Search results for "Brain Edema"
showing 6 items of 56 documents
Mechanisms of arachidonic acid induced glial swelling
2000
Accumulation of arachidonic acid (AA) in the brain during ischaemia may contribute to development of brain oedema. In this study we investigated the effect of selected drugs on AA-induced cytotoxic brain oedema in C6 glioma cells. Suspended C6 glioma cells were preincubated with drugs and AA (0.1 mM) was added. When no drug was administered cell volume increased immediately after the addition of AA with a maximum cell swelling of 13.1+/-1.9% at 15 min (mean +/- S.E. M.). Preincubation of cells with BW 755C, a dual inhibitor of cyclo- and lipoxygenases, showed no reduction in cell swelling from AA, whereas superoxide dismutase, amiloride and the protein kinase inhibitor H-9370 led to a signi…
Effects of Various Therapeutic Management on Raised Intracranial Pressure and on Dynamics Brain Edema in Brain Abscess Model in Cats
1983
In spite of the improved antibiotic treatment of brain abscess, the mortality remains high, between 30% and 40% (2,3). With the help of effective antibiotic treatment it is possible to bring the inflammatory Part of the lesion under control, but not the space-occupying element which is determined by the inflammatory brain edema. Any improvement in the results will therefore have to wait until an effective antiedematous treatment has also been developed. The aim of our previously described investigations on experimental brain abscess in cats (3) was to demonstrate that only the additional treatment with steroids as well as the antibiotics results in an improvement in the final outcome.
The Role of Monoamines in the Development of Cold-Induced Edema
1976
Our results show that even the experimentally induced high concentrations of exogenous 5-HT in the brain tissue during the early phase of edema formation are not able to increase the amount of fluid accumulation in the normal and injured brain tissue. The changes of the endogenous 5-HT levels in the blood and the brain tissue result in similar hemispheric water and RISA differences between the injured and uninjured half of the brain. Moreover, 5-HT concentrations elevated by 100% failed to produce detectable edema in the normal brain tissue of the rat.
Mechanisms of C-reactive protein-induced blood-brain barrier disruption.
2009
Background and Purpose— Increased mortality after stroke is associated with brain edema formation and high plasma levels of the acute phase reactant C-reactive protein (CRP). The aim of this study was to examine whether CRP directly affects blood–brain barrier stability and to analyze the underlying signaling pathways. Methods— We used a cell coculture model of the blood–brain barrier and the guinea pig isolated whole brain preparation. Results— We could show that CRP at clinically relevant concentrations (10 to 20 μg/mL) causes a disruption of the blood–brain barrier in both approaches. The results of our study further demonstrate CRP-induced activation of surface Fcγ receptors CD16/32 fo…
Brain energy metabolism in global brain oedema.
1978
Different degrees of severity in global brain oedema were induced by varying amounts of water intoxication (50, 100, 150, and 200 ml Aqua dest./kg b.wt. intravenously) in groups of six cats, which were functionally nephrectomized. Animals loaded with physiological saline and sham-operated served as controls. Two hours following the water load, the tissue concentrations of CrP, ATP, ADP, AMP, pyruvate, glucose, and lactate were determined by optical enzymatic analysis. The results show disturbances in brain energy metabolism dependent on the severity of the brain oedema. The high energy compounds and in consequence the ATP/ADP-ratio, and respectively the energy charge potential, fall in dire…
Brain Oedema and Intracranial Pressure in Superior Sagittal Sinus Balloon Occlusion. An Experimental Study in Pigs
1990
About 2/3 of all patients with thrombosis of the superior sagittal sinus (SSS) develop signs of increased ICP and/or brain oedema (BE). The time of onset and the spectrum of symptoms in SSS thrombosis vary extremely. This variability might be caused by differences in pathomechanism like BE and rise of ICP, parameters studied in the present contribution.