Puttick R M, Terrar D A
University Department of Pharmacology, Oxford, United Kingdom.
Anesth Analg. 1993 Jul;77(1):55-60. doi: 10.1213/00000539-199307000-00011.
We investigated the possibility that the effects of propofol on sarcoplasmic reticulum (SR) function may contribute to the myocardial depression induced by this anesthetic. With guinea pig isolated papillary muscles, the effects of propofol on transient alterations in contractility (termed "potentiated-state" contractions), after abrupt changes in stimulation frequency and brief periods of rest, were compared with those of enflurane and the inhibitor of SR function, ryanodine. These potentiated-state contractions are mediated by calcium derived largely from the SR. Propofol, enflurane, and ryanodine were applied at concentrations that produced approximately 50%-60% inhibition of "steady-state" contraction. Ryanodine abolished and enflurane attenuated the potentiated-state contractions, whereas propofol had no apparent effect. Although impairment of SR function may contribute to the depression of contractility induced by enflurane, propofol has no major effect on SR function.
我们研究了丙泊酚对肌浆网(SR)功能的影响可能导致这种麻醉剂引起心肌抑制的可能性。在豚鼠离体乳头肌实验中,将丙泊酚在刺激频率突然改变和短暂休息后对收缩性短暂变化(称为“增强状态”收缩)的影响,与恩氟烷和SR功能抑制剂Ryanodine的影响进行了比较。这些增强状态的收缩主要由来自SR的钙介导。丙泊酚、恩氟烷和Ryanodine均以产生约50%-60%“稳态”收缩抑制的浓度应用。Ryanodine消除了增强状态的收缩,恩氟烷使其减弱,而丙泊酚没有明显作用。虽然SR功能受损可能导致恩氟烷引起的收缩性降低,但丙泊酚对SR功能没有主要影响。