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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Acta neurochirurgica 105 (1990), S. 158-168 
    ISSN: 0942-0940
    Keywords: Brain edema ; cerebral blood flow ; brain tissue hydraulic resistance ; somatosensory evoked potential ; intracranial pressure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To evaluate the potency of putative secondary mediators of brain edema and their possible contribution to edema related brain dysfunction an infusion model of brain edema was developed in rats. 100 ul of fluid (saline, 20% nonautologous protein) was infused over one hour into the left forebrain white matter through a stereotaxically placed (+ 1.2 mm ant to bregma, 3 mm lateral and 2.9 mm depth) 25 G needle. Brain tissue hydraulic resistance (Rt), regional cerebral blood flow (rCBF), cortical somatosensory evoked potentials (SEPs) and intracranial pressure (ICP) (intraventricular needle) were monitored during the infusion and rCBF CO2 reactivity (hydrogen clearance), local brain water content (microgravimetry), BBB integrity (Evans Blue 2%) and brain histology (H & E, Solochrome-cyanin) were evaluated after the infusion. Saline infusates caused no physiological dysfunction despite ipsilateral expansion and vacuolation of the subcortical white matter, separation of axonal bundles and a significant decrease (p=3.8×10−5)in local subcortical tissue specific gravity. Cortical histology and specific gravity adjacent to the infusion locus were normal. Rt significantly decreased (p=6.5×10−4) during the infusion but there were only minor increases in ICP. Findings with 20% protein infusates were similar despite a focal 65% decrement in the rCBF CO2 reactivity adjacent to the infusion site. This study has shown that a simple and inexpensive model of infusion brain edema can be created in the rat and that it provides a useful model for assessing the physiological effects of mediator compounds in the infusate. Potential applications and methodological improvements for this model are discussed.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Acta neurochirurgica 115 (1992), S. 53-59 
    ISSN: 0942-0940
    Keywords: Bradykinin ; intracranial pressure ; evoked potentials ; cerebral blood flow ; brain edema ; blood brain barrier
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The feline infusion model of brain edema was used to evaluate the role of bradykinin in the etiology and pathophysiology of vasogenic brain edema. Bradykinin (3 or 90 ug in 600 μL saline) did not alter normocapnic regional cerebral blood flow (rCBF) nor induce specific changes in either the somatosensory (SEP) or motor (MEP) evoked potentials. The mean increases in ICP (from 4.5 to 16.1 mmHg) and peri-infusion white matter water content (from 69.4 to 79.8 ml/100 g tissue), mean decrease in lumped craniospinal compliance (from 0.040 to 0.014 ml/mmHg) and local histological changes were all similar to those after 600 μL saline infusion. The interstitial bradykinin infusion caused focal blood-brain-barrier (BBB) opening to Evans Blue dye and was chemotaxic for granulocytes. After the infusion there was a global loss of rCBF CO2 reactivity but there was no ischemia at normocapnia. These results show that bradykinin in brain edema fluid, at concentrations greater than those found in neuropathological conditions, can open the BBB of normal cerebral parenchymal capillaries and cause vascular dysregulation. In neuropathological conditions bradykinin may therefore potentiate formation of vasogenic brain edema but does not contribute to perilesional brain dysfunction.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 0942-0940
    Keywords: Blood brain barrier ; cerebral blood flow ; intracranial pressure ; arachidonic acid ; brain oedema ; evoked potential
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Arachidonic acid solution (2 to 15 mg/ml) was infused into the right forebrain white matter of anaesthetised cats over three hours to evaluate its contribution to the genesis and pathophysiology of vasogenic brain oedema. The 0.6 ml infusion increased local white matter water content by a mean of 11.3 ml/100 g tissue but did not increase cortical water content. Histological studies revealed local expansion and trabeculation of the white matter with aggregations of granulocytic neutrophils in the venules and perivenular brain. The adjacent cortical cytoarchitecture was normal. The white matter around the infusion site was stained lightly and over a variable area (15–20 mm2) by intravenously administered Evans Blue dye 2%. Regional cerebral blood flow (rCBF) adjacent to the frontal infusion did not change significantly during the period of infusion and remained similar to rCBF in the contralateral hemisphere. Following the arachidonic acid infusion regional CBF CO2 reactivity was normal and three was no asymmetry of either cortical somatosensory evoked potential (SEP) or motor evoked potential (MEP) waveforms. The increase in brain water content and changes in the ICP and ICP related biodynamics (pressure-volume index, lumped craniospinal compliance and CSF outflow resistance) were similar to those seen following infusion of 0.6 ml saline. These studies suggest that free intraparenchymal arachidonic acid, at concentrations exceeding those occurring in most neuropathological conditions, can increase the normal brain parenchymal capillary permeability but does not disrupt focal cerebrovascular and electrophysiological function. The clinical implications of these findings are discussed.
    Type of Medium: Electronic Resource
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