EFFECT OF ALPHA-ADRENERGIC STIMULATION ON ISOLATED VENTRICULAR MYOCYTES

α1-肾上腺素能刺激对大鼠肌力的影响 心肌仍有争议。正性变力作用有 本有很好的记载，而且它的前面通常有一个短暂的 收缩能力下降。此外，持续的负面影响 刺激Alpha1的变力作用也已在 多细胞心脏制剂。这项研究的目的是 以表征刺激α1对胞浆的影响 Ca2(CaI)瞬变及其对单根收缩特性的影响 状态下的心室肌细胞导致 抽动幅度的增强或降低。 分离的大鼠心室肌细胞，用普萘洛尔预处理。 用来研究α-肾上腺素能刺激的作用 苯肾上腺素对抽动幅度(TA)和频率的影响 自发收缩波(CW)，它代表 自发性钙释放的机械性表达 肌浆网(SR)。在1 mm浴缸(CaO)中， 在0.2赫兹的场强刺激下，α1具有正性变力作用 它被哌唑嗪可逆地废除了，并达到相当大的 程度似乎与肌丝反应性增加有关 对Ca~(2+)的作用以及对CaI波幅的增强 与抽搐相关的瞬变。B.在0.2秒的刺激期间 在d mm CaO中，在某些舒张期出现CW。 苯肾上腺素消除了它们，降低了TA。这张底片 效果与平行观察到的积极行动形成对比 在1 mm CaO中研究。在类似的加载心肌细胞的实验中 钙离子探针INDO-1 AM检测α1对TA的负性作用 与CAI波幅的降低有关 转瞬即逝。C.在没有刺激的情况下，在d mm CaO中，字母1 显著且可逆地降低了CW频率。这一效果 可以被α1阻滞剂哌唑嗪所预防。这些发现 都与α1-肾上腺素能 对心肌细胞的刺激可以根据细胞内的不同而不同 (CA2)。

The effect of alpha1-adrenergic stimulation on the inotropy of the myocardium is still controversial. A positive inotropic effect has ben well documented and it is often preceded by a short lived decrease in contractility. Additionally a persistent negative inotropic effect of alpha1 stimulation has also been described in multicellular cardiac preparations. The purpose of this study was to characterized the effect of alpha1 stimulation on the cytosolic Ca2+ (Cai) transient and on the contractile properties of single ventricular myocytes under condition leading either to an enhancement or a decrease in twitch amplitude. Isolated rat ventricular myocytes, pretreated with propranolol were used to investigate the effect of alpha1-adrenergic stimulation with phenylephrine on twitch amplitude (TA) and on the frequency of spontaneous contractile waves (CW), which represent the mechanical expression of spontaneous Ca2+ release from the sarcoplasmic reticulum (SR). In 1 mM bathing (Ca2+) (Cao), during field stimulation at 0.2 Hz, alpha1 had a positive inotropic effect which was reversibly abolished by prazosin and to a considerable extent appeared related to an increased myofilament responsiveness to Ca2+ in addition to some enhancement in the amplitude of the Cai transient associated with the twitch. b. During stimulation at 0.2 hz, in d mM Cao, CW appeared in some of the diastolic intervals. Phenylephrine abolished them and decreased TA. This negative effects was in contrast to the positive action observed in parallel studies in 1 mM Cao. In similar experiments with myocytes loaded with the Ca2+ probe Indo-1 AM the negative effect of alpha1 on TA was associated with a decrease in the amplitude of the Cai transient. c. In the absence of stimulation, in d mM Cao, alpha1 significantly and reversibly reduced CW frequency. This effect could be prevented by the alpha1 blocker prazosin. These findings are consistent with the view that the effect of alpha1-adrenergic stimulation of cardiac cells can vary in relation to intracellular (Ca2+).