[Vitrectomy in Terson' syndrome].
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Biomedical subjects
Publications and source records attributed to I Takáts.
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Earlier we have shown in the dog model mimicking angina on effort a delayed antiischaemic effect of PgI2 and its stable analogue 7-oxo-PgI2-Na, appearing only when the drug induced marked vasodilatation was over [1]. In the present experiments we could show that the protective effect appears at a time when the blood pressure returned to normal and in addition the marked platelet aggregation inhibitory effect has also faded away. In the rat 7-oxo-PgI2 could substantially diminish vasopressine induced T-wave elevation in the ECG if given 2 hours before administration of vasopressin. In addition it could moderate the vasopressin induced metabolic changes appearing as diminution of the myocardial CP and ATP-level and increase of the myocardial lactate content. A similar metabolic protection was found in the heart of rats pretreated with 7-oxo-PgI2 2 hours before taking myocardial samples and exposing them for 1 minute to ischaemia by incubation in Ringer solution. It is concluded that a direct metabolic and hemodynamic effect could be at least partly responsible for the late antiischaemic effect of 7-oxo-PgI2. This effect was also present in the early phase of experimental myocardial infarction in conscious rats if animals were pretreated with 7-oxo-PgI2 2 hours before occlusion. However treatment did not increase survival rate and failed to reduce the incidence and severity of arrhythmias.
Prostaglandin E2 (0.5 microgram in 10 microliter 10% ethanol) was introduced into the anterior chambers of rabbit eyes. Using the horseradish peroxidase method, it was shown under the electron microscope that the endothelial barrier of the iris vessels broke down. The peroxidase penetrated as far as the basis of the posterior epithelial cells, however, without entering their lateral intercellular spaces. The question of whether the effect of prostaglandins on the barrier was a direct effect or at least a partially indirect one, i.e., a haemodynamic action, is discussed.
Experiments on twenty-eight New Zealand albino rabbits have shown that prostaglandin E2 causes contraction of the isolated iris sphincter and is about five times as effective as acetylcholine. Prostaglandin E2 does not act on the cholinergic receptors; the effect of prostaglandin E2 was not increased by eserine, and not abolished by atropine. In high doses indomethacin (3 X 10(-4) M) reversed the prostaglandin effect, but lower concentrations (3 X 10(-5) M) left it unaffected.
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Simultaneous occlusion of both common carotid arteries in female Sprague-Dawley CFY rats produced characteristic symptoms of global cerebral ischemia, such as staggering, circling, convulsions, followed by coma and death. A close correlation existed among these symptoms and the elevation of water and Na+ content, appearing at the stage of staggering; Evans blue extravasation and diminution of K+ content, detected at circling; and the increase in Ca2+ content in the total brain tissue, manifesting itself at the phase of convulsions, indicating the development of cerebral edema due to ischemia. Dexamethasone given subcutaneously in a single 2.0 mg kg-1 dose 5 hours prior to the induction of global cerebral ischemia reduced considerably the morbidity and mortality, the alterations in water and electrolyte content, and albumin leakage in the brain tissue. Actinomycin D, in a dose of 0.5 mg kg-1 injected intravenously 1 hour before steroid treatment, abolished the beneficial effect. This finding suggests that de novo protein synthesis is involved in the cerebroprotective effect of dexamethasone.