Ostman M, Henriksson R, Sundström S, Reiz S
Anesthesiology. 1986 Jun;64(6):734-8. doi: 10.1097/00000542-198606000-00010.
Adrenergic receptor interaction with isoflurane was studied in an in vitro rat parotid gland model in which beta-adrenoceptor agonists evoke amylase release and alpha-adrenoceptor agonists induce potassium secretion from parotid cells. The amylase secretory studies were performed using a batch-incubation technique, and potassium efflux was evaluated using 86Rb+ as a probe for K+. Isoflurane was dissolved in a fat emulsion, which of its own had no secretory effect. Isoflurane induced a dose-dependent amylase release that was unaffected by beta-adrenergic blockade with propranolol and metoprolol. Isoflurane also induced a significant efflux of 86Rb+ that could not be inhibited by the alpha-adrenoceptor antagonist, phentolamine. Dinitrophenol, an uncoupler of oxidative phosphorylation, had no effect on the isoflurane-induced enzyme release, indicating that amylase secretion occurred by passive leakage. It is suggested that isoflurane has no direct action on alpha- or beta-adrenoceptors. Isoflurane, however, induces potent cellular events that might be due to an unspecific effect on the cell membrane, thereby causing changes in membrane permeability.
在体外大鼠腮腺模型中研究了肾上腺素能受体与异氟烷的相互作用，在该模型中，β-肾上腺素能受体激动剂可引起淀粉酶释放，α-肾上腺素能受体激动剂可诱导腮腺细胞分泌钾。淀粉酶分泌研究采用批量孵育技术进行，钾外流用86Rb+作为K+的探针进行评估。异氟烷溶解于脂肪乳剂中，脂肪乳剂本身无分泌作用。异氟烷诱导剂量依赖性的淀粉酶释放，普萘洛尔和美托洛尔对β-肾上腺素能的阻断对此无影响。异氟烷还诱导了显著的86Rb+外流，这不能被α-肾上腺素能受体拮抗剂酚妥拉明抑制。氧化磷酸化解偶联剂二硝基苯酚对异氟烷诱导的酶释放无影响，表明淀粉酶分泌是通过被动渗漏发生的。提示异氟烷对α-或β-肾上腺素能受体无直接作用。然而，异氟烷可诱导强烈的细胞事件，这可能是由于对细胞膜的非特异性作用，从而导致膜通透性改变。
