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epinephrine (epinephrine, Dey / EpiPen / epinephrine, Mylan)

✓ Approved

Mylan · 小分子 · 小分子

什么是 epinephrine？

epinephrine 是一种小分子，由Mylan研发。该药已获批，用于治疗相关适应症，给药途径：Injectable (Others)。

药物档案

商品名epinephrine, Dey, EpiPen, epinephrine, Mylan
公司Mylan
药物类别小分子
给药途径Injectable (Others)
状态Approved
来源： ClinicalTrials.gov, Mylan

治疗适应症

epinephrine 针对 1 个适应症，涉及 1 个治疗领域。

治疗领域疾病/病症分期
Immune system disordersAnaphylactic reaction✓ Approved

相关研究文献

PubMedNaunyn-Schmiedeberg's archives of pharmacology2026-07-27

The evolution of pharmacological recommendations for anaphylaxis: a comparative analysis of established textbooks.

McGuigan Annika Stina AS, Seifert Roland R

Anaphylaxis can be life-threatening-due to its rapid-progressing and often unpredictable nature. Especially in such medical emergencies, robust clinical trials regarding adjunctive therapies can be scarce and recommendations across literature may vary. Hence, the aim of this study is to investigate the evolution of recommendations for the pharmacological management of anaphylaxis in established pharmacology textbooks over time. The following German textbook series were included: Aktories, Lüllmann, and Karow. The US standard work Goodman & Gilman was reviewed for an international comparison. This study focuses on epinephrine, H1R-antagonists, H2R-antagonists, and GCR-agonists-analyzing their potential use in anaphylaxis via predefined criteria and contextualizing it using the current AWMF anaphylaxis guideline. Epinephrine is continuously recommended as first-line treatment in anaphylaxis across textbooks and decades-with a shift towards i.m. use. Differences prevail regarding the anaphylaxis grade at which epinephrine is indicated vs. when H1R-antagonists are considered sufficient. Overall, H1R-antagonists are noted as adjuncts in at least more severe anaphylaxis. H2R-antagonists appear to lack clinical relevance and are inconsistently discussed as adjunctive add-ons. While GCR-agonists are consistently recommended as adjuncts in anaphylaxis, the included US literature deviates from the German consensus of a high-dose approach. Moreover, there are differences regarding fluid resuscitation-some textbooks merely predate the guideline's recommendation to refrain from colloids, whereas others remain at odds with it even in their latest editions. While there is general agreement on epinephrine's central role in anaphylaxis management, recommendations in literature regarding the specific roles of certain adjunctive measures vary-likely reflecting the limited evidence.

PMID 42503525
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PubMedJournal of personalized medicine2026-07-27

Pharmacologic Strategies for Intraoperative Hypotension When Ephedrine Is Unavailable: An Evidence-Based Review.

Duarte-Medrano Gilberto G, Nuño-Lámbarri Natalia N, Chavez-Muñoz Diana D, Elguezabal Rodelo Rebeca Garazi RG et al.

Background/Objectives: Intraoperative hypotension (IOHs) affects up to 87% of patients under general anesthesia and is consistently associated with acute kidney injury, myocardial damage, stroke, and mortality. The intermittent unavailability of ephedrine across healthcare systems underscores the need for evidence-based alternatives. This review critically evaluates pharmacological options for IOH when ephedrine is unavailable, focusing on receptor pharmacodynamics, population-specific evidence, and clinical consequences of inadequately managed hypotension. Methods: A narrative, evidence-based review was conducted examining mechanisms of action, dosing strategies, adverse effect profiles, and clinical applicability of key vasoactive agents: ephedrine, phenylephrine, norepinephrine, and epinephrine. Population-specific evidence across obstetric, pediatric, and elderly cohorts was synthesized from randomized controlled trials, meta-analyses, and observational studies. The clinical impact of IOH on neurological, cardiovascular, and renal outcomes was reviewed. Results: Each vasopressor exhibits a distinct receptor-selectivity profile that determines its hemodynamic effect and optimal clinical context. Norepinephrine's favorable α1/β1 balance tends to preserve cardiac output better than pure α1-agonists and has emerged as a promising alternative in obstetric and elderly populations, although the optimal agent ultimately depends on the underlying mechanism of hypotension and individual patient characteristics. Epinephrine provides combined vasopressor and inotropic support for hypotension with myocardial depression. IOH is associated with a greater than twofold increase in postoperative AKI and significantly elevated risks of myocardial infarction and stroke, with outcomes driven by cumulative hypotensive exposure rather than isolated pressure nadirs. Conclusions: Effective management of IOH requires individualized vasopressor selection guided by underlying pathophysiology, cardiovascular profile, and surgical context. A physiology-based strategy-rather than protocol-driven drug substitution-enables anesthesiologists to achieve precise hemodynamic control and preserve end-organ perfusion even when ephedrine is unavailable.

PMID 42506108
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PubMedCells2026-07-27

Crosstalk Between Gut Microbiota, Epigenome, and Neurotransmitters in Health and Disease.

Nohesara Shabnam S, Mostafavi Abdolmaleky Hamid H, Thiagalingam Sam S

Beyond its established roles in digestion, immune regulation, and enteroendocrine signaling, the gut microbiota (GM) influences distant organs, particularly the brain, by producing or modulating the balance of neurotransmitters (NTs) and regulating their intestinal metabolism through epigenetic mechanisms, thereby shaping gut-brain communication. In this narrative review, first, we provide an overview of the major classes of NTs, such as serotonin, dopamine, GABA, glutamate, acetylcholine, epinephrine, and norepinephrine, and their functions in the body and brain. Second, we discuss the potential epigenetic mechanisms through which alterations in the levels and/or activity of NTs contribute to health and disease. Third, we explore the potential roles of the GM in the production of biologically active metabolites, such as short-chain fatty acids (SCFAs), and in the regulation of NT metabolism and function in health and disease through epigenetic mechanisms. We also highlight how GM-modulating therapies may improve disease outcomes by altering epigenetically mediated intestinal NT metabolism and availability, with downstream effects on NT activity in other organs. Finally, we discuss the current challenges and future directions for elucidating the interplay among the epigenome, the GM, and NTs.

PMID 42505389
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PubMedMedical microbiology and immunology2026-07-27

Immunomodulatory effect of stress hormones on porcine neutrophil functions during Actinobacillus pleuropneumoniae infection.

Bonilla Marta C MC, Lassnig Simon S, Wendt Michael M, Hennig-Pauka Isabel I et al.

Stress contributes to disease outcomes and can influence the signaling and interactions of immune cells. This study aimed to evaluate the influence of three selected stress hormones cortisol, epinephrine and norepinephrine, at in vivo-relevant concentrations, on the antimicrobial activity of porcine neutrophils during infection with Actinobacillus pleuropneumoniae (A.pp). We analyzed whether stress hormones affect the antimicrobial activity of neutrophils. Reactive oxygen species (ROS) production, cell size, and granularity were measured using flow cytometry. Neutrophil extracellular trap (NET) formation was quantified using confocal immunofluorescence microscopy, and transmission electron microscopy was employed to analyze the formation of vesicular NETs. ROS production and NET formation experiments were also conducted under infection with A.pp. The survival of A.pp in the presence of stress hormone-treated neutrophils was assessed. The antimicrobial activity of neutrophils was altered in a concentration-dependent manner by all tested stress hormones: neutrophils produced higher amounts of ROS and released significantly more NETs under A.pp infection, in particular vesicular NET formation. However, A.pp growth in the presence or absence of neutrophils was not affected by stress hormones. Future studies are needed to characterize the role of vesicular NETs as stress response reactions. In conclusion, this study contributes to a better understanding of the innate immune cells, particularly porcine neutrophils, in infections within stressed hosts.

PMID 42507216
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PubMedJAMA pediatrics2026-07-27

Treatment of Multifood Allergy With Omalizumab or Multiallergen Oral Immunotherapy: A Randomized Clinical Trial.

Wood Robert A RA, Togias Alkis A, Burk Caitlin M CM, Sindher Sayantani S et al.

Food allergy is common, affecting up to 8% to 10% of children and adults. Treatment options include oral immunotherapy (OIT) and omalizumab, an anti-immunoglobulin E (IgE) monoclonal antibody. To compare omalizumab with OIT for the treatment of patients with multifood allergy. This was a double-blind, placebo-controlled, randomized clinical trial comparing omalizumab with omalizumab-facilitated multiallergen OIT (MOIT) in participants who completed stage 1 of the Omalizumab as Monotherapy and as Adjunct Therapy to Multiallergen OIT in Children and Adults With Food Allergy (OUTMATCH) trial, which led to the approval of omalizumab. The setting comprised 10 academic centers across the US. Included in this analysis were individuals aged 1 to 55 years with an allergy to peanuts and at least 2 other foods (milk, eggs, wheat, cashews, hazelnuts, walnuts). Eligibility was based on oral food challenge thresholds, requiring dose-limiting symptoms to cumulative doses of 144 mg or less of protein for peanuts and 444 mg or less for nonpeanut allergens. Data were analyzed from October 2024 to February 2026. Participants were randomized to receive MOIT with placebo omalizumab or omalizumab with placebo MOIT. All received 16 weeks of open-label omalizumab; at week 8, active or placebo MOIT was initiated and escalated to goal doses of 1000 mg per food. At week 16, participants transitioned to blinded omalizumab or placebo injections for 44 weeks. The primary end point was cumulative tolerated dose (CTD) of 4044 mg or greater for all 3 foods. Predefined secondary end points included CTDs of 1044, 2044, 4044, 6044, or 8044 mg for 1, 2, or all 3 foods. A total of 117 participants (median [IQR] age, 7 [1-29] years; 64 male [55%]) were randomized to receive active MOIT (n = 58) or active omalizumab (n = 59). A total of 30 participants (51%) receiving active MOIT and 51 (88%) receiving active omalizumab completed the study. In the intention-to-treat (ITT) analysis, omalizumab was superior to MOIT (21 of 58 [36%] vs 11 of 59 [19%]; odds ratio, 2.6; 95% CI, 1.1-6.3; P = .03), with no differences in per-protocol analyses. Omalizumab superiority for CTDs of 4044 mg or greater was also demonstrated for 2 or more foods and for several individual foods. More participants taking active MOIT experienced adverse events (serious adverse events in 18 of 59 [31%] vs 0%; events leading to discontinuation in 13 of 59 [22%] vs 0%; events treated with epinephrine (22 of 59 [37%] vs 4 of 58 [7%]). Although the ITT analysis found a higher rate of treatment success in those receiving omalizumab compared with MOIT, results suggest that the difference was largely driven by the high rate of study discontinuation in the participants treated with MOIT, mostly related to adverse events.

PMID 42507431
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PubMedJournal of thrombosis and haemostasis : JTH2026-07-26

Acute Stress Activates Piezo1 to Drive NETs Formation and Aggravated Arterial Thrombosis.

Yu Chen C, Liu Xuewei X, Li Sonlin S, Meng Xinyu X et al.

Acute stress is a critical driver of arterial thrombosis, yet its regulatory mechanisms involving immune cells remain poorly understood. Increasing evidence underscores the interplay between acute stress and inflammation mediated through the neuro-immune axis. This study aims to elucidate the mechanisms by which acute stress impacts arterial thrombosis, focusing on neutrophil extracellular traps (NETs) and their regulatory pathways. We employed an acute restraint stress model, FeCl3-induced carotid artery thrombosis model and acute myocardial infarction model to investigate the relationship among NETs, acute stress and arterial thrombosis. Neutrophils isolated from human peripheral blood and murine bone marrow were used to investigate the mechanisms of NETs formation. SYTOX green staining, F-04 staining, immunofluorescence and co-immunoprecipitation were used to investigate its underlying mechanism. We found that acute restraint stress trigger NETs formation and promote thrombosis. In vitro and in vivo experiments revealed that epinephrine induced NETs formation. We further investigate that it is Ca2+ influx not reactive oxygen species (ROS) mediates epinephrine-induced NETs formation. While administration of ICI-118551, a β2 adrenergic receptor antagonist, inhibited intracellular Ca2+ elevation, suppressed NETs formation, and slowed thrombosis progression. Mechanistic studies revealed that epinephrine induced cytoskeletal remodeling and activated the Piezo1 channel, leading to increased intracellular calcium levels. Our findings demonstrate that acute stress exacerbates arterial thrombosis via epinephrine-induced NETs formation, with the non-selective Ca2+ channel Piezo1 contributing to intracellular calcium elevation. Targeting Piezo1 and NETs may represent novel therapeutic strategies for managing acute cardiovascular events.

PMID 42501970
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