PubMed Health⌕ Search

Biomedical subjects

E Siemkowicz

Publications and source records attributed to E Siemkowicz.

15 recordsLinked to original sources
PubMed1990

Estimation of cerebral blood flow during cardiopulmonary resuscitation in humans.

Cerebral blood flow (CBF) and cardiac output (CO) were measured during cardiopulmonary resuscitation in patients who were unsuccessfully resuscitated by use of C14-iodoantipyrine injected into the left ventricle. CO varied between 1.3 and 2.2 l/min with mean 1.8 +/- 0.6 l/min (+/- SD) (28 ml/kg/min). The cortical CBF was found between 14 and 211 ml 100 g-1.min-1 with mean 42 ml 100 g-1.min-1 and mean white matter CBF equal to 27 ml 100 g-1.min-1. It is suggested that the external cardiac massage in humans may be of poor efficacy in terms of brain revival. Cortical CBF after long-lasting cardiopulmonary resuscitation showed signs of maldistribution suggestive of a patchy and incomplete perfusion.

Aged↗
PubMed1985

The effect of glucose upon restitution after transient cerebral ischemia: a summary.

The study describes a reproducible model of complete brain ischemia in rats. Rats with different plasma glucose concentrations were exposed to 10 min of complete cerebral ischemia achieved by compression of neck vessels by a pneumatic cuff. All 30 rats, except one, in which pre-ischemic plasma glucose level were lower than 22 mM (range 1.6-22) survived 10 min complete ischemia and made a similar recovery. Ten rats with pre-ischemic plasma glucose levels above 22 mM (range 22-47.2) died from seizures in the post-ischemic period. Post-ischemic treatment of seizures and hyperglycemia in the hyperglycemic rats significantly improved recovery. In conclusion, pre-ischemic hyperglycemia above 22 mM impairs recovery after complete ischemia by inducing seizures, post-ischemic hyperglycemia and lactic acidosis.

Animals↗
PubMed1982

[Simultaneous diffusion of inositol and mannitol in the rat brain].

The diffusion of both inositol and mannitol has been determined simultaneously by the integral bolus method in rat brain. The permeability constant (Kin) of inositol averaged 0.27 +/- 0.02 ml X (100 g)-1 X min-1 or 4 X 10(-7) cm X s-1 at a cerebral capillary surface area of 100 cm2 x g-1. The permeability of mannitol was 0.08 +/- 0.01 ml X (100 g)-1. min-1 or 1 X 10(-7) cm X s-1. Neither glucose nor galactose affected the inositol permeability. Hypoglycemia increased somewhat the Km value for mannitol. The basal ganglia showed an increase Km for both substrates as compared with those obtained for cortex, temporal and parietal tissues.

Animals↗
PubMed1981

Hyperglycemia in the reperfusion period hampers recovery from cerebral ischemia.

Glucose treatment prior to cerebral ischemia is followed by similar metabolic and hemodynamic recovery (Siemkowicz & Gjedde 1980), and normalisation of brain extracellular ions (Siemkowicz & Hansen 1981). In view of this, the present study investigated whether post-ischemic hyperglycemia influenced recovery from cerebral ischemia. In rats which received 50% glucose during a 10 min period of cerebral ischemia, and which had a plasma glucose level of 28.5 mM after 10 min of recirculation, recovery was inferior to that of rats receiving either 8% NaCl or 0.9% NaCl (and hence the rats were normoglycemic). Furthermore, rats which had been rendered hyperglycemic (39 mM) prior to ischemia, and which had plasma glucose lowered to 15 mM by insulin treatment during ischemia, did not recover and died within 4 days. Conversely, rats with somewhat lower preischemic hyperglycemia (28 mM), and which had plasma glucose lowered to 12 mM by insulin treatment during ischemia, recovered as well as the normoglycemic rats. In conclusion, preischemic and postischemic hyperglycemia is detrimental to recovery from cerebral ischemia.

Animals↗
PubMed1981

Brain uptake of mannitol and sucrose after cerebral ischemia: effect of hyperglycemia.

The effect of 10 min cerebral ischemia on blood-brain barrier permeability to mannitol and sucrose was evaluated in normo- and hyperglycemic rats. In the period immediately after ischemia (1-4 min) the PS (permeability-surface area product) for mannitol was 159% +/- 75 of control (0.17 +/- 0.02 mg/100 g min) in the hyperglycemic rats (plasma glucose 8 mM) and 204% +/- 30 of control (0.09 +/- 0.02 mg/100 g min) in the hyperglycemic rats (plasma glucose 28 mM). Two hours after ischemia, PS for mannitol returned to the control levels in the normoglycemic rats and remained elevated in hyperglycemic animals. The mannitol/sucrose ratios-2.3 +/- 0.4 in normoglycemic rats and 2.6 +/- 0.1 in hyperglycemic rats-remained unchanged after ischemia. As there was no significant difference in the effects of ischemia on normo- and hyperglycemic rats, it was concluded that the deleterious effect of hyperglycemic on clinical recovery after cerebral ischemia in rats (Siemkowicz & Hansen 1978) is not related to enhancement of BBB damage.

Animals↗
PubMed1980

Cerebrovascular resistance in ischemia.

The cerebrovascular resistance (CVR) of rat, and its dependence on stagnant blood or endothelial capillary swelling, was studied after 10 min of total ischemia by 10 s single carotid infusion of [14C]butanol in saline. The regional saline flow (CPR) was calculated from the uptake of [14 C]butanol. CVR was estimated at infusion pressures ranging from 8--25 kPa (60--190 mm Hg). At 14.7 kPa (110 mm Hg) infusion pressure, the regional CVR of the non-ischemic group varied between 0.21 and 0.40 kPa 100 g min ml-1. After 10 min of complete global cerebral ischemia, it increased to values between 0.82 and 1.95. Removal of blood from the brain by rinsing prior to ischemia did not change the CVR in ischemia. Increasing the plasma osmolality by 8% with mannitol before ischemia attenuated the CVR increase in ischemia. Thus, although osmotic swelling of endothelial cells contributed, the main cause of the CVR increase in ischemia was constriction of arterioles.

Animals↗
PubMed1978

Cytology of human cerebro-spinal fluid after cardiac arrest.

The cytology of the cerebrospinal fluid (CSF) (obtained by suboccipital puncture) from patients after cardiac arrest was investigated by means of the cytocentrifugation method. In patients with unsuccessful resuscitation an increased number of monocytes and macrophages was found immediately after abandoned resuscitation. A pronounced increase in the number of granulocytes, monocytes, and macrophages was found in patients with poor neurologic restitution. The increase in the number of macrophages was seen immediately after cardiac arrest. The granulocyte increase was most pronounced after 24 h. The CSF from patients with full neurologic restitution after cardiac arrest showed small numbers of lymphocytes and granulocytes and an equal amount of monocytes and macrophages. The findings indicate that monocytes/macrophages appear in the cisternal fluid shortly after anoxic/ischemic damage to the brain and that the increase of macrophages and later granulocytes probably is a result of damage to brain tissue.

Cerebrospinal Fluid↗
PubMed1978

Clinical restitution following cerebral ischemia in hypo-, normo- and hyperglycemic rats.

Rats with different levels of blood glucose concentration were exposed to 10 min of complete brain ischemia achieved by compression of neck vessels by a pneumatic cuff. All normoglycemic rats survived the ischemic period and made the best clinical recovery. Hyperglycemic rats died within 12 h. Seizure activity was observed in all animals in this group. Three of eight hypoglycemic rats died between 3 and 16 days. The clinical recovery was less complete than in the control group. Thus, recovery from cerebral ischemia depends upon preischemic blood glucose concentration. Hyper- and hypoglycemia hamper the clinical recovery after transient cerebral ischemia.

Animals↗
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↗