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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We propose than an alarm mechanism is operative in animals, designed to regulate neuromuscular irritability by regulating [Ca2+]. Epinephrine or corticotropin (ACTH), injected intramuscularly into animals, causes a hypercitricemia, resulting in decreased [Ca2+]. This increases muscular excitability to facilitate escape. To avoid over reaction, [Cl-] is shifted into the plasma without a concomitant shift of Na+, thus generating an acidosis and an increase in ionization of Ca. Plasma pH, pCO2, total CO2, and [K+] decrease, and [Mg2+] increases. The acidosis, decrease in K+, and increase in [Mg2+] serve to counteract the effect of the decrease in [Ca2+], to protect against tetany. In the rabbit the hypercitricemia observed upon ACTH administration is accompained by a severe hypocalcemia and drop in blood pressure, resluting in tetanic convulsions. This seems to indicate calcitonin release, independent of the hypercitricemia. Thyroidectomized rabbits show only mild hypocalcemia when given ACTH, but develop a severe acidosis and typical grand mal epileptiform seizures. Administration of ACTH and then calcitonin to the goat, an animal resistant to the effects of ACTH alone, simulates the effect observed in the rabbit with respect to changes in blood components and blood pressure. Changes in the blood in the goat and rabbit resemble those in humans before an epileptic seizure. alpha-Melanotropin, containing a portion of the ACTH sequence, reacts in a manner similar to ACTH but more rapidly.
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PMID:Clinical biochemistry of epilepsy. II. Observations on two types of epileptiform convulsions induced in rabbits with corticotropin. 22 Nov 37

The relation of endotoxicosis to insulin responsiveness was evaluated in male Holtzman rats. Salmonella enteritidis lipopolysaccharide at 0.5 or 1.0 mg per 300 g rat increased lethality in convulsive seizure deaths to 0.25, 0.50, or 1.0 U insulin sc. The hypoglycemic nadir induced by 0.05, 0.10, or 0.25 U of insulin sc was greater in rats rendered endotoxic with 1 mg of lipopolysaccharide IV. Oxidation of U-14C-D-glucose to 14 CO2 by endotoxic tissues in vitro was augmented in liver slices, epididymal fat pads, hemidiaphragms, and spleen slices; no pronounced glucose oxidation increases occurred in lung, heart, stomach, cerebrum, kidney, or whole blood. Epididymal fat pads from endotoxic rats (100 g) manifested increased basal glucose oxidation as well as an enhanced maximal response to incremental insulin doses of 0.01 to 25 mU/ml. It is suggested that altered tissue responsiveness in concert with hyperinsulinemia underlie the profound alterations in glucose homeostasis during endotoxicosis.
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PMID:Increased insulin responsiveness in endotoxicosis. 37 53

The author discusses some mechanisms, conditioning the double role of carbon dioxide in the genesis of epileptical activity, first as a provocative factor, when carbon dioxide is a background against which the epileptical seizure appears and then as arresting the sequalae during the administration of CO2 during a seizure. It was demonstrated that the different action of CO2 was due to different phases in the changed functional state of the brain. The study was accomplished on 80 rabbits of the chenchille breed. The evalution of phases in changes of the functional state of the brain was performed with the aid of the encephalographic method.
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PMID:[Carbon dioxide gas provoking and stopping an epileptic seizure]. 69 5

EEG, end-tidal CO2, neck muscle EMG, eye movements, and ECG were recorded in 17 children undergoing enflurane anesthesia combined with N2O and O2. All subjects were classified in the lowest risk group and had normal pre-anesthetic EEG recordings. Eleven subjects were breathing spontaneously and six were under controlled ventilation. Thirteen subjects were hyperventilated for short periods. As previously reported for adults, various signs of increased central nervous excitability appeared. At the enflurane concentration of 4% all three cases with PaCO2 below 32 mmHg showed generalized high voltage epileptic activity of grand mal type followed by several minutes of postictal slowing. One of these subjects also showed motor manifestations of the electrographic seizure activity. At 3% enflurane, three out of eight subjects showed electrographic seizure activity of poly-spike-suppression type. One of these children also had motor manifestations during this type of seizure activity at a PaCO2 of 31 mmHg. The results indicate that electrographic seizure activity is common among children with moderate hypocapnia at enflurane concentrations of 3% or more.
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PMID:Electroencephalographic activity in children under enflurane anesthesia. 121 Oct 75

Zinc is a potent inducer of the 72 kD heat shock protein (HSP72). In brain, pathological conditions such as ischemia and seizures increase extracellular zinc. The present study examines the effect of zinc on HSP72 expression in rat primary cortical astrocyte culture. Astrocytes were grown to confluence and exposed to zinc chloride in CO2-equilibrated Earle's buffered salt solution. Expression of HSP72 was examined using immunocytochemistry. HSP72 was induced with zinc concentrations of 5 to 100 microM after 4 h exposures, or 200 to 300 microM after 15 min exposures. At the lower concentrations expression occurred in small clusters of contiguous cells. At concentrations high enough to cause cell death, HSP72-positive astrocytes formed a continuous margin around patches of dead cells. These patterns of HSP72 expression are similar to the patterns seen after cerebral ischemia in vivo. Exposure to zinc at 100 microM for 4 h or 400 microM for 15 min caused greater than 90% cell death. Increases in extracellular zinc may contribute to HSP72 induction and astrocyte death under ischemia and other pathological conditions in brain.
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PMID:Zinc toxicity and induction of the 72 kD heat shock protein in primary astrocyte culture. 133 69

pH regulatory mechanisms in primary cultures of astrocytes from the cerebral cortex of neonatal audiogenic-seizure-susceptible DBA/2J (DBA) and genetically controlled C57BL/6J (C57) mice were studied with [14C]dimethyloxazolidine-2-4-dione (DMO) and [3H]-methyl-D-glucose (MDG). Effects of changing the concentration of Na+, K+, HCO3- or Cl- in medium, and/or of different transport blockers and metabolite inhibitor on intracellular pH (pHi) of cultured astrocytes were also studied. In nominal HCO3(-)-free HEPES-buffered Hanks' balanced salt solution (HEPES HBSS), when the pH of medium (pHo) was maintained at 7.4, the steady-state pHi of cultured astrocytes from DBA mice was 6.98 +/- 0.03, and that from C57 mice was 7.01 +/- 0.03. When the cells were incubated in HBSS containing 25 mM HCO3- and equilibrated with 5% CO2 (HCO3- HBSS, pHo = 7.4), pHi of both DBA and C57 astrocytes was approximately 0.1-0.15 pH units higher than that in HEPES HBSS. Reducing the pH or the Na+ concentration in media (pHo, [Na+]o) of either HEPES HBSS or HCO3- HBSS, pHi of both DBA and C57 astrocytes decreased markedly (0.25-0.45 pH units lower than the controls). The decrease in pHi was greater in HEPES HBSS than in HCO3- HBSS. Reducing the Cl- concentration ([Cl-]o) in either HEPES or HCO3- HBSS, pHi of astrocytes increased by 0.05-0.1 pH units. Increasing the K+ concentration ([K+]o) of or adding Ba2+ to the media increased the pHi of both DBA and C57 astrocytes accordingly. SITS, an anion transport inhibitor, decreased the pHi of both DBA and C57 astrocytes in HCO3- HBSS but not in HEPES HBSS. It enhanced the response of pHi to reduction in pHo. Amiloride, a Na(+)-H+ exchange inhibitor, decreased the pHi of both DBA and C57 astrocytes more in HEPES HBSS than in HCO3- HBSS. It enhanced the response of pHi to reduction in pHo and [Na+]o. Ouabain, an Na+,K(+)-ATPase inhibitor, decreased the pHi of cultured astrocytes in HEPES HBSS, but not in HCO3- HBSS. It also enhanced the response of pHi to changing pHo and [Na+]o in HEPES HBSS. Acetazolamide, a carbonic anhydrase inhibitor, decreased the pHi of astrocytes in both HEPES and HCO3- HBSS. Both bumetanide, an Na+,K+/Cl- cotransport blocker, and KCN, a metabolic inhibitor, produced no significant effect on the steady-state pHi or the response of pHi to changing ionic concentration in media in both DBA and C57 astrocytes.
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PMID:Studies on pH regulatory mechanisms in cultured astrocytes of DBA and C57 mice. 139 16

The topography of CO2 vasoreactivity during hyperventilation in 8 patients with complex partial seizure (CPS) was visualized using the regional cerebral blood flow (rCBF) as measured by H(2)15O-PET (positron emission tomography) and compared with that of 10 normal volunteers. In the normal volunteers, the vascular response to CO2 (VrCO2 = delta CBF%/delta PaCO2) in the temporal lobe was 2.46 +/- 0.56 (%/mmHg). In the patients with CPS, VrCO2 in the temporal lobe of the affected side was 2.08 +/- 0.40 (%/mmHg), while VrCO2 on the contralateral side was 2.30 +/- 0.46 (%/mmHg). There was a significant difference in VrCO2 between the affected side of the temporal lobes and the temporal lobes of the normal volunteers. Furthermore, there was a tendency for VrCO2 to be lower in the affected than in the contralateral side of the temporal lobe in patients with CPS. As CO2 is the main regulator of CBF, this impaired vasoreactivity may reflect the brain dysfunction in the seizure focus and adjacent areas.
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PMID:Temporal lobe CO2 vasoreactivity in patients with complex partial seizures. 143 64

Carbonic anhydrase (CA) activity plays an important role in controlling cerebrospinal fluid production and also influences neuroexcitation and susceptibility to seizures. Until recently, CA II was the only CA demonstrated in brain. Its distribution is limited to the epithelial cells of the choroid plexus and to the myelin-forming cells, the oligodendrocytes. In this report, we present immunoblots, using an antibody raised to CA IV from rat lung, that show that CA IV is also present in rat and mouse brain. Results of immunohistochemistry and immunoelectron microscopy on sections from rat and mouse brain are presented that show the distribution of CA IV to be quite distinct from that of CA II. CA IV is expressed on and is limited to the luminal surface of endothelial cells of cerebral capillaries. These results establish CA IV as a cytochemical marker associated with the blood-brain barrier and suggest an important role for CA IV in CO2 and HCO3- homeostasis in brain.
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PMID:Carbonic anhydrase IV on brain capillary endothelial cells: a marker associated with the blood-brain barrier. 149 71

Seizure is a common problem evaluated in pediatric emergency departments. Serum chemistry analysis is often performed as a routine part of the diagnostic evaluation of children who arrive in the ED with seizure. From this retrospective study, we sought to determine 1) how often serum electrolytes (Na, K, Cl, CO2), total calcium, magnesium, ammonia, and glucose chemistries were performed, 2) the frequency of abnormalities detected, and 3) whether abnormalities resulted in a change in patient care. Three hundred eight ED charts from 12 consecutive months were reviewed. Data collected included age, sex, ED diagnosis, medical history, and physical examination. Charts were also reviewed for diagnostic tests ordered and patient management. Children were classified as having febrile (FS) or nonfebrile seizures (NFS) to establish diagnostic evaluation practices for each group as well as to determine rates of laboratory abnormalities. Three hundred eight children were enrolled, 108 (35%) FS and 200 (65%) NFS. The mean ages of FS and NFS patients were 2.1 and 5.7 years, respectively (P less than 0.05, t-test). One hundred twenty-four of 308 (40%) children had at least one test performed; no abnormal test was thought to have caused seizure; none was treated. One hundred five of 308 (34%) were experiencing their first seizure. There was no difference in the likelihood of having a test ordered for children with a first seizure, regardless of seizure category. We concluded that 1) abnormal serum electrolytes, total calcium, magnesium, and glucose rarely cause seizure in children and 2) routine use of these tests in the ED is costly and does not contribute to seizure therapy.
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PMID:Emergency department laboratory evaluation of children with seizures: dogma or dilemma? 160 83

Tris(2-chloroethyl) phosphate (TRCP) is a flame retardant that has a wide variety of industrial applications. In subchronic studies, oral administration of TRCP to rats and mice has been reported to produce dose-, sex-, and species-dependent lesions in the hippocampal brain region. The present investigation has examined the metabolism, elimination, and regional brain distribution of [14C]TRCP in male and female rats. [14C]TRCP was administered by gavage (0, 175, 350, or 700 mg/kg) and urine, feces, exhaled volatiles, CO2, and selected tissues were collected. Regional brain distribution of 14C was determined 2 hr following single doses of TRCP to male and female rats, and 24 hr after a single dose and the last of 14 daily doses of TRCP to female rats. Results of these studies indicate that TRCP is readily absorbed from the gastrointestinal tract, distributed to all brain regions, and that metabolism and excretion are nearly complete in 72 hr. Most of the TRCP-derived radioactivity was excreted in urine (up to 85%), with feces, volatiles, and CO2 combined accounting for less than 10% of the dose. Predominant signs of toxicity associated with TRCP administration (350 and 700 mg/kg) were seizures within 2 hr of treatment, when most of the TRCP-derived radioactivity present in brain tissue was in the form of the parent compound. Traces of inextractable 14C were detected at later times, but this material was not concentrated in brain relative to other tissues.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Brain distribution and fate of tris(2-chloroethyl) phosphate in Fischer 344 rats. 167 50


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