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Delayed neurologic deterioration following anoxia: brain mitochondrial and metabolic correlates.

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Hyper- but not normoglycemic cats exposed to 8 min of anoxia show neurologic signs (fasciculations, myoclonic jerks, seizures) that develop after a symptom-free period. We examined brain mitochondrial function and metabolite concentrations at 0, 1, 3, and 5 h following exposure to anoxia, to

Delayed decreases in specific brain mitochondrial electron transfer complex activities and cytochrome concentrations following anoxia/ischemia.

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Hyperglycemic, but not normoglycemic cats exposed to anoxia develop neurologic signs following reoxygenation including fasciculations, focal and tonic-clonic seizures and coma after a symptom-free period. These symptomatic hyperglycemic cats may develop brain edema and will show diffuse neuronal

Delayed onset of neurologic deterioration following anoxia/ischemia coincides with appearance of impaired brain mitochondrial respiration and decreased cytochrome oxidase activity.

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We previously demonstrated markedly inhibited brain mitochondrial respiration only in cats that (a) were hyperglycemic at anoxia and (b) had neurologic signs, i.e., fasciculations in tongue or facial muscles or focal seizures following reoxygenation. However, since the relationship between time of

[Motor neuron disease with respiratory insufficiency as primary manifestation].

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A 66-year-old man with dyspnea on exertion suffered a cardiac arrest and was referred to our hospital after emergency room intubation. Chest X-ray films detected no abnormalities. Blood gas analysis showed hypoxemia with normal A-aDO 2, and pulmonary function tests revealed combined ventilatory

Reference cardiopulmonary physiologic parameters for standing, unrestrained white rhinoceroses (Ceratotherium simum).

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Chemical restraint is an important tool for the management and medical care of both captive and free-ranging rhinoceroses. Current anesthetic protocols for the white rhinoceros (Ceratotherium simum) are reported to cause varying degrees of hypertension, tachycardia, muscular stiffness and

[Type I spinal atrophy (Werdnig-Hoffman disease). Case report].

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BACKGROUND We report a case of type I spinal muscular atrophy (SMA), also known as Werdnig-Hoffmann disease. METHODS This was a descriptive case report. The patient was in the pediatric intensive care unit of a medical center. METHODS The patient was a 5 1/2 month-old male admitted to the emergency

The role of diazepam in the treatment of nerve agent poisoning in a civilian population.

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The main site of action of diazepam, as with other benzodiazepines, is at the GABA(A) receptor, although it has been suggested that some of the potentially beneficial actions of diazepam in nerve agent poisoning are mediated through other means. It is likely that convulsions may have long-term

Effect of high-intensity exercise on arterial blood gas tensions and upper airway and cardiac function in clinically normal quarter horses and horses heterozygous and homozygous for hyperkalemic periodic paralysis.

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OBJECTIVE To determine the effect of exercise on arterial blood gas tensions and upper airway and cardiac function in clinically normal Quarter Horses and horses heterozygous and homozygous for hyperkalemic periodic paralysis (HYPP). ANIMALS AND PROCEDURE: 5 clinically normal Quarter Horses, and 5

Kerosene, Camphor, and Naphthalene Poisoning in Children.

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Kerosene poisoning is one of the most common accidental poisoning in children in developing countries due common use of kerosene in house-hold and unsafe storage practices. Aspiration pneumonitis is the most common manifestation of kerosene ingestion due to its low viscosity, high

Assessment of ionizable, zwitterionic oximes as reactivating antidotal agents for organophosphate exposure.

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Since the development in the 1950's of 2-PAM (Pralidoxime), an antidote that reactivates organophosphate conjugated acetylcholinesterase in target tissues upon pesticide or nerve agent exposure, improvements in antidotal therapy have largely involved congeneric pyridinium aldoximes. Despite seminal

Organic phosphorus compounds--nerve agents.

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The organic phosphorous compounds (OPC) include both the military grade nerve agents and the organic phosphorous pesticides. The major mechanism of OPC toxicity is through inhibition of acetylcholinesterase in neuronal synapses leading to excess acetylcholine and overstimulation of target organs.

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