Komai H, Rusy B F
Anesth Analg. 1982 May;61(5):403-9.
The effect of halothane on the availability of different sources of activator calcium for myocardial contraction was evaluated in relationship to the negative inotropic effect on the anesthetic. This was studied in rabbit papillary muscle under various stimulation conditions that are known to vary the importance of one or another of two sources of Ca2+ for production of contraction. The rested-state contraction is known to depend primarily on the transsarcolemmal influx of Ca2+ for its activation whereas the potentiated-state contraction is dependent largely on Ca2+ released from intracellular stores. In the presence of 0.6% halothane (gas phase) the rested-state and potentiated-state contractions were depressed (mean +/- SEM) 38% +/- 5% (n = 15) and 32% +/- 3% (n = 7), respectively (no statistically significant difference). Halothane accelerated the decay of the potentiated state, indicating that it stimulates the loss of Ca2+ from internal stores. Halothane also acted to slow the time course of force increase following restimulation of rested muscles, indicating that it inhibits the filling of internal stores. These observations suggest that the negative inotropic effect of halothane is caused by a combination of quantitatively similar effects of the anesthetic on the transsarcolemmal and intracellular sources of activator Ca2+.
研究了氟烷对心肌收缩时不同激活钙源可用性的影响，并将其与该麻醉药的负性肌力作用联系起来。在兔乳头肌中，于各种已知会改变两种钙源中某一种对收缩产生的重要性的刺激条件下进行了此项研究。已知静息状态下的收缩主要依赖跨肌膜钙内流来激活，而增强状态下的收缩很大程度上依赖于从细胞内储存释放的钙。在存在0.6%氟烷（气相）的情况下，静息状态和增强状态下的收缩分别降低了（平均值±标准误）38%±5%（n = 15）和32%±3%（n = 7）（无统计学显著差异）。氟烷加速了增强状态的衰减，表明它刺激了细胞内储存钙的流失。氟烷还使静息肌肉再次刺激后力量增加的时间进程变慢，表明它抑制了细胞内储存的充盈。这些观察结果表明，氟烷的负性肌力作用是由该麻醉药对跨肌膜和细胞内激活钙源产生的数量上相似的作用共同导致的。
