propranolol has been researched along with Sepsis in 12 studies
Propranolol: A widely used non-cardioselective beta-adrenergic antagonist. Propranolol has been used for MYOCARDIAL INFARCTION; ARRHYTHMIA; ANGINA PECTORIS; HYPERTENSION; HYPERTHYROIDISM; MIGRAINE; PHEOCHROMOCYTOMA; and ANXIETY but adverse effects instigate replacement by newer drugs.
propranolol : A propanolamine that is propan-2-ol substituted by a propan-2-ylamino group at position 1 and a naphthalen-1-yloxy group at position 3.
Sepsis: Systemic inflammatory response syndrome with a proven or suspected infectious etiology. When sepsis is associated with organ dysfunction distant from the site of infection, it is called severe sepsis. When sepsis is accompanied by HYPOTENSION despite adequate fluid infusion, it is called SEPTIC SHOCK.
| Excerpt | Relevance | Reference |
|---|---|---|
| "Propranolol treatment attenuates hypermetabolism and does not cause increased incidence of infection and sepsis." | 9.12 | Propranolol does not increase inflammation, sepsis, or infectious episodes in severely burned children. ( Branski, LK; Finnerty, CC; Herndon, DN; Jeschke, MG; Norbury, WB, 2007) |
| " Thus, we investigated the effect of beta-blockade with propranolol on survival, hemodynamics, lung heat shock protein (HSP) expression, metabolism and inflammatory markers in a rat cecal ligation and puncture (CLP) model of sepsis." | 7.79 | Early propranolol treatment induces lung heme-oxygenase-1, attenuates metabolic dysfunction, and improves survival following experimental sepsis. ( Baird, C; Higgins, D; Hutting, H; Khailova, L; Queensland, K; Serkova, N; Vu Tran, Z; Weitzel, L; Wilson, J; Wischmeyer, PE, 2013) |
| "Sepsis is accompanied by an enormous increase in catecholamine expression, leading to metabolism of lipids and glucose, changes in cardiovascular output, immunomodulatory effects, and changes in protein metabolism, all of which push the body into a catabolic state." | 6.44 | Metabolism modulators in sepsis: propranolol. ( Herndon, DN; Jeschke, MG; Norbury, WB, 2007) |
| "Propranolol treatment attenuates hypermetabolism and does not cause increased incidence of infection and sepsis." | 5.12 | Propranolol does not increase inflammation, sepsis, or infectious episodes in severely burned children. ( Branski, LK; Finnerty, CC; Herndon, DN; Jeschke, MG; Norbury, WB, 2007) |
| " Thus, we investigated the effect of beta-blockade with propranolol on survival, hemodynamics, lung heat shock protein (HSP) expression, metabolism and inflammatory markers in a rat cecal ligation and puncture (CLP) model of sepsis." | 3.79 | Early propranolol treatment induces lung heme-oxygenase-1, attenuates metabolic dysfunction, and improves survival following experimental sepsis. ( Baird, C; Higgins, D; Hutting, H; Khailova, L; Queensland, K; Serkova, N; Vu Tran, Z; Weitzel, L; Wilson, J; Wischmeyer, PE, 2013) |
| "Sepsis is accompanied by an enormous increase in catecholamine expression, leading to metabolism of lipids and glucose, changes in cardiovascular output, immunomodulatory effects, and changes in protein metabolism, all of which push the body into a catabolic state." | 2.44 | Metabolism modulators in sepsis: propranolol. ( Herndon, DN; Jeschke, MG; Norbury, WB, 2007) |
| "Treatment with propranolol augmented the epinephrine-induced increase of splenocyte apoptosis, did not affect the decrease of splenocyte proliferation and IL-2 release, augmented the release of IL-6 and antagonized the mobilization of natural killer cells observed in epinephrine-treated animals." | 1.32 | Adrenergic modulation of survival and cellular immune functions during polymicrobial sepsis. ( Exton, MS; Oberbeck, R; Pehle, B; Schedlowski, M; Schmitz, D; Schüler, M; Wilsenack, K, 2004) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 2 (16.67) | 18.7374 |
| 1990's | 0 (0.00) | 18.2507 |
| 2000's | 5 (41.67) | 29.6817 |
| 2010's | 3 (25.00) | 24.3611 |
| 2020's | 2 (16.67) | 2.80 |
| Authors | Studies |
|---|---|
| Knuth, CM | 1 |
| Auger, C | 1 |
| Jeschke, MG | 3 |
| Özyılmaz, E | 1 |
| Büyüknacar, HSG | 1 |
| Bağır, EK | 1 |
| Sencar, L | 1 |
| Öztürk, ÖG | 1 |
| Eray, IC | 1 |
| Dağlıoğlu, YK | 1 |
| Baydar, O | 1 |
| Seydaoğlu, G | 1 |
| Mete, UÖ | 1 |
| Gümürdülü, D | 1 |
| Kocabaş, A | 1 |
| Chang, YT | 1 |
| Huang, WC | 1 |
| Cheng, CC | 1 |
| Ke, MW | 1 |
| Tsai, JS | 1 |
| Hung, YM | 1 |
| Huang, NC | 1 |
| Huang, MS | 1 |
| Wann, SR | 1 |
| Wilson, J | 1 |
| Higgins, D | 1 |
| Hutting, H | 1 |
| Serkova, N | 1 |
| Baird, C | 1 |
| Khailova, L | 1 |
| Queensland, K | 1 |
| Vu Tran, Z | 1 |
| Weitzel, L | 1 |
| Wischmeyer, PE | 1 |
| Sarullo, FM | 1 |
| Americo, L | 1 |
| Accardo, S | 1 |
| Cicero, S | 1 |
| Schicchi, R | 1 |
| Schirò, M | 1 |
| Castello, A | 1 |
| Rudiger, A | 1 |
| Oberbeck, R | 1 |
| Schmitz, D | 1 |
| Wilsenack, K | 1 |
| Schüler, M | 1 |
| Pehle, B | 1 |
| Schedlowski, M | 1 |
| Exton, MS | 1 |
| Uzuki, M | 1 |
| Yamakage, M | 1 |
| Fujimura, N | 1 |
| Namiki, A | 1 |
| Norbury, WB | 2 |
| Finnerty, CC | 1 |
| Branski, LK | 1 |
| Herndon, DN | 2 |
| Wilmore, DW | 1 |
| Long, JM | 1 |
| Mason, AD | 1 |
| Skreen, RW | 1 |
| Pruitt, BA | 1 |
| Jenkins, WL | 1 |
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| Impact of Early CRRT Intervention in Patients Receiving VA-ECMO Support on 30-day Mortality: A Randomized Controlled Trial[NCT03549923] | Phase 4 | 550 participants (Anticipated) | Interventional | 2018-12-18 | Recruiting | ||
| "Reducing Elevated Heart Rate in Patients With Multiple Organ Dysfunction Syndrome (MODS) by the Funny Channel Current (If) Inhibitor Ivabradine"[NCT01186783] | Phase 2 | 70 participants (Anticipated) | Interventional | 2010-05-31 | Recruiting | ||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
3 reviews available for propranolol and Sepsis
| Article | Year |
|---|---|
Burn-induced hypermetabolism and skeletal muscle dysfunction.
Topics: Burns; Cachexia; Epigenesis, Genetic; Exercise; Human Growth Hormone; Humans; Insulin; Metformin; Mu | 2021 |
Beta-block the septic heart.
Topics: Adrenergic beta-Antagonists; Animals; Cardiotonic Agents; Disease Models, Animal; Heart; Humans; Pro | 2010 |
Metabolism modulators in sepsis: propranolol.
Topics: Adrenergic beta-Antagonists; Cytokines; Energy Metabolism; Humans; Hyperglycemia; Lipolysis; Propran | 2007 |
1 trial available for propranolol and Sepsis
| Article | Year |
|---|---|
Propranolol does not increase inflammation, sepsis, or infectious episodes in severely burned children.
Topics: Adrenergic beta-Antagonists; Anabolic Agents; Burns; Child; Energy Metabolism; Female; Humans; Infla | 2007 |
8 other studies available for propranolol and Sepsis
| Article | Year |
|---|---|
Early propranolol treatment ameliorates endothelial dysfunction in experimental septic lung.
Topics: Acute Lung Injury; Animals; Disease Models, Animal; Ligation; Lung; Male; Propranolol; Rats; Rats, W | 2019 |
Effects of epinephrine on heart rate variability and cytokines in a rat sepsis model.
Topics: Adrenergic alpha-Agonists; Adrenergic beta-1 Receptor Antagonists; Animals; Cytokines; Disease Model | 2020 |
Early propranolol treatment induces lung heme-oxygenase-1, attenuates metabolic dysfunction, and improves survival following experimental sepsis.
Topics: Adrenergic beta-Antagonists; Animals; Drug Administration Schedule; Enzyme Induction; Heme Oxygenase | 2013 |
Tako-tsubo cardiomyopathy observed in a patient with sepsis and transient hyperthyroidism.
Topics: Amlodipine; Anti-Bacterial Agents; Antihypertensive Agents; Antithyroid Agents; Aspirin; Echocardiog | 2009 |
Adrenergic modulation of survival and cellular immune functions during polymicrobial sepsis.
Topics: Adrenergic beta-Antagonists; Animals; Apoptosis; Cell Division; Cytokines; Drug Synergism; Epinephri | 2004 |
Preferable inotropic action of procaterol, a potent bronchodilator, on impaired diaphragmatic contractility in an intraabdominal septic model.
Topics: Adrenergic beta-Antagonists; Animals; Bronchodilator Agents; Cyclic AMP; Diaphragm; In Vitro Techniq | 2006 |
Catecholamines: mediator of the hypermetabolic response to thermal injury.
Topics: Adolescent; Adult; Aged; Body Surface Area; Body Temperature; Body Temperature Regulation; Burns; Ca | 1974 |
Some aspects of the treatment of shock in animals.
Topics: Adrenal Cortex Hormones; Animals; Blood Pressure; Blood Transfusion; Cardiac Output; Digitalis Glyco | 1972 |