Composition of isolated edema fluid in cold-induced brain edema

Gazendam, J.; Kito, Go; Zanten, A. K. Van

doi:10.3171/jns.1979.51.1.0070

Cited by 70 publications

(18 citation statements)

References 10 publications

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“…The model has been successfully utilized in the past to improve understanding of pathophysiologic mechanisms underlying vasogenic brain edema, although it is admitted that the method does not comprehensively reflect all facets of severe head injury. This is also true of other experimental models, however, (Ciasen et al, 1967;Sullivan et al, 1976;Gazendam et al, 1979;Gennarelli et al, 1982;Marmarou et al, 1994).…”

Section: Discussionmentioning

confidence: 68%

Treatment of Vasogenic Brain Edema with the Novel Cl⁻ Transport Inhibitor Torasemide

Staub

Stoffel²,

Berger³

et al. 1994

Journal of Neurotrauma

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The efficacy of the diuretic agent torasemide, which antagonizes the Na+/K+/Cl- cotransport and Cl- channels, was investigated to determine its inhibition of brain edema from a focal cerebral lesion. For this purpose, cold injury of the brain was induced in 50 Sprague-Dawley rats while monitoring arterial blood pressure. The brain was removed for gravimetric assessment of swelling of the traumatized hemisphere 24 h after trauma. The water content was also determined after drying the cerebral hemispheres for 24 h. Animals were divided into five groups. A control group with trauma received vehicle only; two other groups received 1.0 or 10.0 mg torasemide/kg body weight 30 minutes before and 6 h after trauma (n = 10-12). Administration of the drug after the insult was also investigated in animals with application of vehicle or 10.0 mg/kg of torasemide at 30 minutes and 6 h following the brain lesion (n = 8). Torasemide did not affect important physiologic variables, such as the arterial pO2, pCO2, pH, hemoglobin, hematocrit, or plasma osmolality, while increasing blood pressure (p < 0.01). The blood pressure response notwithstanding, treatment significantly attenuated hemispheric brain swelling from trauma. In control animals without treatment, cold injury led to hemispheric swelling of 8.89%. In animals with 1 mg torasemide/kg BW, brain swelling amounted to 8.51% and to 7.04% in animals receiving 10 mg/kg before and after the insult (p < 0.005). Treatment was also found to attenuate the increase in tissue water content from trauma, but without reaching statistical significance. Postinsult treatment with torasemide (10 mg/kg BW) at 30 minutes and 6 h after trauma was again associated with a significant reduction in hemispheric brain swelling, which in this group amounted to 7.46% compared with 9.76% in the untreated controls (p < 0.005). The increase in the cerebral water content from trauma was also significantly blunted in the latter experiments (p < 0.01). The present data indicate a remarkable therapeutic potential of the novel diuretic agent torasemide to reduce vasogenic brain edema from an acute cerebral lesion. It is surmised that the compound specifically interferes with Cl- transport mechanisms, which apparently are activated in edematous brain involving neuronal and glial cells, for example. This conclusion is supported by in vitro observations that torasemide inhibits the swelling of glial cells from acidosis. On the other hand, it is unlikely that gross dehydration of the brain secondary to the induction of diuresis by the agent played a role, because hematocrit and plasma osmolality were not found to be affected.

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Section: Discussionmentioning

confidence: 68%

Treatment of Vasogenic Brain Edema with the Novel Cl⁻ Transport Inhibitor Torasemide

Staub

Stoffel²,

Berger³

et al. 1994

Journal of Neurotrauma

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show abstract

“…On the other hand, the pia mater demonstrates high permeability by water and electrolytes but is far less permeable by macromolecules, such as the proteins found in edema fluid [4]. Moreover, the barrier function of the cerebral cortex, attributable to the intricately intertwining cell processes, presents a structure difficult to overcome in the development of vascular edema [38].…”

Section: Discussionmentioning

confidence: 99%

Alterations in diffusion and perfusion in the pathogenesis of peritumoral brain edema in meningiomas

Bitzer

Klose

et al. 2002

Eur Radiol

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Magnetic resonance perfusion and diffusion studies were undertaken to clarify the significance of ischemia in the pathogenesis of peritumoral brain edema in patients with meningiomas. Included in this study were 26 patients with 27 meningiomas and 5 gliomas. Perfusion-weighted imaging (PWI) was performed using a gradient-echo, echo-planar-imaging (EPI) sequence for calculation of the relative regional cerebral blood volume (rrCBV) and the relative regional cerebral blood flow index (rrCBFi). Furthermore, multi-slice spin-echo EPI sequences were applied in order to obtain anisotropic and isotropic diffusion-weighted imaging (DWI). Apparent diffusion coefficient (ADC) values were then calculated for peritumoral brain parenchyma from tumors, with and without edema, using various diffusion sensitivities. Meningiomas without edema demonstrated a minimal increase of perfusion parameters in the peritumoral brain tissue. In contrast, cases with brain edema had highly significant ( p<0.0005) lower rrCBV and rrCBFi. The edema index (EI) correlated strongly with the rrCBV. A fitting procedure resulted into the following mathematical relation: EI=0.1/rrCBV(2). The DWI showed a significantly larger ADC value within areas of brain edema, compared with the normal white matter (0.74 x 10(-3) vs 1.55 x 10(-3) mm(2)/s; p<0.0001). Increases in EI correlated with increases in ADC values. In 31% of the meningiomas associated with edema, areas with increased signal, probable ischemia, demonstrated significantly lower ADC values, in comparison with the rest of the edematous areas. These areas were confined to tissue immediately adjacent to the tumor. In general, the decrease in rrCBV in brain edema represents a consequence from, rather than a cause of, vasogenic edema. Ischemic alterations can be regarded as secondary, facultative phenomena in the pathogenesis of meningioma-related brain edema.

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“…The dry weight of the edema fluid consists of different proteins and salts. It is known that the protein content of brain edema fluid is about 58% of the blood plasma's protein content (Gazendam et al, 1979). Therefore we assumed that the dry weight of the edema fluid is 58% of the dry weight of the blood plasma.…”

Section: Methodsmentioning

confidence: 99%

Role of Bradykinin B₂Receptors in the Formation of Vasogenic Brain Edema in Rats

Plesnila

Schulz

Stoffel

et al. 2001

Journal of Neurotrauma

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Bradykinin is a mediator of brain edema acting through B2 receptors. However, it is not known if bradykinin mediates the formation of cytotoxic or vasogenic brain swelling. To investigate this question we subjected rats to a cryogenic brain lesion over the left parietal cortex, a model well known to produce predominantly vasogenic brain edema. We inhibited bradykinin B2 receptors with the recently characterized nonpeptide B2 receptor antagonist, LF 16-0687. The animals were assigned to three groups (n = 10, each) receiving 10, or 100 microg/kg/min LF 16-0687 or vehicle (0.9% NaCl). Treatment started 15 min before trauma and was continued for 24 h. Another three groups of animals (n = 10, each) received 10 microg/kg/min LF 16-0687 starting 30 or 60 min after trauma or vehicle (0.9% NaCl) for 24 h. Animals were then sacrificed and swelling and water content of the brain were determined. In the vehicle treated group the traumatized hemisphere swelled by 9.3 +/- 1.1% as compared to the untraumatized contralateral side. Pretreatment with 10 microg/kg/min LF 16-0687 decreased brain swelling significantly to 6.4 +/- 1.3% (p < 0.05). Pre-treatment with 100 microg/kg/min was found to be less effective and did not result in a significant reduction of brain swelling (7.4 + 1.3%). Treatment with LF 16-0687 for 24 h (10 microg/kg/min) started 30 or 60 min after trauma did not reduce brain water content or hemispheric swelling. These results demonstrate that brain injury-mediated bradykinin production induces vasogenic brain edema by B2 receptor stimulation. Our findings further clarify the role of bradykinin in the pathophysiology of brain edema formation and confirm the therapeutic potency of bradykinin B2 receptor inhibition.

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Composition of isolated edema fluid in cold-induced brain edema

Cited by 70 publications

References 10 publications

Treatment of Vasogenic Brain Edema with the Novel Cl⁻ Transport Inhibitor Torasemide

Treatment of Vasogenic Brain Edema with the Novel Cl⁻ Transport Inhibitor Torasemide

Alterations in diffusion and perfusion in the pathogenesis of peritumoral brain edema in meningiomas

Role of Bradykinin B₂Receptors in the Formation of Vasogenic Brain Edema in Rats

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Composition of isolated edema fluid in cold-induced brain edema

Cited by 70 publications

References 10 publications

Treatment of Vasogenic Brain Edema with the Novel Cl− Transport Inhibitor Torasemide

Treatment of Vasogenic Brain Edema with the Novel Cl− Transport Inhibitor Torasemide

Alterations in diffusion and perfusion in the pathogenesis of peritumoral brain edema in meningiomas

Role of Bradykinin B2Receptors in the Formation of Vasogenic Brain Edema in Rats

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Product

Resources

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Treatment of Vasogenic Brain Edema with the Novel Cl⁻ Transport Inhibitor Torasemide

Treatment of Vasogenic Brain Edema with the Novel Cl⁻ Transport Inhibitor Torasemide

Role of Bradykinin B₂Receptors in the Formation of Vasogenic Brain Edema in Rats