更新于：2024-06-29
Isoprenaline Hydrochloride
盐酸异丙肾上腺素
更新于：2024-06-29
概要
基本信息
最高研发阶段批准上市 |
首次获批日期 美国 (1956-03-09) |
最高研发阶段(中国)- |
特殊审评- |
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结构
分子式C11H18ClNO3 |
InChIKeyIROWCYIEJAOFOW-MERQFXBCSA-N |
CAS号5984-95-2 |
关联
20
项与 盐酸异丙肾上腺素 相关的临床试验Comparison of the Clinical Utility of Atropine and Isoprenaline in the Invasive Diagnosis of Arrhythmias
Sympathetic Neurovascular Transduction: Role of Adrenergic Receptors and Sex Differences
Sex Disparities in Hypoxic Vasodilation and Impact of Obesity
100 项与 盐酸异丙肾上腺素 相关的临床结果
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100 项与 盐酸异丙肾上腺素 相关的转化医学
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100 项与 盐酸异丙肾上腺素 相关的专利（医药）
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22,423
项与 盐酸异丙肾上腺素 相关的文献（医药）2024-03-01Journal of molecular and cellular cardiology
Dual effect of cardiac FKBP12.6 overexpression on excitation-contraction coupling and the incidence of ventricular arrhythmia depending on its expression level
Article
作者: Pereira, Laetitia ; Gomez, Susana ; Val-Blasco, Almudena ; Gerbaud, Pascale ; Mercier-Nomé, Françoise ; Mercadier, Jean-Jacques ; Journé, Clément ; Benitah, Jean-Pierre ; Lefebvre, Florence ; Oughlis, Célia ; Courilleau, Delphine ; Gandon-Renard, Marine ; Gómez, Ana Maria
FKBP12.6, a binding protein to the immunosuppressant FK506, which also binds the ryanodine receptor (RyR2) in the heart, has been proposed to regulate RyR2 function and to have antiarrhythmic properties. However, the level of FKBP12.6 expression in normal hearts remains elusive and some controversies still persist regarding its effects, both in basal conditions and during β-adrenergic stimulation. We quantified FKBP12.6 in the left ventricles (LV) of WT (wild-type) mice and in two novel transgenic models expressing distinct levels of FKBP12.6, using a custom-made specific anti-FKBP12.6 antibody and a recombinant protein. FKBP12.6 level in WT LV was very low (0.16 ± 0.02 nmol/g of LV), indicating that <15% RyR2 monomers are bound to the protein. Mice with 14.1 ± 0.2 nmol of FKBP12.6 per g of LV (TG1) had mild cardiac hypertrophy and normal function and were protected against epinephrine/caffeine-evoked arrhythmias. The ventricular myocytes showed higher [Ca2+]i transient amplitudes than WT myocytes and normal SR-Ca2+ load, while fewer myocytes showed Ca2+ sparks. TG1 cardiomyocytes responded to 50 nM Isoproterenol increasing these [Ca2+]i parameters and producing RyR2-Ser2808 phosphorylation. Mice with more than twice the TG1 FKBP12.6 value (TG2) showed marked cardiac hypertrophy with calcineurin activation and more arrhythmias than WT mice during β-adrenergic stimulation, challenging the protective potential of high FKBP12.6. RyR2R420Q CPVT mice overexpressing FKBP12.6 showed fewer proarrhythmic events and decreased incidence and duration of stress-induced bidirectional ventricular tachycardia. Our study, therefore, quantifies for the first time endogenous FKBP12.6 in the mouse heart, questioning its physiological relevance, at least at rest due its low level. By contrast, our work demonstrates that with caution FKBP12.6 remains an interesting target for the development of new antiarrhythmic therapies.
2024-03-01Acta pharmacologica Sinica
Isoproterenol induces MD2 activation by β-AR-cAMP-PKA-ROS signalling axis in cardiomyocytes and macrophages drives inflammatory heart failure
Article
作者: Luo, Wu ; Qian, Jin-Fu ; Wu, Gao-Jun ; Xu, Jia-Chen ; Huang, Wei-Jian ; Liang, Shi-Qi ; Wang, Qin-Yan ; Liang, Guang
Cardiac inflammation contributes to heart failure (HF) induced by isoproterenol (ISO) through activating β-adrenergic receptors (β-AR). Recent evidence shows that myeloid differentiation factor 2 (MD2), a key protein in endotoxin-induced inflammation, mediates inflammatory heart diseases. In this study, we investigated the role of MD2 in ISO-β-AR-induced heart injuries and HF. Mice were infused with ISO (30 mg·kg-1·d-1) via osmotic mini-pumps for 2 weeks. We showed that MD2 in cardiomyocytes and cardiac macrophages was significantly increased and activated in the heart tissues of ISO-challenged mice. Either MD2 knockout or administration of MD2 inhibitor L6H21 (10 mg/kg every 2 days, i.g.) could prevent mouse hearts from ISO-induced inflammation, remodelling and dysfunction. Bone marrow transplantation study revealed that both cardiomyocyte MD2 and bone marrow-derived macrophage MD2 contributed to ISO-induced cardiac inflammation and injuries. In ISO-treated H9c2 cardiomyocyte-like cells, neonatal rat primary cardiomyocytes and primary mouse peritoneal macrophages, MD2 knockout or pre-treatment with L6H21 (10 μM) alleviated ISO-induced inflammatory responses, and the conditioned medium from ISO-challenged macrophages promoted the hypertrophy and fibrosis in cardiomyocytes and fibroblasts. We demonstrated that ISO induced MD2 activation in cardiomyocytes via β1-AR-cAMP-PKA-ROS signalling axis, and induced inflammatory responses in macrophages via β2-AR-cAMP-PKA-ROS axis. This study identifies MD2 as a key inflammatory mediator and a promising therapeutic target for ISO-induced heart failure.
2024-12-01Molecular biology reports
Co-treatment with bone marrow-derived mesenchymal stem cells and curcumin improved angiogenesis in myocardium in a rat model of MI
Article
作者: Abedpour, Neda ; Mirfakhraie, Niki ; Javanmard, Masoumeh Zirak ; Shoorei, Hamed
BACKGROUND:
The cardioprotective properties of mesenchymal stem cells and the therapeutic potential of curcumin (CUR) have been explored. Combining these approaches may enhance stem cell effectiveness and expedite healing. This study aimed to investigate the synergistic effects of co-treating bone marrow mesenchymal stem cells (BMSCs) with curcumin on vascular endothelial growth factor (VEGF) levels, in a rat model of myocardial ischemia (MI).
METHODS AND RESULTS:
Sixty-five male rats were divided into four groups: G1 (healthy control), G2 (MI induced by isoproterenol hydrochloride), G3 (treated with BMSCs), and G4 (co-treated with curcumin and BMSCs). Blood and tissue samples were collected at specific time points (day 1, 7, 15 and 21) after MI induction. Serum levels of lactate dehydrogenase (LDH), creatine kinase (CK), cardiac troponin I (cTnI), aspartate aminotransferase (AST), CK-MB and VEGF were measured. VEGF mRNA and protein expression were evaluated using RT-qPCR and Western blot techniques. Histopathological assessments were performed using H&E staining and CD31 immunofluorescence staining. VEGF expression significantly increased on days 7 and 15 in the CUR-BMSCs group, peaking on day 7. Western blot analysis confirmed elevated VEGF protein expression on days 7 and 15 post-MI. ELISA results demonstrated increased serum VEGF levels on days 7 and 15, reaching the highest level on day 7 in CUR-BMSCs-treated animals. Treated groups showed lower levels of LDH, AST, CK, CK-MB and cTnI compared to the untreated MI group. H&E staining revealed improved myocardial structure, increased formation of new capillaries, in both treatment groups compared to the MI group.
CONCLUSION:
Combining curcumin with BMSCs promotes angiogenesis in the infarcted myocardium after 15 days of MI induction. These findings suggest the potential of this combined therapy approach for enhancing cardiac healing and recovery.
100 项与 盐酸异丙肾上腺素 相关的药物交易
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研发状态
10 条最早获批的记录, 后查看更多信息
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| 适应症 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|
| 心动过缓 | 日本 | 1987-04-16 | |
| 癫痫发作 | 日本 | 1987-04-16 | |
| 眩晕 | 日本 | 1975-12-09 | |
| 阿-斯综合征 | 美国 | 1956-05-25 | |
| 支气管痉挛 | 美国 | 1956-05-25 |
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临床结果
临床结果
适应症
分期
评价
查看全部结果
N/A | 22,435 | Central neuraxial anesthesia+Glycopyrrolate+dopamine+Hydroxyethyl starch solutions+Epinephrine+desflurane+bupivacaine+Sodium Chloride 0.9%+propofol+atropine+Ephedrine+Isoflurane+Dobutamine+Vasopressin+Isoproterenol+norepinephrine+Prilocaine+Benzocaine+Procaine+Terlipressin+Tetracaine+ropivacaine+Articaine+levobupivacaine+Milrinone+phenylephrine+Sevoflurane+Mepivacaine+lidocaine+Chloroprocaine (Usual Care Group) | 鬱觸觸窪憲選遞壓構餘(顧艱繭襯構願壓鑰鹽艱) = 窪艱壓糧齋膚顧獵網糧 齋艱獵廠製襯築繭網簾 (構顧願觸糧窪獵遞鹽鹹, 鑰憲衊鬱艱淵繭襯鏇餘 ~ 醖衊壓鏇齋鏇糧餘鑰廠) 更多 | - | 2019-05-16 | ||
Central neuraxial anesthesia+Glycopyrrolate+dopamine+Hydroxyethyl starch solutions+Epinephrine+desflurane+bupivacaine+Sodium Chloride 0.9%+propofol+atropine+Ephedrine+Isoflurane+Dobutamine+Vasopressin+Isoproterenol+norepinephrine+Prilocaine+Benzocaine+Procaine+Terlipressin+Tetracaine+ropivacaine+Articaine+levobupivacaine+Milrinone+phenylephrine+Sevoflurane+Mepivacaine+lidocaine+Chloroprocaine (Hypotension Decision Support) | 鬱觸觸窪憲選遞壓構餘(顧艱繭襯構願壓鑰鹽艱) = 觸繭蓋製觸餘繭積願顧 齋艱獵廠製襯築繭網簾 (構顧願觸糧窪獵遞鹽鹹, 積鏇廠範鏇網構鏇憲壓 ~ 醖網觸鹹繭醖齋簾齋窪) 更多 | ||||||
N/A | 40 | (Healthy Seniors) | 鏇襯壓願積糧範鬱積鹹(夢積窪網窪蓋獵鬱構選) = 鑰憲範築選觸鬱鬱簾製 壓糧簾憲顧製鏇齋齋觸 (鹽窪鏇鹽膚製範遞壓醖, 淵鏇鏇製築衊積鬱選蓋 ~ 製夢選獵醖鹽襯觸願鑰) 更多 | - | 2019-04-23 | ||
(HFpEF) | 鏇襯壓願積糧範鬱積鹹(夢積窪網窪蓋獵鬱構選) = 簾憲網鹽獵築餘膚襯糧 壓糧簾憲顧製鏇齋齋觸 (鹽窪鏇鹽膚製範遞壓醖, 願獵襯網鑰構網願鏇觸 ~ 醖願築範築鏇憲鏇夢餘) 更多 | ||||||
N/A | 1,712 | isoproterenol | 壓蓋憲繭鬱觸艱餘鬱觸(艱壓齋淵夢廠獵襯鏇艱) = 壓餘壓鑰簾衊膚鏇齋簾 鑰膚觸淵夢艱鹹齋壓窪 (壓築衊糧壓淵衊餘鹹願 ) | - | 2018-03-18 | ||
isoproterenol | 壓蓋憲繭鬱觸艱餘鬱觸(艱壓齋淵夢廠獵襯鏇艱) = 憲壓齋憲鏇鬱築觸憲齋 鑰膚觸淵夢艱鹹齋壓窪 (壓築衊糧壓淵衊餘鹹願 ) | ||||||
临床2期 | 131 | (Adenosine and Isoproterenol) | 鏇淵衊鏇淵醖鏇製窪網(襯鏇壓醖顧積範網選繭) = 繭構鑰艱網餘製遞鑰艱 製願繭蓋鹹簾壓齋窪淵 (廠餘鏇膚淵鏇鹹製網齋, 夢獵鏇憲憲遞鹽鏇廠觸 ~ 壓網衊簾膚鏇襯鬱鑰艱) 更多 | - | 2017-12-13 | ||
(Isoproterenol) | 鏇淵衊鏇淵醖鏇製窪網(襯鏇壓醖顧積範網選繭) = 膚鬱製構蓋蓋鏇積衊鑰 製願繭蓋鹹簾壓齋窪淵 (廠餘鏇膚淵鏇鹹製網齋, 願鬱製襯蓋鏇鏇積顧膚 ~ 構網蓋繭餘衊積餘鬱蓋) 更多 | ||||||
N/A | 224 | 選顧鬱膚憲憲築衊願襯(獵蓋壓窪餘鏇網鹹餘遞) = 醖膚鏇襯顧廠醖艱鏇齋 鏇築積淵選鹹製遞廠築 (選蓋膚蓋鑰鑰積築餘築 ) | - | 2016-08-30 | |||
N/A | 20 | 網遞獵窪膚襯網窪觸鑰(鬱醖獵構繭網築糧選顧) = 鹹選鬱鏇醖觸鹽製鹽製 顧網顧選艱範蓋製淵糧 (憲糧顧夢淵獵窪獵願蓋, 選積繭衊淵鏇選齋獵蓋 ~ 壓鏇餘鬱願網鹹鑰顧築) 更多 | - | 2015-02-23 | |||
临床1/2期 | 10 | 淵選顧範遞糧觸鏇鬱糧(淵壓膚網觸獵鑰淵繭餘) = 願觸積餘艱鏇遞簾衊鹹 鏇顧觸艱襯窪獵襯夢齋 (願觸製窪鬱壓艱鬱糧夢, 遞壓選遞艱鹽範襯繭範 ~ 鏇醖築齋遞醖積鬱鑰鬱) 更多 | - | 2012-06-22 |
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