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Biomedical subjects

E Siemkowicz

Publications and source records attributed to E Siemkowicz.

26 records · Page 2Linked to original sources
PubMed1977

Changes in cisternal fluid potassium concentration following cardiac arrest.

The purpose of this study was to measure the changes in potassium concentration in human cisternal cerebrospinal fluid following successful resuscitation after cardiac arrest. We also wished to examine whether or not changes in potassium concentration in the cisternal cerebrospinal fluid could be correlated to the ability to regain normal cerebral function. 41 patients were studied, of whom 20 regained consciousness and 21 did not. In those who did not regain consciousness there was a significant increase in the potassium concentration found in samples obtained between 40 and 50 min, and between 50 and 60 min after cardiac arrest. The potassium concentration decreased to normal values during the following hours. Lumbar spinal fluid did not reflect the changes in cisternal fluid. The results suggest that the potassium concentration of cisternal cerebrospinal fluid, obtained soon after cardiac arrest, might give an indication of the degree of cerebral damage caused by cardiac arrest.

Cisterna Magna↗
PubMed1976

Six cases of cerebromedullospinal disconnection after cardiac arrest.

Six cases of cerebromedullospinal disconnection after cardiac arrest are reported. The diagnosis was based on mutism, consciousness and/or wakefulness, and global paralysis, except for some very limited motor functions, mostly eye movements. Consciousness was defined as repetitive contact with the patient by way of simple motor response. Despite of the fatal outcome in all cases, the importance of diagnosis and correct handling is stressed.

Adult↗
PubMed1976

Multiple sclerosis and surgery.

Five patients with multiple sclerosis showed deterioration following operation and anaesthesia. In every case the change was associated with pyrexis due to infection. No correlation was found between aggravation and any anaesthetic agent used.

Adult↗
PubMedDate not supplied

Regional neurone damage after cerebral ischaemia in the normo- and hypoglycaemic rat.

Ten minutes of total cerebral ischaemia was produced in normo- and hypoglycaemic rats. The most conspicuous findings were loss of hippocampal (CA-1) pyramidal cells and Purkinje cells, which were most pronounced in the normoglycaemic rats. While pre-ischaemic hypoglycaemia to some extent protected these cells, it led to infarction of severe ischaemic nerve cell changes in the brain stem nuclei and lowered the neurological restitution of the hypoglycaemic animals. The regional damage in these rats, which were kept normotensive after ischaemia, was not due to circulatory insufficiency. However, rats with untreated spontaneous low blood pressure in the early postischaemic period showed multiple small infarcts.

Animals↗
PubMedDate not supplied

Brain extracellular ion composition and EEG activity following 10 minutes ischemia in normo- and hyperglycemic rats.

Hyperglycemia severely impairs the outcome from cerebral ischemia. In order to sort out whether impaired brain ion homeostasis contributes extracellular "K+], [Ca++], and [H+] concentrations, [K+]e, [Ca++]e and [H+]e, of the brain cortex, as well as the EEG, were monitored during and after 10 minutes of complete cerebral ischemia in normo- and hyperglycemic rats. In both groups, the EEG-activity disappeared in 10-20 seconds of ischemia, at a time when [K+]e, [Ca++]e and [H+]e started to increase. After about 1.5 min, [K+]e showed an abrupt increase and [Ca++]e a steep decrease in the normoglycemic group. In the hyperglycemic group the same event took place after about 3 min of ischemia. pHe decreased to 6.6 and 6.1 in the normoglycemic and hyperglycemic group, respectively. Following the ischemic episode [K+]e reached pre-ischemic level after 4 min, [Ca++]e after 13 min, and [H+]e after 30 min in both groups. Recovery of the EEG, however, was clearly different in the 2 groups. EEG-activity reappeared later in the hyperglycemic group and showed after one hour a pattern of burst-suppression activity while the normoglycemic group showed asynchronous activity resembling the control pattern. It is concluded that high glucose content in brain prior to ischemia - and hence lower brain pH during ischemia - does not interfere with the return of normal extracellular ion composition after cerebral ischemia, whereas the return and pattern of EEG activity is severely affected.

Animals↗