Positive inotropic effects of the beta 2-adrenoceptor agonist terbutaline in the human heart: effects of long-term beta 1-adrenoceptor antagonist treatment.
β 2-肾上腺素受体激动剂特布他林对人心脏的正性肌力作用: 长期 β 1-肾上腺素受体拮抗剂治疗的影响。

摘要

OBJECTIVES:This study was conducted to determine whether activation of cardiac beta 2-adrenoceptors increases contractility in humans and whether this is affected by long-term beta 1-adrenoceptor antagonist treatment.
BACKGROUND:Coexistence of beta 1- and beta 2-adrenoceptors in the human heart is generally accepted. The functional importance of cardiac beta 2-adrenoceptors for increases in contractility in humans, however, has not been completely established.
METHODS:We studied 1) the beta-adrenoceptor subtype mediating positive inotropic effects of the beta 2-adrenoceptor agonist terbutaline in vitro (on right atrial and left ventricular preparations from nonfailing human hearts) and increases in contractility (by measurement of systolic time intervals) in vivo in seven healthy male volunteers; and 2) in vivo whether long-term treatment of volunteers with the beta 1-adrenoceptor antagonist bisoprolol affects terbutaline-induced increases in contractility.
RESULTS:In vitro terbutaline caused a concentration-dependent increase in atrial and ventricular adenylate cyclase activity and force of contraction. Terbutaline effects were antagonized only by the beta 2-adrenoceptor antagonist ICI 118,551, indicating that they were mediated by beta 2-adrenoceptor stimulation. In vivo intravenous infusions of terbutaline (dose range 25 to 300 ng/kg body weight per min for 15 min) dose dependently increased heart rate and shortened the pre-ejection period and heart rate-corrected electromechanical systole (QS2) time. These effects are mediated predominantly by beta 2-adrenoceptor stimulation because they were only marginally affected by the beta 1-adrenoceptor antagonist bisoprolol (1 x 10 mg orally), either given 2 h before infusion or long term for 3 weeks.
CONCLUSIONS:Stimulation of cardiac beta 2-adrenoceptors in humans causes not only in vitro but also in vivo positive inotropic effects. Long-term beta 1-adrenoceptor antagonist treatment does not considerably affect beta 2-adrenoceptor-mediated in vivo increases in contractility. Thus, it may be possible to treat patients with chronic heart failure and long-term beta 1-adrenoceptor antagonist therapy with beta 2-adrenoceptor agonists if immediate inotropic support is needed.

译文

目的: 本研究旨在确定心脏 β 2-肾上腺素受体的激活是否会增加人体的收缩力,以及这是否受到长期 β 1-肾上腺素受体拮抗剂治疗的影响。
背景: 人类心脏中 β 1-和 β 2-肾上腺素受体的共存被普遍接受。然而,心脏 β 2-肾上腺素受体对增加人体收缩力的功能重要性尚未完全确定。
方法: 我们研究了 1) β-肾上腺素受体亚型在体外介导 β-肾上腺素受体激动剂特布他林的正性肌力作用 (对来自正常心脏的右心房和左心室制剂) 和七名健康男性志愿者体内收缩力的增加 (通过测量收缩时间间隔); 和 2)体内长期使用 β 1-肾上腺素受体拮抗剂比索洛尔治疗志愿者是否影响特布他林诱导的收缩力增加。
结果: 特布他林在体外引起心房和心室腺苷酸环化酶活性和收缩力的浓度依赖性增加。特布他林效应仅被 β 2-肾上腺素受体拮抗剂 ICI 118,551 所拮抗,这表明它们是由 β 2-肾上腺素受体刺激介导的。特布他林的体内静脉输注 (剂量范围 25 至 300 纳克/千克体重/分钟,持续 15 分钟) 剂量依赖性地增加心率,缩短射血前期和心率校正的机械机械收缩 (QS2) 时间。这些影响主要由 β 2-肾上腺素受体刺激介导,因为它们仅受 β 1-肾上腺素受体拮抗剂比索洛尔 (口服 1 × 10 毫克) 的轻微影响, 输注前 2 小时或长期 3 周。
结论: 人类心脏 β 2-肾上腺素受体的刺激不仅在体外引起,而且在体内引起正性肌力效应。长期 β 1-肾上腺素受体拮抗剂治疗不会显著影响 β 2-肾上腺素受体介导的体内收缩力增加。因此,如果需要即时的正性肌力支持,也许可以用 β 2-肾上腺素受体激动剂治疗慢性心力衰竭患者和长期 β 1-肾上腺素受体拮抗剂治疗。

Terbutaline

呼吸 选择性β2受体激动药 药物
概述  :  

基本信息 药品“喘康速”药物成分为硫酸特布他林。硫酸特布他林化学式:(士)α-[(叔丁氨基)甲基]-3,5-二羟基苯甲醇硫酸盐(2:1)。硫酸特布他林分子式:(C12H19NO3)·H2SO4。硫酸特布他林分子量:548.66。 作用机制特布他林(间羟叔丁肾上腺素)为高选择性β2受体激动药,对支气管β2受体的选择性与沙丁胺醇相似,对心脏的兴奋作用仅为沙丁胺醇的1/10。可舒张支气管平滑肌,并能抑制肥大细胞释放组胺等过敏物质,尚有增加纤毛-黏液毯廓清能力,促进痰液排出,减轻咳嗽症状。&n

terbutaline   /tə'bju:təli:n/ 

       n. 特布他林;间羟舒喘宁;间羟叔丁肾上腺素

       A recent study conducted at Duke University illustrated the risk of terbutaline to infants. 最近杜克大学一项研究说明了特布他林对婴儿的危害。

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