We are analyzing https://link.springer.com/article/10.1007/s13311-011-0087-4.

Title:
Novel Treatment Targets for Cerebral Edema | Neurotherapeutics
Description:
Cerebral edema is a common finding in a variety of neurological conditions, including ischemic stroke, traumatic brain injury, ruptured cerebral aneurysm, and neoplasia. With the possible exception of neoplasia, most pathological processes leading to edema seem to share similar molecular mechanisms of edema formation. Challenges to brain-cell volume homeostasis can have dramatic consequences, given the fixed volume of the rigid skull and the effect of swelling on secondary neuronal injury. With even small changes in cellular and extracellular volume, cerebral edema can compromise regional or global cerebral blood flow and metabolism or result in compression of vital brain structures. Osmotherapy has been the mainstay of pharmacologic therapy and is typically administered as part of an escalating medical treatment algorithm that can include corticosteroids, diuretics, and pharmacological cerebral metabolic suppression. Novel treatment targets for cerebral edema include the Na(+)-K(+)-2Cl(−) co-transporter (NKCC1) and the SUR1-regulated NCCa-ATP (SUR1/TRPM4) channel. These two ion channels have been demonstrated to be critical mediators of edema formation in brain-injured states. Their specific inhibitors, bumetanide and glibenclamide, respectively, are well-characterized Food and Drug Administration-approved drugs with excellent safety profiles. Directed inhibition of these ion transporters has the potential to reduce the development of cerebral edema and is currently being investigated in human clinical trials. Another class of treatment agents for cerebral edema is vasopressin receptor antagonists. Euvolemic hyponatremia is present in a myriad of neurological conditions resulting in cerebral edema. A specific antagonist of the vasopressin V1A- and V2-receptor, conivaptan, promotes water excretion while sparing electrolytes through a process known as aquaresis.
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Keywords {🔍}

google, scholar, article, pubmed, cerebral, edema, cas, brain, treatment, injury, saline, hyponatremia, water, hypertonic, stroke, patients, channel, intracranial, pressure, care, sodium, traumatic, ischemia, nkcc, fluid, channels, vasopressin, effect, surtrpm, conivaptan, infarction, formation, med, volume, inhibition, subarachnoid, hemorrhage, neurol, ischemic, blood, ion, clinical, physiol, simard, neurological, swelling, osmotherapy, cotransporter, development, setting,

Topics {✒️}

na-k-cl cotransporter contributes blood–brain barrier disruption blood–brain barrier integrity atp-sensitive potassium channels voltage-sensitive sodium channels raf/mek/mapk cascade [adenosine triphosphate] atp life-threatening brain edema blood–brain barrier sur1/trpm4 channels represent sur1/trpm4 channels open brain-cell volume homeostasis sur1-regulated ncca-atp sur1- regulated ncca-atp severe head injuries space-occupying cerebral infarction large meta-analysis found drug administration-approved drugs step-wise temporal progression middle cerebral artery open-label randomized trial regulate brain-fluid physiology peptide arginine-vasopressin antagonists �targeting ncca-atp channel null mice exhibit drug administration-approved drug central nervous system brain tissue oxygen placebo-controlled clinical trials subarachnoid hemorrhage-induced hyponatremia transendothelial permeability alterations cerebral blood flow promotes water excretion low-dose glibenclamide reduced acute renal failure traumatic brain injury privacy choices/manage cookies atp-independent passive transport glutamate-mediated excitotoxicity tepas jj 3rd free radical scavengers wijdicks ef cerebral blood vessels hemispheric cerebral infarction sodium flux required lopez-arrieta jm aneurysmal subarachnoid hemorrhage treat cerebral edema systolic blood pressure brain-injured states

Questions {❓}

Aggravation of infarct formation by brain swelling in a large territorial stroke: a target for neuroprotection?
Diuretics and epilepsy: will the past and present meet?
Hyponatremia and cerebral infarction in patients with ruptured intracranial aneurysms: is fluid restriction harmful?
Wrong-way chloride transport: is it a treatable cause of some intractable seizures?

Schema {🗺️}

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         headline:Novel Treatment Targets for Cerebral Edema
         description:Cerebral edema is a common finding in a variety of neurological conditions, including ischemic stroke, traumatic brain injury, ruptured cerebral aneurysm, and neoplasia. With the possible exception of neoplasia, most pathological processes leading to edema seem to share similar molecular mechanisms of edema formation. Challenges to brain-cell volume homeostasis can have dramatic consequences, given the fixed volume of the rigid skull and the effect of swelling on secondary neuronal injury. With even small changes in cellular and extracellular volume, cerebral edema can compromise regional or global cerebral blood flow and metabolism or result in compression of vital brain structures. Osmotherapy has been the mainstay of pharmacologic therapy and is typically administered as part of an escalating medical treatment algorithm that can include corticosteroids, diuretics, and pharmacological cerebral metabolic suppression. Novel treatment targets for cerebral edema include the Na(+)-K(+)-2Cl(−) co-transporter (NKCC1) and the SUR1-regulated NCCa-ATP (SUR1/TRPM4) channel. These two ion channels have been demonstrated to be critical mediators of edema formation in brain-injured states. Their specific inhibitors, bumetanide and glibenclamide, respectively, are well-characterized Food and Drug Administration-approved drugs with excellent safety profiles. Directed inhibition of these ion transporters has the potential to reduce the development of cerebral edema and is currently being investigated in human clinical trials. Another class of treatment agents for cerebral edema is vasopressin receptor antagonists. Euvolemic hyponatremia is present in a myriad of neurological conditions resulting in cerebral edema. A specific antagonist of the vasopressin V1A- and V2-receptor, conivaptan, promotes water excretion while sparing electrolytes through a process known as aquaresis.
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      headline:Novel Treatment Targets for Cerebral Edema
      description:Cerebral edema is a common finding in a variety of neurological conditions, including ischemic stroke, traumatic brain injury, ruptured cerebral aneurysm, and neoplasia. With the possible exception of neoplasia, most pathological processes leading to edema seem to share similar molecular mechanisms of edema formation. Challenges to brain-cell volume homeostasis can have dramatic consequences, given the fixed volume of the rigid skull and the effect of swelling on secondary neuronal injury. With even small changes in cellular and extracellular volume, cerebral edema can compromise regional or global cerebral blood flow and metabolism or result in compression of vital brain structures. Osmotherapy has been the mainstay of pharmacologic therapy and is typically administered as part of an escalating medical treatment algorithm that can include corticosteroids, diuretics, and pharmacological cerebral metabolic suppression. Novel treatment targets for cerebral edema include the Na(+)-K(+)-2Cl(−) co-transporter (NKCC1) and the SUR1-regulated NCCa-ATP (SUR1/TRPM4) channel. These two ion channels have been demonstrated to be critical mediators of edema formation in brain-injured states. Their specific inhibitors, bumetanide and glibenclamide, respectively, are well-characterized Food and Drug Administration-approved drugs with excellent safety profiles. Directed inhibition of these ion transporters has the potential to reduce the development of cerebral edema and is currently being investigated in human clinical trials. Another class of treatment agents for cerebral edema is vasopressin receptor antagonists. Euvolemic hyponatremia is present in a myriad of neurological conditions resulting in cerebral edema. A specific antagonist of the vasopressin V1A- and V2-receptor, conivaptan, promotes water excretion while sparing electrolytes through a process known as aquaresis.
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