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At least 109 records · Page 6Linked to original sources
PubMed1993

Difluoromethylornithine decreases postischemic brain edema and blood-brain barrier breakdown.

Brain polyamines have been associated with posttraumatic vasogenic edema and blood-brain barrier (BBB) breakdown seen in some models of brain injury. We hypothesized that the inhibition of the enzyme responsible for polyamine production with the decarboxylase difluoromethylornithine (DFMO) may decrease BBB breakdown after a focal brain ischemic stroke. Thirty-two cats underwent 8 hours of middle cerebral artery occlusion and one of four treatments: sham operation (Sham), ischemia (Isc), ischemia/DFMO (Isc/DF), and ischemia/DFMO/putrescine (Isc/DF/PU). The regional brain specific gravity and the volume of Evans blue (EB) extravasation were measured at the time of death. The groups were monitored for temperature, heart rate, blood pressure, and arterial blood gases, and the values did not differ outside normal physiological ranges. EB results were expressed as the percentage of the hemisphere stained and showed the following: Sham, 2.23%; Isc, 32.8%; Isc/DF, 5.6%; Isc/DF/PU, 36.3%. As a measure of BBB, ischemia increased EB staining; DFMO pretreatment decreased the amount of EB staining to control levels; and the polyamine putrescine abolished the protective effect of DFMO (all significant at P = 0.05). DFMO pretreatment also resulted in a significant (P = 0.05) return to control values for specific gravity in the EB-stained regions (1.0328) of ischemic animals. This effect was present primarily in the white matter. Treatment with DFMO, an ornithine decarboxylase inhibitor, significantly decreased postischemic BBB breakdown and vasogenic edema in this model.

Animals↗
PubMedDate not supplied

[Effect of benzodiazepine tranquilizers on the development of toxic brain edema].

Experimental nicotinic brain edema in rats was made use of to examine the action of the benzodiazepine tranquilizers, diazepam and phenazepam. It was disclosed that these agents have antiedematous properties. It is suggested that the GABA-ergic mechanisms might participate in the realization of the effect under consideration.

Animals↗
PubMed2000

Induction of colligin may attenuate brain edema following intracerebral hemorrhage.

Brain edema plays an important role in the secondary brain injury following intracerebral hemorrhage (ICH). Edema formation after ICH has been linked to thrombin toxicity. Therefore, the induction of endogenous serine protease inhibitors, which inhibit thrombin prior to ICH may limit edema formation. This study examines whether injection of a low dose of thrombin upregulates such inhibitors and induces tolerance to subsequent ICH. Rats received intracerebral infusions of either one unit thrombin or saline into the right caudate nucleus. After seven days, the rats were either (A) used to examine colligin (a serine protease inhibitor) induction by Western blot analysis, immunohistochemistry and immunofluorescent double labeling, (B) to determine brain water content, or (C) they received a second injection of 50 microL blood and brain edema was determined one day later. Intracerebral infusion of thrombin caused a marked upregulation of colligin, a serine protease inhibitor, in the ipsilateral basal ganglia. Immunocytochemistry and immunofluorescent double labeling showed that colligin was induced in astrocytes. Infusion of this dose of thrombin alone did not affect brain water content but it significantly attenuated subsequent ICH-induced brain edema (79.0 +/- 0.5 vs. 81.4 +/- 0.9%, P < 0.01). Our results demonstrate that low doses of thrombin upregulate brain colligin levels and attenuate edema formation induced by ICH.

Animals↗
PubMed1998

Mild hypothermia prevents the occurrence of cytotoxic brain edema in rats.

Hypothermia maintains the impermeability of the blood-brain barrier to proteins and, therefore, presumably the development of vasogenic brain edema after brain ischemia. We intended to determine whether mild hypothermia would have a protective effect against cytotoxic brain edema, the early stage of ischemic brain edema. Two groups of Wistar rats (37 degrees C and 35 degrees C body temperature) were subjected to 6 h of moderate decrease of cerebral blood flow (CBF) by means of permanent bilateral carotid artery ligation, and compared to a third group of unaffected animals. Carotid artery ligation induced a local cerebral blood flow (LCBF) reduction to 50-80% of baseline values. LCBF in the frontal cortex was restored to a higher level in hypothermic animals than in normothermic ones (P < 0.05). In normothermic animals, an increase of brain water content was detected in the frontoparietal and occipital cortex as well as in the hippocampus (P < 0.05), but only in one region of the frontoparietal cortex in hypothermic animals. The impermeability of the blood-brain barrier to proteins was shown by the absence of staining with Evans blue as an indicator of vasogenic brain edema. We conclude that mild hypothermia offers protection against the development of cytotoxic brain edema.

Animals↗
PubMed1997

Traumatic brain swelling in head injured patients: brain edema or vascular engorgement?

Brain edema and vascular engorgement have been used interchangeably to describe brain swelling associated with severe brain trauma and their relative contribution of these compartments to the swelling process remains controversial. In this report, imaging techniques for measurement of brain water and blood volume have been used to study the relative contribution of blood volume and tissue water to the swelling process in severely brain injured patients. More specifically, magnetic resonance techniques for non-invasive tissue water measures founded on mathematical models and later substantiated in laboratory and clinical studies were used for measure of brain tissue water. These studies were combined with measures of cerebral blood volume utilizing indicator dilution methods. Studies indicated that brain water was increased while blood volume decreased. These studies provide compelling evidence that the major contributor to brain swelling is brain edema and not blood volume. Therapies should now be targeted toward preventing edema development and enhancing edema resolution.

Adolescent↗
PubMed1997

Brain edema: pathogenesis and therapy.

In the brain intravascular and interstitial spaces are separated by a highly specialized endothelial lining, which is the morphological substrate of the blood-brain barrier (BBB). Under physiological conditions the BBB exerts rigid control of water soluble compounds moving from blood into brain and from brain into blood, respectively. Under pathological conditions such as trauma or ischemia, an increase in BBB permeability may occur that allows plasma constituents to escape into the brain tissue. This "opening" of the BBB may, at least in part, be due to a massive release of autacoids, which thus act as mediators of vasogenic brain edema. Five criteria have to be fulfilled by a given autacoid to be considered a mediator candidate: (i) a permeability-enhancing action under physiological conditions; (ii) a vasodilatory action; (iii) the ability of inducing vasogenic brain edema; (iv) an increase of concentration in tissue or interstitial fluid under pathological conditions; and (v) a decrease of brain edema by inhibiting the release or action of a given autacoid. Among the mediator candidates discussed, only bradykinin fulfills all these criteria. Histamine, arachidonic acid and free radicals, including nitric oxide, may also be considered mediator candidates of brain edema, but for each of these compounds evidence is less clear than for bradykinin. Although the concept of autacoids mediating brain edema is well established and supported by experimental data, it has not yet gained entrance into the clinics. Treatment of patients suffering from vasogenic brain edema is symptomatic and mainly concentrated on the control of intracranial pressure.

Arachidonic Acid↗
PubMed1999

[Relationship between brain edema induced by freezing injury and concentration of Evan blues and cytosolic free calcium in brain tissues].

The authors studied the changes of Evan blues(EB) of brain tissues and concentration of cytosolic free calcium ([Ca2+]i), and relationship between them and water content of brain tissues following freezing brain edema in rats, to elucidate mechanism and type of brain edema induced by freezing injury. The results indicated that there were close positive relationship between water content and EB of brain tissues, and between [Ca2+]i and water content. We found that not only cytotoxic brain edema(intracellular edema) occurred but also occurred vasogenic brain edema(extracellular edema) followed by blood brain barrier breakdown after brain edema. Freezing brain edema is mixed brain edema.

Animals↗
PubMed1994

Simple quantitative evaluation of blood-brain barrier disruption in vasogenic brain edema.

Traumatic damage to the brain results in blood-brain barrier disruption with subsequent formation of vasogenic brain edema. The goal of this study was to evaluate a colorimetric assay of Evans blue extravasation for quantitatively studying blood-brain barrier disruption. Vasogenic brain edema was produced by a cortical freezing lesion. 52 male Wistar rats were sacrificed and cardiac perfusion was performed. A volume of dimethylformamide, twice the brain weight, was added to the brain and this was incubated for 72 hours. The supernatant was analyzed spectrophotometrically. Evans blue contents in the lesioned hemisphere was significantly increased within one hour after the lesion production relative to the normal brain and continued to increase for 24 hours (p < 0.01). This quantitative assay of Evans blue is a simple method for evaluation of blood-brain barrier disruption in vasogenic brain edema.

Animals↗
PubMed1979

Electroencephalography in brain edema (127 cases of brain tumor investigated by cranial computerized tomography).

Cranial computerized tomography (CCT) in permitting visualization of cerebral edema in live patients, allows for the first time valid studies concerning the role of reactional edema in the generation of EEG abnormalities related to expanding processes. The authors analyze the results of EEG and CCT in 127 patients presenting cerebral tumor(s), 84 of which were accompanied by reactional edema. The study leads to the conclusion (also demonstrated by certain animal work) that edema per se is only rarely responsible (9.5%) for the EEG abnormalities.

Brain Edema↗
PubMed2004

Importance of aquaporins in the physiopathology of brain edema.

Aquaporins (AQPs) are water channels that mediate the efficient movement of water across the membrane. Among different AQPs, AQP4 is the predominant water channel in the brain and is thought to play a significant role in the physiopathology of brain edema. Brain edema is a major clinical problem since it largely accounts for the cause of death in patients suffering from traumatic brain injury or cerebrovascular accidents. In this review, we have tried to summarize comprehensive information about the pathological events conducting to brain edema. In addition, we also have summarized active investigation in the field of AQPs and cerebral edema to find plausible explanations and to deduce potential future directions for the treatment of this clinical condition.

Animals↗
PubMed1998

The effects of methylprednisolone on prevention of brain edema after experimental moderate diffuse brain injury in rats--comparison between dosage, injection time, and treatment methods.

Our study was designed to determine whether methylprednisolone exerts a beneficial effect after experimental moderate diffuse brain injury and whether this possible beneficial effect is affected by the dosage, the timing of administration, and the methods of treatment. A total of 200 anesthetized adult rats were injured utilizing a weight-drop device through a Plexiglas guide tube. These rats were divided into eight groups: Group 1 (n = 35) was assigned to receive no methylprednisolone after impact (control group), Group 2 (n = 25) received an initial intraperitoneal administration of methylprednisolone with a dose of 5 mg/kg at 1 hour after cranial impact, followed by administration with a maintenance dose of 5 mg/kg/4 hours. Group 3 (n = 25), group 5 (n = 25), and group 7 (n = 20) received an initial 30 mg/kg at 1 hour, 4 hours, and 8 hours, respectively without a maintenance dose. Group 4 (n = 25), group 6 (n = 25), and group 8 (n = 20) received an initial 30 mg/kg at 1 hour, 4 hours, and 8 hours after impact, with a maintenance dose of 15 mg/kg/4 hours. Measured water content of brain tissue expressed the amount of water as the difference between fresh and dry weight. At 48 hours after impact, the water content in group 4 and 6 were significantly lower than group 1. Mean +/- SD was 61.4 +/- 0.37% in group 4 (p < 0.03), 61.5 +/- 0.34% in group 6 (p < 0.001), and 63.6 +/- 0.48% in group 1. Compared to group 1, the difference was not statistically significant in group 2 (p > 0.1), group 3 (p > 0.5), group 5 (p > 0.6), group 7 (p > 0.1), and group 8 (p > 0.5). Groups treated with mega dose before 4 hours after head injury, including maintenance dose, showed beneficial effects. Our study suggests that the efficacy of methylprednisolone in head injury was related to the dosage, the timing of administration, and method of treatment.

Animals↗
PubMed1979

Composition of isolated edema fluid in cold-induced brain edema.

Edema fluid isolated from cats with cold-induced brain edema was subjected to analysis of electrolyte content, enzyme activities, colloid osmotic pressure and the radioactivity of intravenously injected 99mTc-labeled albumin. The findings corroborate the essential features of vasogenic edema, such as its origin from the blood plasma, its rapid propagation into the white matter of the brain as contrasted with the delayed spread into gray matter, and its contribution to composition of cerebrospinal fluid. Moreover, the elevated activities of cellular enzymes and K+ content of edema fluid point to the admixture with cellular contents due to the freezing damage.

Albumins↗