bumetanide has been researched along with Brain Edema in 23 studies
Brain Edema: Increased intracellular or extracellular fluid in brain tissue. Cytotoxic brain edema (swelling due to increased intracellular fluid) is indicative of a disturbance in cell metabolism, and is commonly associated with hypoxic or ischemic injuries (see HYPOXIA, BRAIN). An increase in extracellular fluid may be caused by increased brain capillary permeability (vasogenic edema), an osmotic gradient, local blockages in interstitial fluid pathways, or by obstruction of CSF flow (e.g., obstructive HYDROCEPHALUS). (From Childs Nerv Syst 1992 Sep; 8(6):301-6)
| Excerpt | Relevance | Reference |
|---|---|---|
| " The present study has been performed to establish, whether furosemide or bumetanide directly modify intracranial pressure in cytotoxic brain edema." | 7.67 | Effect of furosemide, bumetanide and mannitol on intracranial pressure in experimental brain edema of the rat. ( Plangger, C; Völkl, H, 1989) |
| "Bumetanide treatment increased ATP/Pi and PCr/Pi and ameliorated the declines in these values with insulin/saline treatment." | 5.36 | Cerebral metabolic alterations in rats with diabetic ketoacidosis: effects of treatment with insulin and intravenous fluids and effects of bumetanide. ( Anderson, SE; Glaser, N; O'Donnell, ME; Tancredi, DJ; Yuen, N, 2010) |
| "The mechanisms responsible for cerebral edema formation in diabetic ketoacidosis (DKA) are not well understood, although evidence suggests ischemia as a contributing factor." | 5.33 | Bumetanide reduces cerebral edema formation in rats with diabetic ketoacidosis. ( Anderson, SE; Glaser, N; Lam, TI; O'Donnell, ME, 2005) |
| "These data suggest that bumetanide exerts its neuroprotective and anti-edema effects partly via blockade of the perivascular pool of AQP4 and may have therapeutic potential for ischemic stroke in the clinical setting." | 3.76 | Na(+)-K (+)-2Cl (-) cotransport inhibitor attenuates cerebral edema following experimental stroke via the perivascular pool of aquaporin-4. ( Adams, ME; Amiry-Moghaddam, M; Bhardwaj, A; Froehner, SC; Migliati, ER; Ottersen, OP, 2010) |
| " The present study has been performed to establish, whether furosemide or bumetanide directly modify intracranial pressure in cytotoxic brain edema." | 3.67 | Effect of furosemide, bumetanide and mannitol on intracranial pressure in experimental brain edema of the rat. ( Plangger, C; Völkl, H, 1989) |
| "Novel treatment targets for cerebral edema include the Na(+)-K(+)-2Cl(-) co-transporter (NKCC1) and the SUR1-regulated NC(Ca-ATP) (SUR1/TRPM4) channel." | 2.48 | Novel treatment targets for cerebral edema. ( Kahle, KT; Simard, JM; Walcott, BP, 2012) |
| "The development of cytotoxic brain edema resulting in increased intracranial pressure is a major cause of death occurring in the early phase of traumatic brain injury (TBI)." | 1.37 | Aquaporin-4 expression in cultured astrocytes after fluid percussion injury. ( Curtis, KM; Norenberg, MD; Rao, KV; Reddy, PV, 2011) |
| "In the early hours of ischemic stroke, cerebral edema forms as Na, Cl, and water are secreted across the blood-brain barrier (BBB) and astrocytes swell." | 1.37 | Effects of estradiol on ischemic factor-induced astrocyte swelling and AQP4 protein abundance. ( O'Donnell, ME; Rutkowsky, JM; Wallace, BK; Wise, PM, 2011) |
| "Bumetanide treatment increased ATP/Pi and PCr/Pi and ameliorated the declines in these values with insulin/saline treatment." | 1.36 | Cerebral metabolic alterations in rats with diabetic ketoacidosis: effects of treatment with insulin and intravenous fluids and effects of bumetanide. ( Anderson, SE; Glaser, N; O'Donnell, ME; Tancredi, DJ; Yuen, N, 2010) |
| "An important contributor to cerebral edema formation is the Na-K-Cl cotransporter (NKCC)." | 1.36 | Expression of Na-K-Cl cotransporter and edema formation are age dependent after ischemic stroke. ( Akella, P; Benashski, SE; Liu, F; McCullough, LD; Xu, Y, 2010) |
| "The mechanisms responsible for cerebral edema formation in diabetic ketoacidosis (DKA) are not well understood, although evidence suggests ischemia as a contributing factor." | 1.33 | Bumetanide reduces cerebral edema formation in rats with diabetic ketoacidosis. ( Anderson, SE; Glaser, N; Lam, TI; O'Donnell, ME, 2005) |
| "Cerebral edema was evaluated in rats subjected to permanent middle cerebral artery occlusion (MCAO) by magnetic resonance diffusion-weighted imaging and calculation of apparent diffusion coefficients (ADC)." | 1.32 | Bumetanide inhibition of the blood-brain barrier Na-K-Cl cotransporter reduces edema formation in the rat middle cerebral artery occlusion model of stroke. ( Anderson, SE; Lam, TI; Liu, XB; O'Donnell, ME; Tran, L, 2004) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 1 (4.35) | 18.7374 |
| 1990's | 0 (0.00) | 18.2507 |
| 2000's | 10 (43.48) | 29.6817 |
| 2010's | 11 (47.83) | 24.3611 |
| 2020's | 1 (4.35) | 2.80 |
| Authors | Studies |
|---|---|
| Tóth, K | 1 |
| Lénárt, N | 1 |
| Berki, P | 1 |
| Fekete, R | 1 |
| Szabadits, E | 1 |
| Pósfai, B | 1 |
| Cserép, C | 1 |
| Alatshan, A | 1 |
| Benkő, S | 1 |
| Kiss, D | 1 |
| Hübner, CA | 1 |
| Gulyás, A | 1 |
| Kaila, K | 1 |
| Környei, Z | 1 |
| Dénes, Á | 1 |
| Zhang, J | 1 |
| Pu, H | 1 |
| Zhang, H | 1 |
| Wei, Z | 1 |
| Jiang, X | 1 |
| Xu, M | 1 |
| Zhang, L | 1 |
| Zhang, W | 1 |
| Liu, J | 1 |
| Meng, H | 1 |
| Stetler, RA | 1 |
| Sun, D | 4 |
| Chen, J | 1 |
| Gao, Y | 1 |
| Chen, L | 1 |
| Zhang, M | 1 |
| Cui, Z | 1 |
| Cui, H | 1 |
| Cao, Y | 1 |
| Zhong, C | 1 |
| Wang, Y | 1 |
| Lu, KT | 3 |
| Huang, TC | 1 |
| Tsai, YH | 1 |
| Yang, YL | 3 |
| Yuen, N | 2 |
| Anderson, SE | 5 |
| Glaser, N | 3 |
| Tancredi, DJ | 2 |
| O'Donnell, ME | 7 |
| Lam, TI | 4 |
| Tran, L | 2 |
| Liu, F | 1 |
| Akella, P | 1 |
| Benashski, SE | 1 |
| Xu, Y | 1 |
| McCullough, LD | 1 |
| Migliati, ER | 1 |
| Amiry-Moghaddam, M | 1 |
| Froehner, SC | 1 |
| Adams, ME | 1 |
| Ottersen, OP | 1 |
| Bhardwaj, A | 1 |
| Jayakumar, AR | 1 |
| Valdes, V | 1 |
| Norenberg, MD | 2 |
| Cai, L | 1 |
| Du, T | 1 |
| Song, D | 1 |
| Li, B | 1 |
| Hertz, L | 1 |
| Peng, L | 1 |
| Rao, KV | 1 |
| Reddy, PV | 1 |
| Curtis, KM | 1 |
| Rutkowsky, JM | 2 |
| Wallace, BK | 1 |
| Wise, PM | 1 |
| Walcott, BP | 1 |
| Kahle, KT | 1 |
| Simard, JM | 1 |
| Yan, Y | 2 |
| Dempsey, RJ | 2 |
| Flemmer, A | 1 |
| Forbush, B | 1 |
| Liu, XB | 1 |
| Chen, H | 1 |
| Luo, J | 1 |
| Kintner, DB | 1 |
| Shull, GE | 1 |
| Wu, CY | 2 |
| Cheng, NC | 1 |
| Wo, YY | 1 |
| Yang, JT | 1 |
| Yen, HH | 2 |
| Peng, JH | 1 |
| Wang, CL | 1 |
| Brillault, J | 1 |
| Foroutan, S | 1 |
| Plangger, C | 1 |
| Völkl, H | 1 |
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| Conivaptan for the Reduction of Cerebral Edema in Intracerebral Hemorrhage- A Safety and Tolerability Study[NCT03000283] | Phase 1 | 7 participants (Actual) | Interventional | 2017-03-22 | Completed | ||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
Changes in cerebral edema (CE) as measured on CT. Goal is a -5 to -10% change in CE over time. Change will be measured both as absolute change in volume, calculated as the final volume minus the baseline volume measure and converted to a percentage of the baseline volume measure. (NCT03000283)
Timeframe: Baseline to 168 hours post-enrollment
| Intervention | percentage of change from baseline (Mean) |
|---|---|
| Conivaptan Treatment Group | -37.1 |
Cost as measured by length of stay in the neuro ICU. (NCT03000283)
Timeframe: Enrollment through hospital discharge, up to 3 weeks
| Intervention | days (Mean) |
|---|---|
| Conivaptan Treatment Group | 14.4 |
All-cause deaths during hospitalization (NCT03000283)
Timeframe: Enrollment through hospital discharge, up to 3 weeks
| Intervention | Participants (Count of Participants) |
|---|---|
| Conivaptan Treatment Group | 0 |
Modified Rankin Scale (0 to 6) at discharge from the hospital. A score of 0 indicates no disability and a score of 6 indicates the patient died. Functional independence is defined as a score of 2 or less. (NCT03000283)
Timeframe: At discharge from ICU and from hospital, up to 3 weeks
| Intervention | score on a scale (Median) |
|---|---|
| Conivaptan Treatment Group | 5 |
"Cost as measured by:~Need for external ventricular drain (EVD)/bolt or surgical procedures (craniectomy, clot evacuation,VPS) for reduction/management of CE.~Need for central venous lines, arterial lines, peripherally inserted central venous catheter (PICC) lines, tracheostomy/percutaneous endoscopic gastrostomies (PEGs).~Number of patients requiring a ventilator." (NCT03000283)
Timeframe: Baseline to 168 hours post-enrollment
| Intervention | Participants (Count of Participants) | ||
|---|---|---|---|
| EVD/bolt or surgical procedures | Lines or tracheostomy/PEG | Ventilator | |
| Conivaptan Treatment Group | 0 | 7 | 1 |
The number of participants with abnormal seizure activity and/or abnormal lab values and/or increase in infection rate and/or any drug-related adverse events. (NCT03000283)
Timeframe: Baseline to 168 hours post-enrollment
| Intervention | Participants (Count of Participants) | |||
|---|---|---|---|---|
| Abnormal Seizure Activity | Abnormal Lab Values | Infections | Drug-related Adverse Events | |
| Conivaptan Treatment Group | 0 | 0 | 1 | 0 |
1 review available for bumetanide and Brain Edema
| Article | Year |
|---|---|
Novel treatment targets for cerebral edema.
Topics: Antidiuretic Hormone Receptor Antagonists; ATP-Binding Cassette Transporters; Benzazepines; Brain Ed | 2012 |
22 other studies available for bumetanide and Brain Edema
| Article | Year |
|---|---|
The NKCC1 ion transporter modulates microglial phenotype and inflammatory response to brain injury in a cell-autonomous manner.
Topics: Animals; Brain Edema; Brain Injuries; Bumetanide; Embryo, Mammalian; Gene Expression Regulation; Hip | 2022 |
Inhibition of Na
Topics: Animals; Blood-Brain Barrier; Brain; Brain Edema; Brain Injuries, Traumatic; Bumetanide; Disease Mod | 2017 |
Astaxanthin alleviates cerebral edema by modulating NKCC1 and AQP4 expression after traumatic brain injury in mice.
Topics: Animals; Aquaporin 4; Brain; Brain Edema; Brain Injuries, Traumatic; Bumetanide; Capillary Permeabil | 2016 |
Transient receptor potential vanilloid type 4 channels mediate Na-K-Cl-co-transporter-induced brain edema after traumatic brain injury.
Topics: Animals; Body Water; Brain; Brain Edema; Brain Injuries, Traumatic; Bumetanide; Hippocampus; Male; M | 2017 |
Cerebral blood flow and cerebral edema in rats with diabetic ketoacidosis.
Topics: Animals; Brain Edema; Bumetanide; Cerebrovascular Circulation; Diabetic Ketoacidosis; Magnetic Reson | 2008 |
The role of the blood-brain barrier Na-K-2Cl cotransporter in stroke.
Topics: Animals; Astrocytes; Blood-Brain Barrier; Brain Edema; Brain Ischemia; Bumetanide; Cerebral Infarcti | 2004 |
Cerebral metabolic alterations in rats with diabetic ketoacidosis: effects of treatment with insulin and intravenous fluids and effects of bumetanide.
Topics: Animals; Aspartic Acid; Brain; Brain Edema; Bumetanide; Cerebrovascular Circulation; Creatinine; Dia | 2010 |
Expression of Na-K-Cl cotransporter and edema formation are age dependent after ischemic stroke.
Topics: Aging; Animals; Brain; Brain Edema; Bumetanide; Infarction, Middle Cerebral Artery; Ischemic Attack, | 2010 |
Na(+)-K (+)-2Cl (-) cotransport inhibitor attenuates cerebral edema following experimental stroke via the perivascular pool of aquaporin-4.
Topics: alpha-Synuclein; Animals; Aquaporin 4; Brain Edema; Bumetanide; Cerebral Infarction; Male; Mice; Mic | 2010 |
The Na-K-Cl cotransporter in the brain edema of acute liver failure.
Topics: Animals; Brain Edema; Bumetanide; Liver Failure, Acute; Male; Phosphorylation; Rats; Rats, Wistar; S | 2011 |
Astrocyte ERK phosphorylation precedes K(+)-induced swelling but follows hypotonicity-induced swelling.
Topics: ADAM Proteins; ADAM17 Protein; Animals; Astrocytes; Brain Edema; Bumetanide; Cell Division; Cells, C | 2011 |
Aquaporin-4 expression in cultured astrocytes after fluid percussion injury.
Topics: Analysis of Variance; Animals; Aquaporin 4; Astrocytes; Blotting, Western; Brain Edema; Brain Injuri | 2011 |
Effects of estradiol on ischemic factor-induced astrocyte swelling and AQP4 protein abundance.
Topics: Animals; Aquaporin 4; Arginine Vasopressin; Astrocytes; Blotting, Far-Western; Brain Edema; Bumetani | 2011 |
Inhibition of Na(+)-K(+)-Cl(-) cotransporter during focal cerebral ischemia decreases edema and neuronal damage.
Topics: Animals; Brain; Brain Edema; Brain Ischemia; Bumetanide; Cerebral Infarction; Drug Administration Sc | 2003 |
Bumetanide inhibition of the blood-brain barrier Na-K-Cl cotransporter reduces edema formation in the rat middle cerebral artery occlusion model of stroke.
Topics: Animals; Blood-Brain Barrier; Brain Edema; Bumetanide; Diffusion Magnetic Resonance Imaging; Diureti | 2004 |
Bumetanide reduces cerebral edema formation in rats with diabetic ketoacidosis.
Topics: Animals; Blood Glucose; Blood Urea Nitrogen; Brain Edema; Bumetanide; Carbon Dioxide; Diabetic Ketoa | 2005 |
Na(+)-dependent chloride transporter (NKCC1)-null mice exhibit less gray and white matter damage after focal cerebral ischemia.
Topics: Amyloid beta-Protein Precursor; Animals; Astrocytes; Brain Edema; Brain Infarction; Brain Ischemia; | 2005 |
Inhibition of the Na+ -K+ -2Cl- -cotransporter in choroid plexus attenuates traumatic brain injury-induced brain edema and neuronal damage.
Topics: Animals; Brain Edema; Brain Injuries; Bumetanide; Choroid Plexus; Diuretics; Male; Neurons; Neuropro | 2006 |
Bumetanide administration attenuated traumatic brain injury through IL-1 overexpression.
Topics: Analysis of Variance; Animals; Brain Edema; Brain Injuries; Bumetanide; Disease Models, Animal; Hipp | 2007 |
Hypoxia effects on cell volume and ion uptake of cerebral microvascular endothelial cells.
Topics: Animals; Blood-Brain Barrier; Brain; Brain Edema; Bumetanide; Cattle; Cell Hypoxia; Cell Size; Cells | 2008 |
Na+-K+-Cl- cotransporter in rat focal cerebral ischemia.
Topics: Animals; Astrocytes; Autoradiography; Brain Chemistry; Brain Edema; Bumetanide; Carrier Proteins; Ce | 2001 |
Effect of furosemide, bumetanide and mannitol on intracranial pressure in experimental brain edema of the rat.
Topics: Animals; Brain Edema; Bumetanide; Diuretics; Furosemide; Intracranial Pressure; Male; Mannitol; Neph | 1989 |