Search PubMed⌕ Search

Biomedical subjects

E Siemkowicz

Publications and source records attributed to E Siemkowicz.

At least 19 recordsLinked to original sources
PubMed2003

Role of staphylococcal enterotoxin A in a fatal case of endocarditis.

A young female with no identifiable risk factors developed rapid, overwhelming Staphylococcus aureus endocarditis. Despite rapid sterilization of the blood and the mitral valve with optimal antimicrobials, she had persistent septic shock. In order to investigate this, the toxin-producing capacity of the infecting strain and the patient's ability to produce antibodies were determined. The strain produced high levels of both alpha-toxin and staphylococcal enterotoxin A (SEA), whilst the patient responded with modestly high levels of antibodies to alpha-toxin and low-normal levels to SEA. The patient was most probably susceptible to the actions of SEA and developed a toxic-shock-syndrome-like disease that further aggravated her valvular dysfunction. This case illustrates that optimal antimicrobial therapy alone is not sufficient treatment in patients with persistent toxic shock and that there is a need to evaluate immunomodulatory strategies in such patients.

Adult↗
PubMed1997

Magnesium sulfate solution dramatically improves immediate recovery of rats from hypoxia.

This study in rats investigated the effects of 0.5 mEq/1 kg body weight of magnesium sulfate solution upon hypoxic left cardiac ventricular pressure (Part 1), optimal timing for injection of magnesium sulfate solution for successful resuscitation (Part 2) and survival benefits of magnesium sulfate after 8 or 12 min of hypoxia (Part 3) in rats resuscitated by single bolus arterial reperfusion using 2 ml of arterial blood and 6-9 micrograms epinephrine. A total of 153 pentobarbital anesthetized rats were subjected to 8 or 12 min 0.75% O2:99.25% N2 hypoxia in order to induce cardiac arrest. In Part 1, 13 rats (six control and seven injected with magnesium sulfate solution) were subjected to 12 min hypoxia and cardiac left ventricular pressure (LVP) was measured. In Part 2, 47 rats were exposed to 12 min of hypoxia. Normal saline or magnesium sulfate solution was injected prior to hypoxia, at 2 or 4 min of hypoxia, to find the optimal timing of magnesium sulfate injection for successful resuscitation by arterial reperfusion. In Part 3, 90 rats were studied to determine 7-day survival. Two control groups were injected with saline during 8 min (29 rats) or 12 min (18 rats) of hypoxia and two groups received magnesium sulfate solution during 8 min (14 rats) and 12 min (29 rats) of hypoxia. Magnesium sulfate fully reversed the hypoxic increase of LVP and improved survival after 12 min of hypoxia from approximately 15 (control) to 100% if given during the first 2.5 min of hypoxia. The main cause of the progressive resuscitation failure after 8 or 12 min control hypoxia was a progressive increase in acute cardiac failure. Although magnesium sulfate solution significantly improved immediate recovery after hypoxia (8 and 12 min), mortality due to reperfusion injury (para or tetraplegia) was observed in 62% of rats surviving longer than 1 day after 8 min and 100% after 12 min hypoxia (in control rats-50 and 100%, respectively). The overall survival after hypoxia, with or without reperfusion injury, was relatively low: 28% in control groups after 8 min and 17% after 12 min. In the magnesium sulfate groups these numbers were only slightly higher, 36 and 21%, respectively. It is concluded that in conjunction with arterial reperfusion magnesium sulfate infusion is very effective in improving acute cardiac recovery after 8-12 min of hypoxia. The likely mechanism of magnesium sulfate action is decreased incidence of ventricular fibrillation (VF) and asystole, and possibly myocardial relaxation during and after hypoxia, a property which may qualify MgSO4 as an ischemic preconditioning agent. Poor long-term survival rates of rats exposed to hypoxia and resuscitated by intraarterial reperfusion do not support its use in resuscitation.

Animals↗
PubMed1995

Post-ischemic hypothermia ameliorates ischemic brain damage but not post-ischemic audiogenic seizures in rats.

AIM: The objective of this study was to describe a pattern of recovery and histological nerve cell loss in Sprague-Dawley rats exposed to severe brain ischemia and to compare it to that of Wistar rats. METHODS: Ether- and ketamine-anesthetized Sprague-Dawley rats were exposed to 3, 5, 6 and 10 min of normothermic severe brain ischemia (4 groups) induced by hypotension and neck compression. In group No. 5, the brain temperature was rapidly lowered, after 10 min of ischemia, to 30 degrees C during 45-50 min of recirculation. Wistar rats (group No. 6) served as controls (10-min normothermic ischemia). RESULTS: In Sprague-Dawley (S-D) rats, post-ischemic audiogenic seizures (PAS) increased with the duration of ischemia and reached 86% (6/7 rats), after 10 min of ischemia. Mortality rate was high (50% = 7/14 rats). No seizure activity was observed after 10 min of ischemia in 6 Wistar (W) rats, and all survived. In the S-D rats, 10 min of ischemia produced histopathological damage in all brain regions examined, except in the thalamus. Damage was less severe in the W rats. Post-ischemic hypothermia ameliorated hippocampal and cortical nerve cell damage, but had no effect on the incidence of PAS activity and mortality. In W rats, hippocampal nerve cell loss was much less severe than in the S-D rats and cortical damage was not observed. CONCLUSION: Sprague-Dawley rats develop post-ischemic audiogenic seizures more frequently than Wistar rats and mortality rate is high. The incidence of post-ischemic audiogenic seizures and mortality correlates well with the duration of ischemia. Post-ischemic moderate hypothermia (30 degrees C) significantly ameliorated the hippocampal and cortical nerve cell losses after 10 min of severe brain ischemia, but did not improve outcome. It appears that the high mortality rate of S-D rats following brain ischemia is related to frequent post-ischemic audiogenic seizures.

Acoustic Stimulation↗
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

Hyperglycemic ischemia of rat brain: the effect of post-ischemic insulin on metabolic rate.

To identify the mechanism by which hyperglycemia impairs recovery after cerebral ischemia, cortical blood flow (CBF), cortical metabolic rate for oxygen (CMRO2), and the cortical phosphorylation rate for glucose (CPRg1c) were measured in rats 1 h after a global ischemic insult of the brain. A control group remained hyperglycemic after ischemia. The experimental group received insulin which reduced plasma glucose during the period of recirculation after ischemia. Thus, the brains of both groups were hyperglycemic before and during ischemia. The CMRO2 after ischemia was higher in insulin-treated rats than in hyperglycemic rats (250 vs 168 mumol . 100 g-1 . min-1) while the CPRg1c was lower (22 vs 58 mumol . 100 g-1 . min-1). We conclude that glucose-induced inhibition of oxygen consumption in brain contributes to the impaired recovery after ischemia.

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

Extracellular potassium and blood flow in the post-ischemic rat brain.

The concentration of extracellular potassium, [K+]e, was measured in parietal cortex and basal ganglia of rats during and after ten minutes of complete cerebral ischemia. The post-ischemic normalization of [K+]e was considerably delayed in parietal cortex compared to basal ganglia, but in both regions, [K+]e reached its normal concentration within 4 min of the end of the ischemia. Also, in both regions blood flow was elevated at the time of maximal [K+]e decrease. Our findings suggest that the normalization of [K+]e and cerebrovascular resistance after ischemia are related by positive feed-back, possibly via the stimulation of Na+-K+-ATPase.

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↗
PubMed1980

Improvement of restitution from cerebral ischemia in hyperglycemic rats by pentobarbital or diazepam.

Hyperglycemic rats were exposed to 10 min of complete cerebral ischemia. Rats with 26 mM (range 23-27 mM) plasma glucose levels died. Rats with the same degree of hyperglycemia, treated after ischemia with pentobarbital (75-95 mg/kg) or diazepam (10-13 mg/kg), survived the observation period of 21 days and recovered, albeit incompletely. The same treatment given to rats with higher degrees of hyperglycemia did not prevent death. It is concluded that postischemic treatment with anticonvulsive drugs may improve clinical restitution from ischemia in moderately hyperglycemic rats.

Animals↗
PubMed1980

Rapid simultaneous determination of regional blood flow and blood-brain glucose transfer in brain of rat.

A new method was developed and used in rat to measure regional and whole-brain blood flow and blood-brain glucose transfer simultaneously and in 20 s. This simple method consisted of i.v. bolus injection of labeled butanol and tracer glucose, determination of the average arterial tracer concentration and subsequent assay of cerebral tissue activity 20 s after bolus injection. The whole-brain blood flow rate averaged 129 ml (100 g)-1 min-1. The unidirectional blood-brain glucose transfer was twice as high as previously estimated in similar studies on rat, or 144 mumol (100 g)-1 min-1 at 10 mM glucose in plasma. The magnitude is sufficient to explain the high cerebral glucose consumption rates recently determined by means of autoradiographic 2-deoxy-D-glucose method of Sokoloff et al. (1977).

Animals↗
PubMed1980

Post-ischemic coma in rat: effect of different pre-ischemic blood glucose levels on cerebral metabolic recovery after ischemia.

Hyper-, normo-, and hypoglycemic rats were exposed to 10 min of complete cerebral ischemia. Regional cerebral blood flow (CBF), blood-brain glucose transfer, and cerebral consumption of oxygen and glucose were measured before, as well as three and 60 minutes after ischemia. Three min after ischemia, no differences were observed between the 3 groups of rats. One h after ischemia, the hyperglycemic rats in comparison to those of the other groups had similar whole-brain CBF and glucose consumption but appreciately lower oxygen consumption, indicating continued non-oxidative use of glucose in the hyperglycemic group. In general, regional CBF values exceeded the control value by 100-200% 3 min after ischemia and were reduced to 50% of control at 1 h after ischemia, at which time the rats were still comatose. In the brain stem of hyperglycemic rats, blood flow, however, remained elevated after ischemia. Thus, the significantly increased mortality observed in rats hyperglycemic before, during and after ischemia (Siemkowicz & Hansen 1978) was the result, not of impaired postischemic CBF, but of ischemic or postischemic damage to brain cells. We suggest that the damaging factor in the hyperglycemic group is increased lactacidosis associated with prolonged anaerobic glycolysis.

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↗