Nuffield Department of Anaesthetics, John Radcliffe Hospital, Oxford, UK.
Adv Exp Med Biol. 2010;669:201-4. doi: 10.1007/978-1-4419-5692-7_40.
The purpose of this study was to ascertain if effects of halothane and sevoflurane (0.18-1.45 MAC) on the magnitude of the rise in intracellular calcium ([Ca(2+)]i with approximately 90s hypoxia (measured using indo-1 dye) in rat pup carotid body type I glomus cells. paralleled their known effects on the human hypoxic ventilatory response, where halothane is more depressive. We also assessed these agents' effect on [Ca(2+)]i response to 100 mM K(+). Halothane depressed the [Ca(2+])i transient in hypoxia more than sevoflurane (p = 0.036). Both agents also depressed the [Ca(2+)]i response to K+ - halothane more than sevoflurane (p = 0.004). These actions reflect their known influence on human hypoxic ventilatory response, consistent with the notion that the cellular process underlies the whole-body effect. The responses to K(+), which depolarises the cell membrane, indicates that in addition to a putative effect on K(+) channels, voltage-activated Ca(2+) channels may also be involved in the anaesthetic effect.
本研究旨在确定氟烷和七氟醚(0.18-1.45MAC)对大鼠幼仔颈动脉体 I 型球细胞内钙浓度升高幅度的影响[Ca(2+)]i 在大约 90s 缺氧(用 indo-1 染料测量),类似于它们对人类缺氧性呼吸反应的已知影响,其中氟烷的抑制作用更强。我们还评估了这些药物对 100mM K(+)诱导的[Ca(2+)]i 反应的影响。氟烷对缺氧时[Ca(2+)]i 瞬变的抑制作用强于七氟醚(p=0.036)。两种药物对 K+诱导的[Ca(2+)]i 反应的抑制作用也强于七氟醚(p=0.004)。这些作用反映了它们对人类缺氧性呼吸反应的已知影响,与细胞过程是全身效应基础的观点一致。对细胞膜去极化的 K(+)的反应表明,除了对 K(+)通道的假定作用外,电压激活的 Ca(2+)通道也可能参与麻醉作用。