bumetanide has been researched along with Brain Swelling in 23 studies
| 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 Swelling
| 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 Swelling
| 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 |