusion of excess calcium in the rat: effects on sleep states, behavior and cortical EEG. 21 97

Adenovirus type 12 was recovered from the CSF of a 36-year-old woman with adenoviral meningoencephalitis and lead toxicity. The serum level of lead was 199 micrograms/dL and the CSF level was 7 micrograms/dL. After therapy with edetate disodium calcium (Calcium Disodium Versenate), she had an uneventful recovery. The possibility of exacerbation of lead poisoning with encephalopathy due to adenovirus type 12 meningoencephalitis is raised.
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PMID:Adenoviral meningoencephalitis in a patient with lead toxicity. 22 48

In a study of electrolytes in lumbar cerebrospinal fluid (csf) from psychiatric patients, the authors found a positive correlation between calcium concentration and symptom severity in hospitalized depressed patients. CSF calcium levels tended to decrease as patients improved. In four rapidly cycling patients, CSF calcium was higher during depression than during mania. Mean CSF calcium for the depressed patients as a group was not significantly different from neurological controls or other psychiatric patients. Symptom remission from acute psychosis in schizophrenic patients was accompanied by a significant increase in CSF calcium concentration. These findings are discussed in relationship to calcium-induced alterations in neuronal and physiological excitability.
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PMID:CSF calcium: clinical correlates in affective illness and schizophrenia. 42 Sep 7

The posterior hypothalamus of anaesthetized cats was superfused with artificial cerebrospinal fluid through a push-pull cannula and the release of endogenous GABA from the hypothalamus into the superfusate was studied. The resting release of GABA varied rhythmically, since phases of high rate of release were separated from each other by phases of low rate of release. The time interval between two adjacent phases of high rate of release was about 70 min. Electrical stimulation of the posterior hypothalamus with the tip of the cannula enhanced the rate of release of GABA in a frequency-dependent way. Superfusion of the hypothalamus with CSF which contained a high concentration of potassium and a low concentration of sodium increased the rate of release of GABA; this effect was dependent on the presence of calcium ions in the superfusing fluid. Pretreatment of the cats with reserpine reduced the levels of GABA in hypothalamus and rest of brain and the concentration of GABA in the superfusate as well. Stimulation of the locus coeruleus with a bipolar electrode elicited an increased release of GABA in the hypothalamus.
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PMID:In vivo release of endogenous GABA in the cat hypothalamus. 50 46

IN AN EFFORT TO DOCUMENT THE ROLE OF THE LIVER IN THE CATABOLISM OF VASOACTIVE INTESTINAL PEPTIDE, SEVERAL DIFFERENT TYPES OF EXPERIMENTS WERE CARRIED OUT, INCLUDING: 1) simultaneous measurement of portal and systemic immunoreactive vasoactive intestinal peptide, both in the basal state and following calcium stimulation; 2) by measuring plasma concentrations of immunoreactive vasoactive intestinal peptide before and after portacaval shunt; 3) by measuring plasma VIP before and after portacaval shunt following calcium, prostigmine and pentagastrin stimulation; 4) by determining plasma VIP levels in patients with liver disease and in hepatic failure, and in patients with variceal hemorrhage before and serially after portal systemic shunt; 5) by measuring CSF vasoactive intestinal peptide in dogs before and after portacaval shunt and when the animals finally succumb to hepatic failure. The results consistently suggest that the shunting of portal blood away from the liver does not result in significant elevation of basal peripheral plasma levels of vasoactive intestinal peptide. Following stimulation however, increased amounts of peripheral plasma VIP are detected, following calcium, pentagastrin and prostigmine release of VIP. Portal vein levels are always significantly higher than peripheral plasma VIP again, confirming a catabolic role for the liver. In patients, elevation of peripheral plasma VIP is seen in hepatic failure, but not after portacaval shunt. Finally, cerebrospinal fluid VIP is elevated in dogs following hepatic failure, confirming the presence of a neural-gut axis and suggesting an influence of hepatic catabolism of VIP not only in the periphery, but also within the central nervous system.
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PMID:Hepatic inactivation of vasoactive intestinal peptide in man and dog. 66 73

In anaesthetized cats, in which the cerebrospinal fluid bicarbonate concentration was varied by a ventriculocisternal perfusion technique, the ventilatory response to CO2 during hyperoxia could be satisfactorily described by VE = S(PCSFCO2 -B). Both the slope S and the intercept B were positively and linearly related to the CSF bicarbonate concentration. Assuming that the PCSFCO2 is equal to the PCO2 in extracellular fluid, it can be shown that VE is a linear, but not a unique function of the [H+] at the site of the chemoreceptors; the slope of this relation varies with the bicarbonate concentration at that site, possibly due to chemical complex formation between HCO-3 and Ca2+ or Mg2+. Changes in the B-value were related to the location of the central chemoreceptors with the models of Pappenheimer and Berndt aand their coworkers. It was found that changes in the CSF bicarbonate concentration are reflected for 60 per cent at the site of the central chemoreceptors, and that this was independent of the cerebral perfusion. Using Berndt's model a distance between CSF and central chemoreceptors of approximately 100 micron was found; this calculated distance is relatively insensitive to relationship (logarithmic or not) between ventilation and H+ concentration and to changes in cerebral perfusion, owing to the approximate nature of the diffusion model.
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PMID:Influence of the CSF bicarbonate concentration on the ventilatory response to CO2 in relation to the location of the central chemoreceptors. 74 Nov 4


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