Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038220 (status epilepticus)
 7,272 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The influence of hypercapnia, hypoxia and status epilepticus on cerebral cortex concentrations of adenosine, adenine nucleotides and cyclic AMP was studied on lightly anaesthetized (70% N2O) and artificially ventilated rats. Neither hypercapnia (arterial PCO2 about 80 and about 300 mmHg) nor hypoxia (minimal values of 19 mmHg) altered tissue concentrations of AMP, cyclic AMP or adenosine. Bicuculline-induced status epilepticus was accompanied by increased concentrations of cyclic AMP but adenosine concentration did not change. Experiments with ischemia, and those in which tissue hypoxia was exaggerated by unilateral carotid artery ligation, showed that tissue adenosine concentrations were elevated only when AMP concentration rose. It is concluded that the marked increase in cerebral blood flow which occurs in hypoxia and status epilepticus is unrelated to changes in tissue adenosine concentration and that the increase in cyclic AMP during neuronal hyperactivity is triggered by other mechanisms than adenosine accumulation.
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PMID:Adenosine and cyclic AMP in cerebral cortex of rats in hypoxia, status epilepticus and hypercapnia. 21 98

In order to study effects of catecholamines on cerebral oxygen consumption (CMRo2) and blood flow (CBF), rats maintained on 75% N2O and 25% O2 were infused i.v. with noradrenaline (2, 5, or 8 microgram.kg-1.min-1) or adrenaline (2 or 8 microgram.kg-1.min-1) for 10 min before CBF and CMRo2 were measured. In about 50% of animals infused with 2--8 microgram.kg-1.min-1 of noradrenaline, CMRo2 (and CBF) rose. However, there was no dose-dependent response, and CMRo2 did not exceed 150% of control. The effects of noradrenaline in a dose of 5 microgram.kg-1.min-1 on CMRo2 and CBF were blocked by propranolol (2.5 mg.kg-1). In animals infused with adrenaline (8 microgram.kg-1.min-1) CMRo2 was doubled and, in many, CBF rose 4- to 6-fold. It is concluded that, when given in sufficient amounts, catecholamines have pronounced effects on cerebral metabolism and blood flow, the effects of adrenaline on CMRo2 and CBF resembling those observed in status epilepticus.
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PMID:Influence of intravenously administered catecholamines on cerebral oxygen consumption and blood flow in the rat. 69 50

The objective of the present study was to explore if lesions of the ascending noradrenergic pathways, originating in the locus coeruleus, modulate the cerebral metabolic response to bicuculline-induced seizures in rats. Bilateral noradrenergic lesions were performed by 6-hydroxydopamine injections in the caudal mesencephalon, 12-22 days before seizures were induced in animals ventilated on N2O:O2 (75:25). After 5 min of seizures the brain was frozen in situ and cerebral cortex and hippocampus were sampled for analysis. Labile phosphates, glycolytic metabolites, cyclic nucleotides, and free fatty acids were measured. In another series, lesioned animals were used for measurements of cerebral oxygen consumption. The noradrenergic lesions neither modified the electroencephalographically recorded seizure discharge, nor did they alter cerebral oxygen consumption or cerebral energy state. However, when compared to sham-operated animals, those with noradrenergic lesions had significantly higher (115% and 68%) glycogen concentrations and lower (50% and 52%) cyclic AMP concentrations in cerebral cortex and hippocampus, respectively, demonstrating the marked influence of noradrenergic activity on adenylate cyclase activity and glycogenolysis. The lesions failed to modulate the rise in free fatty acids in the cerebral cortex, or the cyclic GMP concentrations in the cerebral cortex and hippocampus. Thus, increased noradrenergic activity during status epilepticus does not seem responsible for lipolysis or for activation of guanylate cyclase.
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PMID:Influence of lesions of the noradrenergic locus coeruleus system on the cerebral metabolic response to bicuculline-induced seizures. 630 1

A model is described in which transient ischemia is induced in rats anaesthetized with N2O:O2 (70:30) by bilateral carotid artery clamping combined with a lowering of mean arterial blood pressure to 50 mm Hg, the latter being achieved by bleeding, or by bleeding supplemented with administration of trimetaphan or phentolamine. By the use of intubation, muscle paralysis with suxamethonium chloride, and insertion of tail arterial and venous catheters, it was possible to induce reversible ischemia for long-term recovery studies. Autoradiographic measurements of local CBF showed that the procedure reduced CBF in neocortical areas, hippocampus, and caudoputamen to near-zero values, flow rates in a number of subcortical areas being variable. Administration of trimethaphane or phentolamine did not affect ischemic and postischemic flow rates, nor did they alter recovery of EEG and sensory-evoked responses, but trimetaphan blunted the changes in plasma concentrations of adrenaline and noradrenaline. Recovery experiments showed that 10 min of ischemia gave rise to clear signs of permanent brain damage, with a small number of animals developing postischemic seizures that led to the death of the animals in status epilepticus. After 15 min of ischemia, such alterations were more pronounced, and the majority of animals died. It is concluded that the short revival times noted are explained by the fact that the model induces near-complete ischemia, and that recovery following forebrain ischemia is critically dependent on residual flow rates during the period of ischemia.
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PMID:Models for studying long-term recovery following forebrain ischemia in the rat. 2. A 2-vessel occlusion model. 646 70

In order to evaluate the possible contribution of regional insufficiency in blood flow to the development of epileptic brain damage, we have measured changes in total and regional cerebral blood flow (tCBF and rCBF) during the course of prolonged sustained seizures. We have used both a particle distribution method (radioactively labelled microspheres) and a diffusible tracer method (iodo [14C]antipyrine). Seizures were induced with bicuculline (1.2 mg/kg, i.v.) in rats with neuromuscular paralysis, mechanically ventilated with 70% N2O/30% O2, rCBF was determined in 13 brain regions after 10, 30, 60 and 120 min of seizure activity. Microsphere and iodo[14C]antipyrine methods gave identical control values for tCBF (0.88 +/- 0.02 vs 0.86 +/- 0.07 ml/g brain/min) and closely similar rCBF values. The increases in tCBF after 10 and 30 min seizure activity were less as measured with microspheres than with iodo [14C]antipyrine (2.42 +/- 0.29 vs. 4.99 +/- 0.94 and 1.79 +/- 0.18 vs 3.05 +/- 0.30 mg/g brain/min, respectively). With microspheres, rCBF values showed considerable interhemisphere variability, but did not do so with iodo [14C]antipyrine. The regional pattern of flow changed during seizures. Changes in neocortical rCBF tended to match changes in tCBF. Consistent decreases in rCBF relative to tCBF were seen in the pons-medulla and cerebellum at all seizures times. Relative increases in rCBF were seen at all seizure times in the thalamus, and at 10 and 30 min in colliculi and midbrain. In the hippocampus, rCBF was unchanged (relative to tCBF) at 10 and 30 min, but was increased at 60 and 120 min of seizure activity. Thus, regions developing epileptic brain damage in this model of status epilepticus (hippocampus, thalamus, neocortex) show increases in rCBF greater than those in regions not showing brain damage (cerebellum, brain stem).
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PMID:Regional cerebral blood flow in the rat during prolonged seizure activity. 676 47