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)

Acid hydrolases and lysosomal membrane properties were studied at various ages in the normal human brain. In CSF and four brain regions, the inferior olive, the cerebellar cortex, the caudate nucleus and the frontal cortex were thus beta-galactosidase, beta-glucosidase, alpha-mannosidase, hexosaminidase and acid phosphatase biochemically quantitated at ages varying between 2 and 89 years of age. Also the membrane latency for acid phosphatase was studied in these regions. No major regional quantitative differences were found with regard to the enzymes studied. Their kinetic properties were also defined. There appeared to exist a regional and intra-areal variation in lysosomal membrane permeability. There was, however, no age related increase in total enzyme contents. The possibility significance of these findings are discussed with reference to the aging process.
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PMID:Regional study of acid hydrolases and lysosomal membrane properties in the normal human brain at various ages. 0 May 61

The lactate and pyruvate content in the arterial blood and CSF of 24 patients operated on the brain under fluothane anesthesia with artificial ventilation of the lungs was measured. Towards the end of the operation and anesthesia a sizably elevated lactate level and accumulation of its excess in the blood were noted, these shifts having been more marked with hypocapnic ventilation of the lungs. An increased concentration of lactate and pyruvate in the cerebrospinal fluid was not attended by accumulation of lactate excess.
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PMID:[Changes in cerebrospinal fluid lactate and pyruvate levels during brain surgery under fluotane anesthesia]. 0 4

Arteriolar diameters and venular erythrocyte velocities in the small pial vessels on the surface of the cat brain were measured by TV methods during induced epileptic seizures through a cranial window. Grand mal seizures maximally dilated arterioles and increased venular erythrocyte velocity up to 400%. High positive correlation existed between changes in CSF hydrogen ion concentration and pial arteriolar diameter, suggesting metabolic regulation of CBF through CSF/interstitial fluid hydrogen ion alterations during the seizure.
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PMID:Brain microvascular hemodynamic responses to induced seizures. 0 70

Cerebral hemispheric blood flow and metabolism were measured before and after therapy with intracarotid infusion of combined PBZ and PPL in 15 patients with recent cerebral infarction. HBF was unaltered despite decrease in cerebral perfusion pressure. Cerebral hemispheric oxygen comsumption and carbon dioxide production decreased while cerebral hemispheric lactate production increased. Biphasic cerebral uptake of tyrosine was observed during and immediately after PBZ and PPL infusion. CSF HVA increased, indicating altered DA turnover. CSF 5HIAA levels also increased, suggesting altered 5HT turnover after PBZ and PPL. Release of cyclic AMP from ischemic brain into cerebral venous blood seen in the steady state was abolished after therapy. Cerebral hemodynamic studies suggest a functional balance between monaminergic neurogenic influences in the control of cerebral circulation. Imbalance of such controlling factors in ischemic brain may lead to paradoxical vascular responses to induced hypertension and hypotension. PBZ and PPL enhance such responses perhaps by increasing central neurotransmitter turnover and release. Further shift toward cerebral anaerobic metabolism may occur in ischemic brain following the use of phenoxybenzamine and propranolol. Worsening of neurological deficit occurred in four cases. Combined therapy with PBZ and PPL does not appear beneficial in the therapy of patients with recent stroke.
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PMID:Influence of adrenergic receptor blockade on circulatory and metabolic effects of disordered neurotransmitter function in stroke patients. 0 7

In case of cranial trauma, early respiratory troubles either of central or peripheral origin often accelerate the deterioration of the neurological situation. The different values of PCO2, PO2, pH and alcaline reserve measured on samples of CSF in comatose patients prove the central acidosis related to metabolic and vascular disorders in the damaged areas. Our results confirm the correlation between the importance of this disturbances and the severity of the trauma. It is thus necessary to insure patients of satisfactory respiration conditions. The tracheobronchial cleansing is applicable to intubated or tracheotomized patients by an instillation of 5ml of simple or bicarbonated physiological serum 4 to 6 times a day, followed by repeated aspirations and associated to a preventive endotracheal instillation of 80 mg of Gentamycin 4 times a day. Moreover we use controlled respiration which does not modify the gazometric parameters in the CSF but which assures patients a normoxia and moderate hypocapnia with a decrease of intracranial hypertension. Treatment by controlled hyperventilation must be precocious, because the recuperation at the level of the damaged zones is very slow.
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PMID:Treatment of comatose patients by mechanical hyperventilation. 0 50

To evaluate the metabolic adaptations of the brain to acute respiratory acid-base disturbances, a method was developed to measure intracellular pH (pHi) in the brain of dogs under conditions in which arterial pH is rapidly altered. Brain pHi was determined by measuring the distribution of 14C-labeled dimethadione (DMO) in brain relative to cortical CSF. Brain extracellular space (ECS) was evaluated as the 35SO4 = space relative to cortical CSF, and arterial Po2 was maintained at 82-110 mmHg. In normal dogs, brain (cerebral cortex) pHi was 7.05, and after 1 h of hypercapnia (arterial pH = 7.07) it fell to 6.93. However, after 3 h with arterial Pco2 maintained at 85 mmHg brain pHi was normal (7.06), and during this time brain bicarbonate had risen from 11.3 to 24.4 meq/kg H2O. These changes were not prevented by intravenous doses of acetazolamide,
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PMID:Intracellular pH of brain: alterations in acute respiratory acidosis and alkalosis. 0 79

We have previoulsy shown pH compensation to be similar in CSF and arterial blood during chronic hypoxemic hypocapnia in man and pony, and postulated that the compensatory reduction in CSF [HCO3] was dependent upon corresponding changes in [HCO3]a. We tested this hypothesis in anesthetized, paralyzed dogs by determining the effects of 7 or 14 hours of hypocapnia (PaCO2 20 and 30 mm Hg), hypoxemia (PaO2 30, 38 and 48 mm Hg) and hypocapnic hypoxemia on CSF acid-base status. [hco3]a was either permitted to fall normally or was held near control levels by NaHCO3 infusion. In hypocapnia and hypoxemic hypocapnia, the decrease in [HCO3] and % pH compensation in CSF were less than or equal to that in arterial blood. Most (51-89%) of the compensatory decrease in CSF [HCO3] was prevented by preventing the corresponding reduction in [HCO3]a. This dependence of changes in CSF on plasma [HCO3] required a concurrent decrease in CSF PCO2, but was largely independent of variations in plasma pH. A minor but significant portion of the decrease in CSF [HCO3] was achieved independently of corresponding changes in [HCO3]a. The contribution of this local mechanism to CSF [HCO3] regulation increased with increasing severity of hypocapnia or hypoxemia and was usually associated with a selective increase in CSF lactate. It was concluded that [HCO3] regulation in the CSF during hypoxemic hypocapnia was primarily dependent upon, and therefore limited by, the concomitant decrease in plasma [HCO3].
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PMID:Dependence of CSF on plasma bicarbonate during hypocapnia and hypoxemic hypocapnia. 0 65

1. The acid-base balance (pH, pCO2 and HCO-3) of 23 normal subjects was determined both in arterialized capillary blood and in the CSF. 2. Statistically significant correlations (determined by means of Spearman's rank correlation) were found between: pCO2 in arterialized blood and CSF pH (Rs=--0.372, p is less than 0.05), pCO2 in the CSF and CSF pH (Rs=--0.421, p is less than 0.05), HCO-3 in the CSF and in arterialized blood (Rs=0.623, p is less than 0.05), blood pH and CSF pH (Rs=0.485, p is less than 0.025), pCO2 in the CSF and HCO-3 in the CSF (Rs=0.559, p is less than 0.005). 3. The regulatory mechanisms of the CSF acid-base balance in normal subjects and also in patients with extra-neural or CNS disturbances are discussed.
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PMID:[The acid-base balance in the CSF of normal subjects regulatory mechanisms (author's transl)]. 0 11

Regulation of CSF HCO3-in respiratory acidosis was studied in light of the "dual contribution theory," which proposed that there were two sources for the CSF HCO3-increase: 1) HCO3-by diffusion from plasma and 2) HCO3-generated in the CNS and catalyzed by the local carbonic anhydrase (J. Appl. Physiol. 38: 504-512, 1975). In anesthetized dogs with an increase in Paco2 of 30 mmHg for 4 h the plasma HCO3 increased 2 meq/1 and CSF 6 meq/1. In combined respiratory and metabolic acidosis, plasma HCO3-did not increase but CSF HCO3-increased 6 meq/1. In combined acidosis and intraventricular injections of acetazolamide no increase in plasma or CSF HCO3-occurred. In combined respiratory acidosis and metabolic alkalosis and intraventricular acetazolamide, plasma HCO3-increased 15 meq/1 but CSF HCO3-increased 6 meq/1. Brain and CSF ammonia increased linearly and selectively with the increase in the relative contribution of CNS HCO3-increase. Therefore regulation of CSF HCO3-in respiratory acidosis depends on both components of the dual contribution theory, where each component can provide the total CSF HCO3-increase under appropriate experimental conditions. The control mechanism may be sensitive to changes in [H+] on the brain side of the blood-brain barrier.
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PMID:Dual contribution theory of regulation of CSF HCO3 in respiratory acidosis. 0 20

In respiratory alkalosis the fall in CSF bicarbonate is in part due to increased CSF lactate. The rest of CSF HCO3 fall may be actively regulated or as more recent evidence suggests is dependent on plasma HCO3 fall. Therefore, the relationship between plasma and CSF HCO3 changes was studied during 4 hours of respiratory alkalosis (PaCO2=20 mm Hg) in anesthetized dogs when plasma HCO3: (1) fell normally, (2) kept 'normal' by NaHCO3 infusion, (3) increased by infusing more NaHCO3, and (4) reduced by infusing HCl. In respiratory alkalosis plasma and CSF HCO3 fell 4.6 and 3.8 mEQ/L, respectively. In hypocapnia and 'normal' plasma HCO3 CSF HCO3 fell 2 mEq/L and lactate increased 1.33 mEq/L. In hypocapnia and metabolic alkalosis plasma HCO3 increased 6.5 mEq/L and CSF HCO3 remained unchanged and lactate increased 2.12 mEq/L. In combined hypocapnia and metabolic acidosis plasma HCO3 fall 10.5 mEq/L but CSF HCO3 fell 3.1 mEq/L and CSF pH returned to normal at 4 hours. Therefore CSF HCO3 fall in hypocapnia is primarily and critically dependent on the simultaneous fall in plasma HCO3 content, with a minimal contribution from CNS lactate increase. When CSF PH has returned to normal, however, CSF HCO3 fall is stopped despite further falls in plasma HCO3.
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PMID:Importance of changes in plasma HCO-3 on regulation of CSF HCO-3 in respiratory alkalosis. 0 12


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