Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: HUMANGGP:021525 (albumin)
 60,984 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three single CSF proteins with different molecular size (albumin, immunoglobulin G, and alpha2-macroglobulin) were determined by the method of electroimmunoassay in 61 children with febrile convulsions (FC) in order to evaluate the permeability of the blood-CSF barrier (B-CSF-B). Forty-two children with acute extracerebral infection served as controls. In contrast to a group of 22 children who suffered from acute meningoencephalitis or encephalitis, the CSF values of 48 children with FC were within normal limits. Thus even a very mild form of inflammatory encephalopathy-undetectable with conventional CSF investigation-was excluded in the majority of the children with FC. In 11 patients, however, CSF concentrations of albumin and alpha2-macroglobulin were abnormally raised, indicating a B-CSF-B distrubance. Elevated albumin values were found most frequently. In several children with FC lasting more than 20-30 min, B-CSF-B damage was probably caused by prolonged seizure activity since there is a linear correlation between albumin concentration and duration of convulsions. Several other factors known to raise the children's risk of developing epilepsy in later life were associated with the protein pattern of B-CSF-B disturbance in some of the children. In these cases, the cause of abnormal permeability of B-CSF-B is unknown and the condition might have existed prior to the occurrence of seizures.
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PMID:Febrile convulsions and blood-cerebrospinal fluid barrier. 7 3

The effect of electrically induced seizures on the permeability of the rat blood-brain barrier was investigated. The small radioactive tracers sodium (24Na+), chloride (36Cl-) carbon labelled thiourea (14C-thiourea) and glucose (14C-D-glucose) were studied in indicator dilution experiments with indium labelled diethylenetriaminepenta-acetic acid (113mIn-DTPA) as reference substance. This method allows a quantitative estimate of the transcapillary loss of solutes, the extraction (E), during a single passage through the brain. Passage of macromolecules was studied using as marker substance Evans Blue which binds to plasma albumin. In the resting state ENa, ECl, Ethiourea and Eglucose were 2.9, 4.8, 9.3 and 12.5%, respectively. During seizures and during shortlasting hypercapnia E glucose decreased while E for the other tracers was unchanged. As cerebral blood flow increased, there must be an increased transfer of test substances into the brain. This finding is in agreement with recent human studies [15]. When Evans Blue was injected intravenously prior to electroshock, there was no staining of brain tissue after one electroshock but following repeated electroshocks some staining was observed. In an attempt quantify this transcapillary loss of albumin by means of indicator dilution, 51Cr-labelled erythrocytes were used as intravascular reference substance against 113mIn-DTPA (a plasma tracer). However, the albumin loss (by pinocytosis or otherwise) occurring after ten electroshocks could not be detected during a single passage through the brain.
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PMID:Blood-brain barrier during electroshock seizures in the rat. 40 65

The purpose of this study was to determine the effect of activation of sympathetic pathways during seizures on cerebral blood flow and integrity of the blood-brain barrier. We measured cerebral blood flow with microspheres and disruption of the blood-brain barrier with labeled albumin in cats. One cerebral hemisphere was denervated by cutting the superior cervical sympathetic trunk on one side. During bicuculline-induced seizures, superior cervical sympathetic nerve activity increased about threefold. Blood flow to the innervated hemibrain was significantly lower than flow to denervated hemibrain. However, in relation to the total increase in flow, this effect of nerves was minor. Blood-brain barrier permeability increased about sixfold during seizures, but there was no difference between the innervated and denervated sides of the brain. We conclude that sympathetic nerves attenuate the increase in cerebral blood flow during seizures, despite the increase in metabolism, but this effect is small. Activation of sympathetic nerves does not reduce disruption of the blood-brain barrier during seizures.
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PMID:Effect of sympathetic nerves on cerebral vessels during seizures. 46 10

Stimulation of the sympathetic nerves to the brain is known to make the resistance vessels able to withstand a higher blood pressure, i.e. to prevent blood-brain barrier (BBB) dysfunction and overperfusion in acute hypertension. When hypertension occurs concomitantly with a metabolic vasodilatation e.g. during epileptic seizures and after amphetamine-administration, protein leakage in the brain is more pronounced than in hypertension per se. Unilateral stimulation of the cervical sympathetic chain during the administration of amphetamine or bicuculline--the latter a GABA-receptor blocking substance that induces epileptic activity--attenuated the leakage of Evans blue-albumin and 125IHSA into the brain. Our results thus indicate a prophylactic effect of sympathetic stimulation also when hypertension is combined with a metabolically induced vasodilatation. The sympathetic nerves may constrict both extracerebral arteries and intracerebral resistance vessels. Unexpectedly the effect on the BBB of unilateral stimulation was to a great extent bilateral under the present experimental conditions.
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PMID:Effect of sympathetic stimulation on the blood brain barrier dysfunction induced by amphetamine and by epileptic seizures. 71 82

During experimental seizures, the blood-brain barrier (BBB) is broken; tracer substances such as I131-albumin, Evans blue and horseradish peroxidase (HRP) geographically locate the barrier breakdown primarily in the diencephalon. Using rats, we have induced seizures with electroshocks and demonstrated the breakdown of the BBB with Evans blue and HRP. We have shown that (1) the BBB breakdown is proportional to the number of electroconvulsant shocks (ES) given; (2) the mechanism of increased barrier permeability is primarily by micropinocytosis in the cerebral capillaries, arterioles, and, to a lesser extent, venules; and (3) the stimulus for micropinocytosis and hence BBB breakdown is associated with the abrupt rise in systemic blood pressure and cerebral vasodilatation that accompanies each ES. If the systolic hypertension is abolished via cervical cordotomy, there is little to no breakdown in the BBB.
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PMID:Ultrastructural characteristics of the brain and blood-brain barrier in experimental seizures. 86 58

Twenty-eight women with severe pre-eclampsia were misdiagnosed and initially thought to have disorders unrelated to pregnancy. Their chief complaints included failing vision, liver or gallbladder dysfunction, renal failure, hemorrhage, seizures, and heart failure. Laboratory studies usually demonstrated thrombocytopenia and high hematocrit values. The development of these symptoms appears to begin with failure of the primigravida to appropriately increase her blood volume commensurate with the increase in size of her uterus. Expanding the severly pre-eclamptic patient's blood volume with intravenous albumin appears to be an effective and appropriate therapy.
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PMID:Severe pre-eclampsia: another great imitator. 94 95

Sex related differences of the blood brain barrier permeability was investigated during bicuculline-induced seizures in Wistar rats. The rats were anesthetized with diethyl-ether. Evans-blue, which was used as a blood brain barrier tracer, was injected into femoral vein 5 minutes before administering bicuculline to induced grand mal seizures. Evans-blue albumin extravasation was determined as a macroscopical finding; and a quantitative estimation with spectrophotometer using homogenized brain to release the dye was also performed to evaluate the macroscopic findings. During convulsions the mean arterial blood pressure increased in both female and male rats, but the difference was in the extravasation of Evans-blue being more pronounced in the females. Blood brain barrier lesions were present in 85% of female rats and 61% of male rats. Mean value for Evans-blue dye in the whole brain was found to be 1.197 +/- .402 mg % in the group consisting of all the female rats, and .755 +/- .247 mg % in the group of all male rats during bicuculline-induced seizure. This difference between female and male rats was found to be statistically significant (p < .001). Severe protein leakage was seen in the thalamus, hypothalamus, hippocampus, globus pallidus, nucleus caudatus, periaqueductal gray and mesencephalon bilaterally in female rats. However, in male rats, Evans-blue leakage was similar to that of female rats except that the frequency and intensity of blood brain barrier breakdown was less after convulsions. Our results showed that the extravasation of Evans-blue albumin was most pronounced in the brains of female rats compared to male rats after bicuculline induced seizure.
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PMID:Influence of sex on the blood brain barrier permeability during bicuculline-induced seizures. 134 74

The substantia nigra has a gating function controlling the spread of epileptic seizure activity. Additionally, in models of prolonged status epilepticus the pars reticulata of substantia nigra (SNR) suffers from a massive lesion which may arise from a massive metabolic derangement and hyperexcitation developing in the activated SNR. In this study, status epilepticus was induced by systemic injection of pilocarpine in rats. The neuropathology of SNR was investigated using immunohistochemical techniques with the major emphasis on the time-course of changes in neurons and astrocytes. Animals surviving 20, 30, 40, 60 min, 2, 3, 6 hours, 1, 2, and 3 days after induction of status epilepticus were perfusion-fixed, and brains processed for immunohistochemical staining of SNR. Nissl-staining and antibodies against the neuron-specific calcium-binding protein, parvalbumin, served to detect neuronal damage in SNR. Antibodies against the astroglia-specific cytoskeletal protein, glial fibrillary acidic protein (GFAP), and against the glial calcium-binding protein, S-100 protein, were used to assess the status of astrocytes. Immunohistochemical staining for serum-albumin and immunoglobulins in brain tissue was taken as indicator of blood-brain barrier disturbances and vasogenic edema formation. Immunohistochemical staining indicated loss of GFAP-staining already at 30 min after induction of seizures in an oval focus situated in the center of SNR while sparing medial and lateral aspects. At 1 h there was additional vacuolation in S-100 protein staining. By 2 hours, parvalbumin-staining changed in the central SNR indicating neuronal damage, and Nissl-staining visualized some neuronal distortion. Staining for serum-proteins occurred in a patchy manner throughout the forebrain during the first hours. By 6 h, vasogenic edema covered the lesioned SNR. By 24 h, glial and neuronal markers indicated a massive lesion in the center of SNR. By 48-72 h, astrocytes surrounding the lesion increased in size, and polymorphic phagocytotic cells invaded the damaged area. In a further group of animals surviving 1 to 5 days, conventional paraffin-sections confirmed the neuronal and glial damage of SNR. Additional pathology of similar quality was found in the globus pallidus. Since astrocytes were always damaged in parallel with neurons in SNR it is proposed that the anatomical and functional interrelationship between neurons and astrocytes is particularly tight in SNR. Both cell elements may suffer in common from metabolic disturbance and neurotransmitter dysfunction as occur during massive status epilepticus.
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PMID:Damage of substantia nigra pars reticulata during pilocarpine-induced status epilepticus in the rat: immunohistochemical study of neurons, astrocytes and serum-protein extravasation. 175 84

The effect of chronic electroconvulsive seizure on the blood brain barrier permeability to albumin was investigated in the male rats. Evans blue was used as a blood brain barrier tracer. The following situations were studied: Acute electroshock: a. one electroshock stimulus, b. ten electroshock stimuli. Chronic electroshock: a) group of animals were pretreated with electroshock given as one electroshock (ES) every other day (ES x 7); b) chronic electroshock + one electroshock, c) chronic electroshock + ten repeated electroshocks. As a result, chronic electroshock per se does not effect the blood-brain barrier permeability.
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PMID:Blood-brain barrier permeability during acute and chronic electroconvulsive seizures. 181 Dec 18

Seizure prophylaxis is standard intrapartum therapy for patients with pregnancy-induced hypertension. Magnesium sulfate is used in the United States in spite of limited literature comparing its efficacy with other anticonvulsants. Fifty patients with pregnancy-induced hypertension were prospectively randomized to receive magnesium sulfate or phenytoin for seizure prophylaxis. Patients were observed for toxicity, side effects, and labor outcomes, and the neonates were evaluated for side effects of the therapy. Three patients were excluded with adverse reactions to medications (one in magnesium sulfate group, two in phenytoin group). No differences were found in patient tolerance, adverse reactions, or neonatal outcomes between groups. Maternal free phenytoin levels were 13.0% +/- 0.4% of total phenytoin (serum albumin, 2.5 to 3.5 gm/dl), significantly higher than in nonpregnant patients. Neither free phenytoin levels nor percentage of total phenytoin that was free correlated significantly with maternal albumin levels. The pharmacokinetics of phenytoin loading in the massively obese pregnant patient may differ and require further evaluation. Phenytoin is a well-tolerated alternative to magnesium sulfate for seizure prophylaxis in the patient with mild pregnancy-induced hypertension.
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PMID:Magnesium sulfate versus phenytoin for seizure prophylaxis in pregnancy-induced hypertension. 195 52


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