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

The time course of changes in cortical tissue pH (pHi) and blood flow during cortical seizures in halothane-anesthetized cats was examined. The clearance of the molecular form of umbelliferone (Um) was used to estimate focal cortical blood flow (CBFu), whereas the ratio of the molecular to the ionic form of the molecule was used to concurrently calculate the local pHi. Resting pHi and flow in normocarbic animals was 7.116 +/- 0.008 and 46 +/- 8 ml/100 g/min, respectively. Respiratory induced alterations of PaCO2 over a range of 20-60 torr revealed a correlated change in pHi from 7.39 +/- 0.05 to 7.01 +/- 0.03 and a monotonic increase in the rate of Um clearance (slope 0.89 +/- 0.13 ml/100 g/min/torr). Focal electrical stimulation of the cortex resulted in a rapid vasodilation (50% dilation = 1-3 s) of pial arterioles and venules and an increase in Um clearance. pHi showed no significant change until around 10 s. The maximum fall in pHi occurred by 30-60 s (6.85 +/- 0.054). Longer intervals of stimulation (10 min) resulted in no further decline in pHi, but upon cessation of stimulation. pHi remained acidotic for poststimulation periods up to 10 min, with a mild but statistically significant acidosis being observed at 20 min. The absolute decline in pH observed following stimulation appeared to be closely regulated, as comparable levels following stimulation were observed during hypocarbia and hypercarbia. These observations thus suggest that pHi regulation during intense cortical activation may be considered in three phases: following the onset of activity, an initial acute regulation of pHi at control levels; an intracellular acidosis of around 6.8, which is closely regulated and which can be readily reversed upon termination of stimulation; and during continued stimulation, a change in state where in spite of no further change in pHi, the ability of the cortex to return to control pHi appears to be significantly impaired.
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PMID:In vivo studies on intracellular pH, focal flow, and vessel diameter in the cat cerebral cortex: effects of altered CO2 and electrical stimulation. 310 71

1. The goal of this study was to examine the regulation of resistance in the large arteries and small vessels that supply the brain stem. 2. We used a new method in anaesthetized cats to measure blood flow to the medulla (microspheres) and pressure (servo-null) in branches of the basilar artery that supply the medulla. Resistance was determined during normocapnia, hypercapnia, hypocapnia and seizures (produced with intravenous bicuculline). 3. Pressure in arteries that supply the medulla (150 microns internal diameter) was 71 +/- 4% (mean +/- S.E. of mean) of aortic pressure and large artery resistance was 31 +/- 4% of the total resistance in the medulla. Hypercapnia and seizures decreased large artery resistance by 67 and 50%, respectively, and hypocapnia increased large artery resistance by 58%. Small vessel resistance decreased by 82% during hypercapnia and by 43% during seizures, and increased by 96% during hypocapnia. 4. Thus, resistance of the large arteries (greater than 150 microns diameter) accounts for about one-third of the total vascular resistance in the brain stem. Both large arteries and small vessels respond to alterations in arterial carbon dioxide tension and seizures, and contribute to the regulation of blood flow to the brain stem.
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PMID:Role of large arteries in regulation of blood flow to brain stem in cats. 311 12

A placebo-controlled, randomized study of the effect of a 10-day infusion of morphine (MOR) upon fetal survival and fetal breathing movements was done in late gestation lambs. MOR infusion at a rate of 3 mg.hr-1 did not affect fetal survival or the response of fetal breathing movements to hypercapnia. Chronic exposure to MOR increased the height of the integrated diaphragmatic electromyogram signal (IDIA), respiratory drive and inspiratory effort during periods of eucapnia. Respiratory drive was determined by the product of IDIA height and breathing frequency, and inspiratory effort was the quotient of IDIA height divided by inspiratory time. These effects may be related to accumulation of morphine-3-beta-D-glucuronide. Higher doses of MOR, 10 (n = 3) and 30 (n = 1) mg.hr-1, caused seizures and decreased fetal survival.
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PMID:Comparison of chronic morphine and placebo infusion in late gestation fetal lambs: effect upon survival and breathing movements. 313 63

The noncontroversial fact regarding ECT seems to be that controversy exists in almost every area of its use, its art, and its science. The nature of the treatment itself, its history of abuse, unfavorable media presentations, special attention by the legal system, uneven distribution of use among facilities and practitioners, and lack of certified standards for psychiatric training in ECT have tended, in the past 2 decades, to swing the pendulum towards the use of tricyclic and other antidepressant agents for the treatment of severe depression. Despite recommendations for continual review of data and of clinical and research experience, few pertinent reports by anesthesiologists have appeared. Guidelines for the anesthesiologist have not been established. Due to the pervading presence in earlier studies of hypoxia, hypercarbia, and acidosis, it is futile to compare findings of unmodified ECT to modified ECT. More recent studies relating especially to cardiovascular abnormalities have also been difficult to evaluate because of widely varying formats, use of different agents and dosages, continuance or discontinuance of psychotropic drugs, and variability of ventilation and concentrations of oxygen. ECT is a modality that has not outlived its usefulness. With proper pretreatment, selection and evaluation of patients, use of appropriate modification techniques, and careful clinical management and monitoring during treatment, ECT can be both safe and effective, even in relatively high-risk patients. ECT provides an exciting challenge for concerned physicians to explore the role of brain function and behavior, and the effects of seizures on neuroendocrine mechanisms, neurohumoral mechanisms, cerebral metabolism, the blood-brain barrier, and ion transport systems. It may lead to further understanding of the action of general anesthetics, CNS depressant drugs, and the effects of stimulation of the central autonomic nervous system and the endocrine systems. A close interaction between basic and clinically oriented researchers holds the key to designing studies that can answer these critical questions, rather than continuation of studies that merely generate more data.
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PMID:Electroconvulsive therapy--1987. 330 31

Local brain tissue oxygen tension, temperature, and electrical potential were continuously and simultaneously measured at each of two different depths in anesthetized, paralyzed rat brain. Brain tissue temperature increases up to 1 degree C were recorded in response to direct electrical stimulation, spreading depression, PTZ-induced seizures, hypercapnia, and hypoxia. An increase in brain tissue temperature was also recorded during reoxygenation after hypoxia. Thus, we have shown that, in this preparation, increases in either blood flow or oxidative metabolism lead to transient warming of the brain.
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PMID:Brain tissue temperature: activation-induced changes determined with a new multisensor probe. 336 63

Nimodipine, a dihydropyridine that interacts with a Ca++ channel-associated binding site, when delivered (30 to 150 micrograms/kg) intra-arterially (ia) to enflurane-anesthetized cats, produced a dose-dependent suppression of seizures evoked by pentylenetetrazol. A comparable suppression was produced by clonazepam (1 to 30 micrograms/kg, ia). Phenytoin was maximally effective only at nearly lethal doses (90 mg/kg, ia). Verapamil, a diphenylalkylamine that interacts with a separate Ca++ channel-associated site, at the maximum nonlethal dose (6 mg/kg, ia) resulted in a mild facilitation of seizure activity. The drug vehicle used in these studies (50% polyethylene glycol-400) had no effect when given alone. Regional cerebral blood flow (rCBF) as measured by the clearance of xenon-133 was markedly elevated immediately after the onset of seizure activity (89 +/- 3 to 168 +/- 4 ml/100 gm/min). Concurrent with their resolution of the seizure activity, both nimodipine and clonazepam reduced rCBF to near preseizure levels and preserved the rCBF response to hypercarbia which would otherwise have been abolished following prolonged seizure activity. Moreover, the effect of nimodipine on rCBF and seizures occurred without any prominent alterations in mean arterial blood pressure as compared to preseizure levels. These data support the proposition that a dihydropyridine Ca++ channel binding site may play a role in modulating paroxysmal neuronal activity, and suggest that this class of agents may reflect a novel group of antiepileptic drugs.
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PMID:Effect of dihydropyridines and diphenylalkylamines on pentylenetetrazol-induced seizures and cerebral blood flow in cats. 361 73

The influence of arterial O2 and CO2 tensions on electroconvulsive seizure duration was investigated in five mongrel dogs under consistent anaesthetic conditions. Seizure durations were measured in a randomized protocol of nine possible combinations of arterial gas tension spanning increased, normal or decreased levels of PaO2 and PaCO2. Seizure duration was directly related to PaO2 (p less than 0.00001) and inversely related to PaCO2 (p less than 0.0001). A significant synergism was evident at the extremes of PaO2 and PaCO2, with seizure duration being greater than predicted for hyperoxia-hypocapnia and hypoxia-hypercapnia and shorter than predicted for hypoxia-hypocapnia and hyperoxia-hypercapnia. We conclude that arterial gas tensions strongly influence ECT-induced seizure duration and through this may influence the therapeutic efficacy of electroconvulsive therapy.
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PMID:Arterial PaO2 and PaCO2 influence seizure duration in dogs receiving electroconvulsive therapy. 366 9

The intrinsic processes involved in the initiation and arrest of seizures are not completely understood. Cortical and cerebellar inhibitory mechanisms, accumulation of metabolic products, and glial uptake of extracellular potassium (K+o), anions, and released neurotransmitters are all important processes that limit focal firing and terminate a seizure once it has been initiated. Of these, the intrinsic cortical inhibitory mechanisms--i.e., recurrent and surround inhibition--appear to be the most important. Active cation and anion transport processes are two metabolic events that have yet to be elucidated but clearly could be involved in terminating a seizure discharge. For example, without an active mechanism to transport chloride, opening of the chloride channel by the inhibitory transmitter GABA would not result in increased chloride permeability. The transient hypoxia and hypercapnia and lactic acidosis that follows a severe tonic-clonic seizure produces a mixed systemic metabolic and respiratory acidosis. In experimental animals, the hypercapnia that results is sufficient to block seizure discharges. Increasing the CO2 concentration significantly reduces the extension to flexion (E/F) ratio of mice given maximal electroshock seizures (MES) and increases the time required for 50% of the animals to recover sufficiently from a first MES to be able to have another MES. The decreased E/F ratio and the increased recovery time (RT50) are both indicative of a decrease in seizure activity. Since the extent to which CO2 is allowed to accumulate in the brain is regulated by the glial specific enzyme carbonic anhydrase (CA), it follows that the glial cell has an integral role in the mechanisms involved in arresting seizure activity. In contrast, hypoxia increased the E/F ratio and decreased the RT50, evidence that seizure activity was enhanced. Another metabolic factor affecting duration of seizure activity, susceptibility to seizures, and recovery from seizures is glucose. Recovery from seizures depends in part on an adequate supply of this energy source. An inverse correlation (R = 0.95) between RT50 and blood sugar was found when the blood sugar was altered experimentally by treatments that altered the endocrine status (pancreatectomy, treatment with alloxan, cortisol, insulin, glucagon, and dextrose). Since glial cells contain (as glycogen) the small amount of glucose present in the brain, they probably hasten the ability of the brain to recover normal function following a seizure.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Role of glial cation and anion transport mechanisms in etiology and arrest of seizures. 370 23

The effect of generalized seizures on local cerebral blood flow was studied autoradiographically in 21 immature marmoset monkeys, using either [123I]- or [131I]isopropyliodoamphetamine. Generalized convulsions were induced in ketamine-anesthetized and awake monkeys with bicuculline and continued for 4-59 min. During convulsions in marmosets less than 3 weeks of age, there was a striking rearrangement of blood flow in favor of the brainstem pontomedullary region. The ratios of blood flow in pons-medulla to blood flow in cerebral cortex, putamen, ventroposterior thalamic nuclei, lateral geniculate nuclei, cerebellum and hemispheric white matter increased 1 1/2 to 2 times compared to controls. In seizure animals 4-8 weeks of age, the redistribution of blood flow to brainstem did not occur. Although metabolic acidosis developed after 30 min of bicuculline-induced seizures, mean arterial blood pressure, temperature, arterial pO2 and pCO2 did not differ significantly from controls, indicating that hypoxemia, hypercapnia and hypotension cannot explain the altered cerebral blood flow pattern. The redistribution phenomenon could be explained by more pronounced vasodilatation in brainstem than many other brain regions during generalized seizures in newborn monkeys. Lack of significant vasodilatation in forebrain structures such as cerebral cortex could contribute to neuronal damage by limiting substrate supply at a time of increased metabolic activity.
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PMID:Preferential blood flow to brainstem during generalized seizures in the newborn marmoset monkey. 380 66

This article reviews normal acid-base regulation, related laboratory tests, and the potential disorders if the body's ability to compensate is disrupted. Acid derived from the oxidation of proteins and through tissue metabolism must be excreted or neutralized daily by the kidneys and lungs to maintain a proper acid-base balance. Acid-base homeostasis is normally maintained by chemical buffering, changes in renal hydrogen-ion excretion, and alterations in the rate and volume of alveolar ventilation. Metabolic disorders are characterized by disturbances in bicarbonate (HCO3-) concentration, and respiratory disorders develop with primary alterations in the partial pressure of carbon dioxide (Pco2). Metabolic acidosis is characterized by low pH, low serum HCO3- concentrations, and a compensatory decrease in Pco2 with hyperventilation. Bicarbonate administration can correct this disorder, and equations for calculating the necessary amount of HCO3- are presented. Metabolic alkalosis is characterized by a primary increase in HCO3-, compensatory hypoventilation, and an increase in Pco2 (hypercapnia). The drug therapy for this disorder is directed at either saline-responsive alkalosis or saline-resistant alkalosis. Formulas for estimating the volume requirements of patients and appropriate doses of acidifying agents are presented. Respiratory acidosis and alkalosis are also discussed. The initial therapy for the hypercapnia associated with respiratory acidosis requires reversing the underlying pulmonary disease with steroids, bronchodilators, or antibiotics. The increased Pco2 in this conditions must be lowered slowly to avoid precipitating cardiac arrhythmias and seizures. The correction of respiratory alkalosis requires elevating the Pco2 and again treating the underlying disease. Pharmacists should be knowledgeable about acid-base regulation and the disorders that frequently occur with disease because drugs are capable of inducing or exacerbating these disorders and are often key elements in therapy.
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PMID:Simple acid-base disorders. 393 55


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