Department of Physiology, University of Alberta, Alberta, Canada.
Adv Exp Med Biol. 2010;669:123-7. doi: 10.1007/978-1-4419-5692-7_25.
Caffeine counters endogenous or drug-evoked depression of breathing in (preterm) infants. Despite its common clinical use, little is known on central nervous mechanisms of its stimulatory respiratory action. We show that millimolar concentrations of caffeine are needed in perinatal rat en bloc medullas and medullary slices for stimulation of fictive inspiratory rhythms that were either endogenously slow in fetuses or depressed by prostagandins or opioids. Findings suggests that caffeine blocks phospodiesterase-4 thus raising cAMP in rhythmogenic pre-Bötzinger complex (preBötC) networks and/or cells driving the inspiratory preBötC.
咖啡因可对抗（早产儿）婴儿内源性或药物引起的呼吸抑制。尽管其在临床上被广泛应用，但对于其刺激呼吸作用的中枢神经机制知之甚少。我们的研究表明，在围产期大鼠整体脑髓和脑髓切片中，需要用到毫摩尔浓度的咖啡因，才能刺激内源性呼吸频率较慢的胎儿的模拟吸气节律，或刺激由前列腺素或阿片类药物引起的呼吸抑制。这些发现表明，咖啡因可阻断磷酸二酯酶-4，从而使呼吸节律生成区（pre-Bötzinger 复合体，preBötC）网络和/或驱动吸气 preBötC 的细胞中的 cAMP 升高。
