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基本信息
去甲腎上腺素鹽酸鹽[干冰運(yùn)輸
levophedhydrochloride
L-ARTERENOL HYDROCHLORIDE
(-)-ARTERENOL HYDROCHLORIDE
L-NORADRENALINE HYDROCHLORIDE
L-NOREPINEPHRINE HYDROCHLORIDE
[2-(3,4-dihydroxyphenyl)-2-hydroxyethyl]azanium chloride
[2-(3,4-dihydroxyphenyl)-2-hydroxy-ethyl]azanium chloride
[2-(3,4-dihydroxyphenyl)-2-hydroxy-ethyl]ammonium chloride
(R)-4-(2-Amino-1-hydroxyethyl)benzene-1,2-diol hydrochloride
物理化學(xué)性質(zhì)
安全數(shù)據(jù)
常見(jiàn)問(wèn)題列表
去甲腎上腺素鹽酸鹽既是一種神經(jīng)遞質(zhì),主要由交感節(jié)后神經(jīng)元和腦內(nèi)腎上腺素能神經(jīng)末梢合成和分泌,是后者釋放的主要遞質(zhì),也是一種激素,由腎上腺髓質(zhì)合成和分泌,但含量較少。循環(huán)血液中的去甲腎上腺素主要來(lái)自腎上腺髓質(zhì)。對(duì)α受體具有強(qiáng)大激動(dòng)作用,對(duì)心臟β1受體作用較弱,對(duì)β2受體幾無(wú)作用。
去甲腎上腺素(Norepinephrine),學(xué)名1?(3,4?二羥苯基)?2?氨基 乙醇,是腎上腺素去掉N?甲基后形成的物質(zhì), 去甲腎上腺素既是一種神經(jīng)遞質(zhì),主要由交感節(jié)后神經(jīng)元和腦內(nèi) 腎上腺素能神經(jīng)末梢合成和分泌,是后者釋放的主要遞質(zhì),也是一種激素,由腎上腺髓質(zhì)合成和分泌,但含量較少。循環(huán)血液中的去甲腎 上腺素主要來(lái)自腎上腺髓質(zhì)。
藥用去甲腎上腺素是一種腎上腺素受體激動(dòng)藥,有收縮血管、升高血壓的作用,主要用于搶救急性低血癥和周?chē)軘U(kuò)張所引起的休克等。去甲腎上腺素中具有旋光性,左旋體療效較右旋體大27倍。藥用去甲腎上腺素主要由人工合成。
在補(bǔ)足血容量的前提下,用5%葡萄糖或葡萄糖鹽水稀釋后靜滴,成人開(kāi)始以8~12μg/min速度滴注,調(diào)整滴速使血壓升至理想水平。維持量為2~4μg/min。在必要時(shí)可超越以上劑量。小兒常以每分鐘0.02~0.1μg/kg速度滴注,按需要調(diào)節(jié)滴速。本品不宜皮下或肌內(nèi)注射。
藥液外漏可引起局部組織壞死。靜脈輸注時(shí)沿靜脈徑路皮膚變白、紫紺。嚴(yán)重眩暈。本品可使生命器官血流減少,在缺氧、電解質(zhì)失衡等條件下或過(guò)量時(shí)可出現(xiàn)高血壓、心律失常、心率緩慢,頭痛嘔吐甚至抽搐。常有焦慮不安、眩暈、頭痛、蒼白、心跳重感、失眠等持續(xù)不良反應(yīng)。本品有過(guò)敏反應(yīng),孕婦及哺乳期婦女、缺氧、閉塞性血管病、血栓形成者慎用。
應(yīng)用中必須監(jiān)測(cè)中心靜脈壓、肺動(dòng)脈舒張壓、尿量、心電圖等。本品與全麻藥必須同用時(shí)要減量;與β受體阻滯劑、降壓藥、洋地黃類(lèi)分別合用時(shí)可引起高血壓、心律失常;與麥角制劑、三環(huán)類(lèi)抗抑郁藥、甲狀腺激素同時(shí)使用時(shí),血管收縮作用增強(qiáng)。
EC50: 5.37 μM (β 1 -selective adrenergic receptor)
Norepinephrine (NE) bitartrate monohydrate is generally considered to be a β 1 -subtype selective adrenergic agonist. Norepinephrine(NE) also has direct activity at the β 2 -adrenoceptor in higher concentrations. Adipocytes from the inguinal fat pad (iWA) or the interscapular fat pad (BA) are isolated from neonatal wild-type C57BL/6J mice and cultured. To examine the effect of activating AT2 upon β-adrenergic signaling, cAMP production is first assessed in response to Norepinephrine (NE, 10 μM) with or without CGP (10 nM) co-treatment. Norepinephrine (NE) increases cAMP as expected in iWA, and CGP does not alter this effect. Norepinephrine (NE) is also known to induce lipolysis, and liberated fatty acids are required to functionally activate UCP1 protein and to stimulate heat production. CREB phosphorylation at Ser133 is increased after Norepinephrine (NE) treatment and significantly attenuated with CGP co-treatment in mouse iWA.