Drug Database
NI

nitroglycerin (Adesitrin / Deponit / Cordipatch)

✓ Approved

Takeda · 小分子 · 小分子

什么是 nitroglycerin?

nitroglycerin 是一种小分子,由Takeda研发。该药已获批,用于治疗相关适应症,给药途径:Topical、Transdermal。

药物档案

商品名Adesitrin, Deponit, Cordipatch
公司Takeda
药物类别小分子
给药途径Topical, Transdermal
状态Approved

治疗适应症

nitroglycerin 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
Cardiac disordersAngina pectoris✓ Approved

相关研究文献

PubMedJournal of cardiovascular electrophysiology2026-10-25

Cavotricuspid Isthmus Ablation Using a Variable Loop Pulsed Field Ablation Catheter: A Single-Center Descriptive Analysis.

Wiederkehr Caroline C, Breitenstein Alexander A, Jeger Raban R, Müller Andreas A et al.

Cavotricuspid isthmus (CTI) ablation is frequently performed concomitant with pulmonary vein isolation (PVI). Pulsed field ablation (PFA) has emerged as the preferred energy source for PVI, but it is unclear whether CTI ablation can be performed with PFA catheters. We retrospectively analyzed data from patients who underwent PVI and CTI ablation using a variable-loop PFA catheter for feasibility, efficacy, and safety. Twenty-three patients (mean age 65 years, 57% male) were included in this analysis. Systemic intravenous nitroglycerin was administered to all subjects to prevent vasospasm. Acute CTI block could be documented in all patients at the end of the ablation procedure without complications and with low fluoroscopy exposure. We observed one symptomatic recurrence of possible typical atrial flutter during a mean follow-up of 218 days. CTI ablation using a variable-loop PFA ablation catheter was feasible, efficient, and safe in the acute setting. Prospective studies with larger patient numbers are needed to evaluate the long-term efficacy and safety of this approach.

PMID 42927637
阅读全文 →
PubMedCureus2026-10-25

Could Climate Change Be Silently Damaging Medicines We Keep at Home?

Helito Paulo P, Al-Baker Alanoud A AA, Khalil Zeyad Z, Osman Taha T et al.

Climate change is increasing the likelihood of medicines being exposed to temperatures outside recommended storage conditions after dispensing. Unlike controlled pharmaceutical storage and stability testing environments, everyday settings such as homes, vehicles, bags, delivery packages, domestic refrigerators, and periods of power interruption may subject medicines to fluctuating or extreme temperatures. The clinical significance of these exposures, however, remains uncertain and is likely to vary considerably between products. This scoping review maps the available evidence on post-dispensing temperature exposure and medication stability, with particular attention to real-world storage conditions, physicochemical integrity, biological activity, potential clinical consequences, and practical strategies for reducing temperature-related risk. Evidence was considered across a range of temperature-sensitive and commonly used medicines, including insulin, refrigerated biologics, epinephrine, inhaled medicines, nitroglycerin, and oral formulations, together with studies evaluating household refrigeration, vehicle exposure, and low-resource cooling approaches. The available literature indicates that medicines may frequently encounter conditions outside labelled storage recommendations after leaving formal supply chains. Nevertheless, exposure beyond a labelled temperature range should not be interpreted automatically as loss of pharmaceutical quality or clinical effectiveness. Thermal stability varies substantially according to formulation, temperature intensity, duration of exposure, cumulative thermal history, packaging, and storage conditions. Current evidence is strongest for selected temperature-sensitive medicines but remains fragmented across many other drug classes. Overall, the literature supports a plausible climate-sensitive pathway linking increasing environmental heat with post-dispensing medication-quality risk, but evidence is currently insufficient to quantify the associated clinical burden at population level. Important priorities include characterising cumulative real-world thermal exposure, establishing clinically meaningful degradation thresholds, linking temperature histories with patient outcomes, and evaluating feasible adaptation measures. Climate-resilient medication management will require clearer storage guidance, improved patient education, practical cooling solutions, more reliable refrigeration, temperature-monitoring technologies, and stronger surveillance of medicines after dispensing.

PMID 42924385
阅读全文 →
PubMedThe European journal of neuroscience2026-10-23

Spinorphin Ameliorates Nitroglycerin-Induced Migraine-Like Responses and Trigeminovascular Neuroinflammation Potentially Through Opioid Receptor-Mediated Mechanisms.

Demir Cemalettin C, Torun Ibrahim Ethem IE, Baranoglu Kilinc Yasemin Y, Kilinc Erkan E

Enhancement of endogenous opioid signaling through inhibition of enkephalin degradation has emerged as a potential strategy for pain control, yet its role in migraine remains unclear. This study investigated whether spinorphin, an endogenous inhibitor of multiple enkephalinases, attenuates trigeminovascular activation and migraine-like responses in experimental migraine. Migraine-like pain was induced in male Wistar rats by nitroglycerin. The effects of spinorphin were evaluated using periorbital and plantar von Frey tests, followed by assessment of c-Fos levels in the trigeminal nucleus caudalis (TNC), calcitonin gene-related peptide (CGRP) levels in the trigeminal ganglion (TG) and TNC, and meningeal mast cell degranulation. Opioid receptor involvement was examined using nalmefene. In complementary ex vivo hemiskull preparations, capsaicin-evoked CGRP release was quantified, and the interaction between spinorphin and sumatriptan was investigated. Spinorphin dose-dependently alleviated cephalic and extracephalic mechanical hypersensitivity, reduced c-Fos levels, decreased CGRP concentrations in the TG and TNC, and inhibited meningeal mast cell degranulation. These protective effects were markedly attenuated by nalmefene, supporting the involvement of opioid receptor-mediated mechanisms. In ex vivo preparations, spinorphin selectively reduced capsaicin-induced CGRP levels in the superfusates without affecting basal CGRP levels, and this effect was abolished by nalmefene. Moreover, spinorphin enhanced the inhibitory effect of sumatriptan on capsaicin-stimulated CGRP levels. Spinorphin attenuates behavioral, neurochemical, and neuroinflammatory features of experimental migraine, at least partly through mechanisms involving endogenous opioid signaling. These findings suggest enkephalinase inhibition as a promising therapeutic approach for migraine and support further investigation of spinorphin as a potential adjunct to established antimigraine therapies.

PMID 42919102
阅读全文 →
PubMedActa otorrinolaringologica espanola2026-10-23

Compromised nasal skin in functional rhinoplasty: a literature review and proposal of a clinical management protocol.

Martínez-Villasmil Virginia V, Fernández-Míguez Marta M, Casanova-Ramón María M, Caldas-Pozuelo Carmen C et al.

Rhinoplasty is one of the most complex procedures in facial surgery, particularly in the context of revision surgery. The integrity of the nasal skin-soft tissue envelope (SSTE) is a critical factor for both aesthetic and functional outcomes, and vascular compromise of this structure may lead to one of the most feared complications: cutaneous necrosis. The aim of this review is to synthesize the available evidence regarding risk factors and therapeutic strategies in the management of compromised nasal skin following rhinoplasty. A literature review was conducted in PubMed and Embase to identify studies describing cutaneous necrosis following rhinoplasty surgery. The main risk factors identified were revision surgery, smoking, and aggressive thinning of the cutaneous flap. The available literature suggests that early initiation of therapies such as topical nitroglycerin, hyperbaric oxygen therapy, and pentoxifylline may improve tissue salvage in selected cases. A clinical protocol integrating preoperative assessment and an early intraoperative and postoperative management algorithm is proposed. Early identification of high-risk patients and the implementation of a standardized multimodal approach may help optimize skin viability in complex rhinoplasty procedures.

PMID 42914090
阅读全文 →
PubMedBMC cardiovascular disorders2026-10-23

Percutaneous closure of an iatrogenic left atrial-aortic perforation complicated by cardiac tamponade and coronary vasospasm during transseptal puncture: a case report.

Lee Jinho J, Lee Young Shin YS

Iatrogenic atrial-aortic perforation during transseptal puncture is a rare but potentially life-threatening complication. Percutaneous closure using dedicated occluder devices has emerged as a less invasive alternative to surgical repair in selected patients. A 68-year-old woman with hypertension and long-standing persistent atrial fibrillation (≥ 12 years) underwent catheter ablation. Pre-procedural imaging showed a markedly elevated left atrial (LA) volume (171 mL) with predominantly lateral enlargement. During a second transseptal puncture attempt, the sheath-dilator system inadvertently advanced through the LA wall and perforated the sinotubular junction of the aorta, confirmed by aortography. Although the sheath initially tamponaded the perforation, subsequent migration led to rapid hemopericardium requiring cardiopulmonary resuscitation (CPR) and emergent pericardiocentesis. With the access tract preserved, a 12/10 mm Amplatzer Duct Occluder was delivered percutaneously, achieving successful closure. Following device deployment, sudden cardiac arrest occurred due to diffuse coronary vasospasm, which resolved rapidly with intracoronary nitroglycerin. The patient was discharged in stable condition on an oral anticoagulant, a calcium channel blocker, and long-term nitrates. This case describes the successful percutaneous management of an iatrogenic LA-to-ascending aorta perforation during transseptal catheterization, complicated by cardiac tamponade and coronary vasospasm. This case suggests that careful attention is warranted not only during the septal puncture itself, but also during subsequent sheath advancement, even after successful entry into the LA has been confirmed.

PMID 42919139
阅读全文 →
PubMedThe journal of headache and pain2026-10-21

Targeting neuronal FKBP5 attenuates mechanical allodynia by suppressing NF-κB-mediated neuroinflammation in an NTG-induced chronic migraine mouse model.

Peng Cheng C, Fan Tianhua T, Zhou Gang G, Zhao Min M et al.

Chronic migraine (CM) is a debilitating neurological disorder characterized by persistent trigeminovascular sensitization and neuroinflammation. While FK506-binding protein 51 (FKBP5) modulates spinal neuroinflammation in chronic pain, its specific role in trigeminovascular nociceptive processing and CM pathogenesis remains largely unknown. We used a nitroglycerin (NTG)-induced CM mouse model. Following RNA-sequencing (RNA-seq) of total RNA isolated from trigeminal nucleus caudalis (TNC) tissue lysates, target expression was validated via reverse transcription quantitative PCR (RT-qPCR), Western blotting, and immunofluorescence. To establish causality, we used a neuron-specific CRISPR-Cas9 editing system for Fkbp5 knockout within the TNC, alongside pharmacological interventions using the specific FKBP5 antagonist SAFit2 and the nuclear factor kappa B (NF-κB) inhibitor PDTC. Migraine-like behaviors were evaluated using von Frey filaments, coupled with biochemical analyses of NF-κB cascade activation and trigeminovascular neuroinflammation. RNA-seq, RT-qPCR, Western blotting, and immunofluorescence consistently confirmed a marked upregulation of Fkbp5 mRNA and FKBP5 protein in the TNC of NTG-treated mice, predominantly localized to neurons. Concurrently, significant microglial and astrocytic activation was observed in the TNC. Both neuron-specific Fkbp5 knockout and pharmacological inhibition with SAFit2 significantly attenuated NTG-induced periorbital and hind paw mechanical allodynia. Furthermore, FKBP5 deficiency blunted the NTG-triggered phosphorylation of p65 and IκBα, effectively suppressing the downstream release of pro-inflammatory cytokines, including interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α), as well as the upregulation of calcitonin gene-related peptide (CGRP) and c-Fos. Crucially, targeted blockade of the NF-κB cascade with PDTC recapitulated the protective behavioral and biochemical effects of FKBP5 deficiency. We demonstrate that neuronal FKBP5 is significantly associated with CM pathogenesis. FKBP5 sustains mechanical allodynia by activating the NF-κB-mediated neuroinflammatory cascade. Consequently, targeting FKBP5 represents a promising therapeutic strategy for CM.

PMID 42902147
阅读全文 →

注册免费账户还可查看另外 9996 篇文献

免费注册查看全部文献 →

了解更多nitroglycerin