Biomedical subjects
W Rieder
Publications and source records attributed to W Rieder.
[Successful resuscitation by laymen after lightning stroke].
Explore the source record for details and available documents.
[Labetalol for the management of hypertensive crises during surgery of cerebral aneurysm; a haemodynamic study (author's transl)].
The haemodynamic effects of Labetalol, an alpha- and beta blocking agent were investigated during neurosurgery in 11 patients with cerebral aneurysm and hypertensive episodes. All operations were performed in neuroleptanalgesia and controlled ventilation (PaCO2 = 30 mmHg). Immediately after intravenous injection of Labetalol there was a significant fall in the following haemodynamic parameters: arterial pressure -20 percent, pulmonary artery pressure -17 per cent, heart work index (right ventricle -32 percent, left ventricle -30 percent) and cardiac effort index -25 percent. Heart rate, cardiac index, stroke volume, total systemic and total pulmonary resistance were not appreciably altered. Labetalol appears to be of value in neurosurgical operations, where an increase in blood pressure, heart rate and myocardial oxygen consumption is undesirable.
Diffuse cerebral ischemia in the cat: II. Regional metabolites during severe ischemia and recirculation.
Metabolite levels were measured in seven brain regions in cats after 15 or 30 minutes of a severe ischemic insult and after a 90-minute period of recirculation following 15 or 30 minutes of ischemia. Brain levels of phosphocreatine were depleted after a 15- or 30-minute insult, and lactate levels were extremely high at both times. The adenosine triphosphate (ATP) content in many brain areas and the presence of microregions of low reduced nicotinamine-adenine dinucleotide in the brains of the animals that had 15 minutes of ischemia suggested that the ischemia, though severe, was not complete. Recirculation following a 15-minute insult restored brain levels of ATP and phosphocreatine to 70 to 100% of control values in all regions analyzed. In contrast, metabolic recovery from a 30-minute insult was regionally heterogeneous. Thus, there was persistent depression of ATP and phosphocreatine and elevation of lactate, which was localized in discrete cortical foci near the longitudinal midline. The factors governing the localization of metabolic failure must have become manifest during the recirculation period since the ischemic insult itself caused similar metabolic perturbations in all cortical regions.
Evaluation of in situ freezing of cat brain by NADH fluorescence.
Explore the source record for details and available documents.
Regional changes in metabolism in hypoxia-ischemia.
Explore the source record for details and available documents.
Two distinct types of inhomogeneous metabolic failure in cerebral oligemia.
Explore the source record for details and available documents.
Laryngectomy with preservation of the air passages.
Explore the source record for details and available documents.
[Laryngectomy with preservation of air passage].
Explore the source record for details and available documents.
[Experiences with cricohyoidopexy].
Explore the source record for details and available documents.
[Possibilities of partial or horizontal laryngectomy with preservation of the respiratory pathways].
Explore the source record for details and available documents.
[Professor Dr. Max Loeweneck on his 70th birthday].
Explore the source record for details and available documents.
Deleterious effect of glucose pretreatment on recovery from diffuse cerebral ischemia in the cat. II. Regional metabolite levels.
Glucose was infused intravenously into cats prior to cerebral ischemia. Brain concentrations of glucose, measured in 7 regions, were elevated 2.5-fold compared to those of non-infused animals. Ischemia of 15 or 30 minutes duration caused a greater accumulation of lactic acid in the brain of glucose-infused animals. Post-ischemic restitution of cerebral ATP, phosphocreatine, and lactate during 90 minutes of recirculation was severely impaired in the brain of animals pretreated with glucose compared to untreated animals. Thus, excess lactic acidosis may be a major factor interfering with metabolic restitution following cerebral ischemia.