Mechanisms of Brain Ion Homeostasis during Acute and Chronic Variations of Plasma Potassium

Stummer, Walter; Betz, A. Lorris; Keep, Richard F.

doi:10.1038/jcbfm.1995.39

Cited by 15 publications

(7 citation statements)

References 28 publications

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“…20 Indeed, we were able to detect CD16 and CD32 expression by immunostainings, which is in line with other studies demonstrating CD16 expression at the human and rat BBB. 31,32 Pretreatment with neutralizing anti-CD16 or anti-CD32 antibodies significantly reduced the barrier-disrupting effect of CRP.…”

Section: Discussionmentioning

confidence: 99%

Mechanisms of C-Reactive Protein-Induced Blood–Brain Barrier Disruption

Kuhlmann

Librizzi

Closhen³

et al. 2009

Stroke

105

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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 g/mL) causes a disruption of the blood-brain barrier in both approaches. The results of our study further demonstrate CRP-induced activation of surface Fc␥ receptors CD16/32 followed by p38-mitogen-activated protein kinase-dependent reactive oxygen species formation by the NAD(P)H-oxidase. The resulting oxidative stress increased myosin light chain kinase activity leading to an activation of the contractile machinery. Blocking myosin light chain phosphorylation prevented the CRP-induced blood-brain barrier breakdown and the disruption of tight junctions. Conclusions-Our data identify a previously unrecognized mechanism linking CRP and brain edema formation and present a signaling pathway that offers new sites of therapeutic intervention.

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Section: Discussionmentioning

confidence: 99%

Mechanisms of C-Reactive Protein-Induced Blood–Brain Barrier Disruption

Kuhlmann

Librizzi

Closhen³

et al. 2009

Stroke

105

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“…In this study, it was reported that deprivation of K + can reduce the binding of furosemide in its areas of action. Moreover, this phenomenon may be related to the findings of Stummer et al [12], which suggest that the increased influx of K + to the intracellular environment in acute hypokalemia is compensated by the stimulation of K+ efflux via Na + -K + -ATPase to restore the balance of K + in cerebrospinal fluid. However, this was not observed in our study.…”

Section: Discussionmentioning

confidence: 87%

Influência do veículo na eficácia da reposição de potássio em ratos hipocalêmicos

Petenusso

Valenti

Abreu³

et al. 2009

Rev Bras Cir Cardiovasc

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Influência do veículo na eficácia da reposição de potássio em ratos hipocalêmicosVehicle influence on potassium replacement effectiveness in hypokalemic rats Abstract Introduction: Patients who undergo cardiac surgery are commonly treated with diuretic therapy for the management of volume overload. The concern of hypokalemia in adult before, during and after surgery has already been described since there is risk of cardiac arrhythmia. Clinically, intravenous potassium (K+) replacement dilution is only recommended with sodium chloride 0.9% solution (SF0.9%), likely due to the putative effects of glucose solution 5% (SG5%) on insulin secretion, which influence K+ replacement quality. However, it is not yet experimentally proved the influence of SF0.9% and SG5% on K+ replacement quality in patients with hypokalemia.Objectives: To assess the effects of different vehicles of K+ replacement on blood K+ levels in furosemide hypokalemic rats.Methods: Male Wistar rats were divided into four groups: K++SF, K++SG, SF and SG. Jugular vein was cannulated for K+ replacement and femoral vein was cannulated for blood analysis were performed. Furosemide (50mg/kg) was injected S.C. to induce hypokalemia. It was analyzed potassium plasmatic levels 24 hours before furosemide injection, 24 hours after furosemide injection and after 30 minutes post-replacement.Results: There was reduction in post-injection of K+ levels when compared to the basal values (pre-furosemide) in all groups. However, the levels [K+] returned to baseline in both groups receiving K++SF or K++SG, which was not observed in groups receiving only SF and SG. Only K+SF presented increased after K+ replacement (P< 0.05).Conclusion: K+ replacement diluted both in SF and SG did not affect blood K+ levels in rats. 368 PETENUSSO, M ET AL -Vehicle influence on potassium replacement effectiveness in hypokalemic rats Bras Cir Cardiovasc 2009; 24(3): 367-372 Descriptors Rev

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“…3, 4). Permeability to K + is regulated through a specialized Na + /K + ‐ATPase located on the membrane of the brain capillary endothelial cell (Stummer et al, 1995). When the blocker of the Na + /K + pump ouabain (10 μM) was coperfused for 5 min with the high‐K + solution (n = 8), a gradual increase in [K + ] PC and [K + ] EC was observed (Fig.…”

Section: Resultsmentioning

confidence: 99%

Blood–brain barrier preservation in the in vitro isolated guinea pig brain preparation

Librizzi

Janigro

Biasi

et al. 2001

J of Neuroscience Research

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The morphofunctional preservation of the blood-brain barrier (BBB) was evaluated in the isolated guinea pig brain maintained in vitro by arterial perfusion. Electron microscopy evaluation after 5 hr in vitro demonstrated that cerebral capillaries and BBB specializations in this preparation retain features compatible with structural integrity. BBB-impermeable and -permeable atropine derivatives arterially perfused to antagonize carbachol-induced fast oscillatory activity confirmed the functional preservation of the BBB in vitro. To study BBB function further, changes in extracellular K+ concentration during arterial perfusion of a high-K+ solution were measured with K+-sensitive electrodes positioned in the cortex and, as control, at the brain venous outlet, where the solution perfused through the brain arterial system was collected. After 5 hr in vitro, the [K+](o) values measured during high-K+ perfusion in the piriform and entorhinal cortices were 5.02 +/- 0.17 mM (mean +/- SE) and 5.2 +/- 0.21 mM, respectively (n = 6). Coperfusion of the high-K+ solution with the Na+/K+ pump blocker ouabain (10 microM; n = 4) induced consistently spreading depression preceded by a rise in [K+](o). Finally, sporadic, isolated spots of extravasation of the fluorescent marker fluorescein isothiocyanate (FITC)-dextran preferentially circumscribed to deep cortical layers was observed in brains perfused with FITC-dextran after 5 hr in vitro. The study demonstrates that the in vitro isolated guinea pig brain is viable for studying cerebrovascular interactions and BBB permeability of compounds active in the central nervous system.

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Mechanisms of Brain Ion Homeostasis during Acute and Chronic Variations of Plasma Potassium

Cited by 15 publications

References 28 publications

Mechanisms of C-Reactive Protein-Induced Blood–Brain Barrier Disruption

Mechanisms of C-Reactive Protein-Induced Blood–Brain Barrier Disruption

Influência do veículo na eficácia da reposição de potássio em ratos hipocalêmicos

Blood–brain barrier preservation in the in vitro isolated guinea pig brain preparation

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