Effects of chloride flux modulators in an in vitro model of brain edema formation

Kumar, Vikas; Naik, Runa S.; Hillert, Markus; Klein, Jochen

doi:10.1016/j.brainres.2006.09.012

Cited by 15 publications

(10 citation statements)

References 48 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It is widely accepted that NKCC plays an important role in cerebral edema formation after ischemia (Chen and Sun, 2005, Kumar et al, 2006). NKCC can be activated by decreasing pHi and contributes to acidosis-induced cytotoxic brain edema (Ringel et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

Expression of Na–K–Cl cotransporter and edema formation are age dependent after ischemic stroke

Akella¹,

Benashski²,

Xu³

et al. 2010

Experimental Neurology

View full text Add to dashboard Cite

Age is the most important independent risk factor for stroke; however aging animals are rarely used in stroke studies. Previous work demonstrated that young male mice had more edema formation after an induced stroke than aging animals. An important contributor to cerebral edema formation is the Na-K-Cl cotransporter (NKCC). We examined the expression of NKCC in young (10-12 week) and aging (15-16 months) C57BL6 male mice after middle cerebral artery occlusion (MCAO) and investigated the effect of pharmacological inhibition of NKCC with Bumetanide on cerebral edema formation. Both immunofluorescent staining and Western blotting analysis showed that NKCC expression was significantly higher in the ischemic penumbra of young compared to aging mice after stroke. Edema formation was significantly more robust in young mice and was reduced with Bumetanide. Bumetanide had no effect on cerebral edema in aging mice after MCAO. This suggests that NKCC expression and edema formation are age dependent after ischemic stroke.

show abstract

Section: Discussionmentioning

confidence: 99%

Expression of Na–K–Cl cotransporter and edema formation are age dependent after ischemic stroke

Akella¹,

Benashski²,

Xu³

et al. 2010

Experimental Neurology

View full text Add to dashboard Cite

show abstract

“…It has been reported that permanent MCAO (24 h) creates predictable neuronal injury that is caused by both cytotoxic and vasogenic edema (Kumar et al, 2006;Mdzinarishvili et al, 2007). The brains were quickly removed and sectioned coronally into slices of 1 mm thickness using McIlwain Tissue Chopper.…”

Section: Methodsmentioning

confidence: 99%

Nicotine Exacerbates Brain Edema during In Vitro and In Vivo Focal Ischemic Conditions

Paulson¹,

Yang²,

Selvaraj³

et al. 2009

J Pharmacol Exp Ther

Self Cite

View full text Add to dashboard Cite

We have previously shown that nicotine, the addictive component of tobacco products, alters the blood-brain barrier (BBB) Na ϩ ,K ϩ ,2Cl Ϫ cotransporter (NKCC) during in vitro hypoxiaaglycemia exposure. Attenuation of abluminal NKCC suggests that accumulation of ions in the brain extracellular fluid would result in an increase of fluid or cytotoxic edema in the brain during hypoxia-aglycemia or stroke conditions. To further investigate whether nicotine products have the potential to worsen stroke outcome by increasing edema formation, two separate models to mimic stroke conditions were utilized to decipher the effects of short-term and long-term administrations of nicotine products on brain edema following stroke. Oxygen glucose deprivation (OGD) was studied in rat hippocampal slices with short-term or long-term exposure to nicotine and cigarette smoke constituents. During short-term exposure, the presence of nicotine at a concentration mimicking heavy smokers increased water content of hippocampal slices during OGD. Furthermore, long-term 1-week administration of nicotine increased water content in hippocampal slices that could be attenuated with nicotine acetylcholine receptor (nAChR) antagonists, suggesting nicotine increase edema during OGD via nAChRs. A second model of focal ischemia, middle cerebral artery occlusion, showed an increase of infarct size during short-term exposure to nicotine and an increase of edema during both short-term and long-term administration of nicotine, compared with saline controls. These findings support the paradigm that nicotine products not only increase the incidence of stroke but also have the potential to worsen stroke outcome by increased edema formation.

show abstract

“…* P < 0.01 versus vehicle-treated WT. AQP4 expression is attenuated with bumetanide treatment in WT but not in a-syn -/-mice cerebral edema [40,41]. Previous in vitro studies have suggested that furosemide was only effective in inhibiting water permeability in AQP4 channels when administered intracellularly [39].…”

Section: Discussionmentioning

confidence: 96%

Na+–K+–2Cl− Cotransport Inhibitor Attenuates Cerebral Edema Following Experimental Stroke via the Perivascular Pool of Aquaporin-4

et al. 2010

View full text Add to dashboard Cite

show abstract

Effects of chloride flux modulators in an in vitro model of brain edema formation

Cited by 15 publications

References 48 publications

Expression of Na–K–Cl cotransporter and edema formation are age dependent after ischemic stroke

Expression of Na–K–Cl cotransporter and edema formation are age dependent after ischemic stroke

Nicotine Exacerbates Brain Edema during In Vitro and In Vivo Focal Ischemic Conditions

Na+–K+–2Cl− Cotransport Inhibitor Attenuates Cerebral Edema Following Experimental Stroke via the Perivascular Pool of Aquaporin-4

Contact Info

Product

Resources

About