[The central anticholinergic syndrome. An overview].
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Biomedical subjects
Publications and source records attributed to W Erdmann.
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Exposure of rats to high concentrations of oxygen (greater than 95%) at 1 ATA pressure (101 kPa) is lethal within three days. Rats treated with a small dose of endotoxin are protected against these lethal effects of hyperoxia. Recently, we found that the lysine salt of acetylsalicylic acid antagonises this protective action of endotoxin. This suggests that prostaglandin metabolism plays an important role in the protective action of endotoxin against pulmonary oxygen toxicity. Therefore, we measured the plasma levels of 6KPGF1 alpha, a stable degradation product of prostacyclin (PGI2), PGE2 and thromboxane B2, the stable degradation product of thromboxane A2, in rats exposed to air or greater than 95% oxygen for 48 hours. We compared these with the plasma levels of rats treated with endotoxin (Salmonella typhimurium lipopolysaccharide 1 mg/kg) and exposed to air or greater than 95% oxygen for 48 hours. We found that exposure of rats to greater than 95% oxygen for 48 hours leads to a significant rise in the 6KPGF1 alpha levels. Rats exposed to greater than 95% oxygen for 48 hours and treated with endotoxin had significantly higher PGE2 and significantly lower 6KPGF1 alpha plasma levels than saline-treated rats exposed to greater than 95% oxygen for 48 hours.
This paper reports investigations on the effects on gastrointestinal transit of subcutaneous or intrathecal administration of opiates: morphine, sufentanil and alfentanil. Subcutaneous administration of opiates produced a significant dose-dependent decrease in transit of a charcoal meal test. Intrathecal administration of morphine to Wistar rats with catheter chronically implanted in the subarachnoid space did not cause a decrease in gastrointestinal transit. However, in freshly prepared rats with intrathecal catheter in the subarachnoid space, morphine significantly decreased intestinal transit of charcoal meal. In addition, sufentanil and alfentanil, on intrathecal administration in rats with chronically implanted catheters, caused a marked dose-dependent slowing of the passage of meal. Prior s.c. administration of the opiate antagonist naloxone completely blocked the depression of gastrointestinal transit caused by high doses of intrathecal sufentanil and s.c. administered morphine.
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Ketamine is normally considered as being anti-dysrhythmic. A case report is presented here in which small subanaesthetic doses of ketamine were administered to reinforce spinal analgesia. Initial doses were followed by a dysrhythmia, which appeared to be repeatedly counteracted by further small doses of the drug. The cardiac pharmacology of ketamine is discussed, as is the relevance of the chance finding of mitral valve prolapse.
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The effect of haemodilution with dextran or with oxygen transporting fluorocarbons (Fluosol-DA 20%) on myocardial oxygen tension (PmO2) during experimental myocardial ischaemia was studied in pigs. Polarographic oxygen microelectrodes were introduced 3 mm to the left ventricle wall and the distal one-third of the left anterior descending coronary artery (LAD) was occluded. Anaesthesia was maintained with 0.5% halothane in oxygen to ensure maximal oxygen content of the fluorocarbons. The animals were divided into three groups of five animals each. In group I no treatment was given and in groups II and III, after bleeding 20 ml kg-1, haemodilution was performed with Fluosol-DA 20% or 5% dextran respectively. Occlusion of the LAD caused no significant changes in cardiovascular vascular variables and only in group III (dextran) were significant effects of haemodilution observed. LAD occlusion caused highly significant decreases in PmO2. After haemodilution, PmO2 in the Fluosol group II (in contrast to groups I and III) was no longer significantly different from pre-occlusion values. After 5 h of occlusion, mean PmO2 in this group had returned to 92.2% of the pre-occlusion values, whereas in groups I and III it was 27.8% and 33.7%, respectively.
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Intrathecal and intracarotid effects of ketamine were investigated in anaesthetized rats. Ketamine was administered in the subarachnoid space in doses ranging from 300 to 1500 micrograms X kg-1. In these doses ketamine produced a short-lasting hypotension and bradycardia which may be due to inhibition of sympathetic outflow from thoraco-lumbar region. On the other hand when ketamine (5 mg X kg-1) was injected into the cerebral circulation it produced a rise in blood pressure and heart rate, probably through a cholinergic mechanism.
The present study was designed to investigate the pain relief mechanism of electrical stimulation to the pituitary and the relationship between hypothalamic and pituitary analgesic mechanism through the observation of monkey behavior and characteristics of tooth pulp-evoked potentials. The results suggest that pituitary-stimulating analgesia should be differentiated from hypothalamic-stimulating effect. In view of the facts, the theory of the Pituitary Inhibitory System is proposed.
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