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机构地区:[1]中国科学院上海生理研究所
出 处:《生理学报》1991年第6期589-593,共5页Acta Physiologica Sinica
基 金:国家自然科学基金资助;No.370227
摘 要:实验在去双侧外周化学感受器传入的麻醉雄性家兔上进行。给动物吸低氧混合气(10%O_2于N_2中)导致通气抑制后,从动物侧脑室注入β-内啡肽拮抗剂纳洛酮使抑制的通气被“翻转”;注入拟似剂羟甲芬太尼则使抑制更加深化。此时中枢5-羟色胺含量均较给药前明显升高。给动物注入外源性5-羟色胺后,中枢β-内啡肽含量较给药前明显下降,此时通气回复至对照水平。结果提示:中枢β-内啡肽系统是引起低氧通气抑制的基本和直接因素,而5-羟色胺系统则是作为一种神经调质,通过调制其β-内啡肽活动而间接对低氧通气反应产生影响。Experiments were performed on anesthetized bilaterally chemodenervatedrabbits.After giving hypoxic gas mixture(10% O_2 in N_2)to animals to causeventiIatory inhibition,lateral ventricle applications of β-endorphins(β-EP)antagonist naloxone(Nix)and agonist ohmefentanyl(OMF)respectivelyreduced and enhanced hypoxia-induced ventilatory inhibition.Meanwhile thelevel of central serotonin(5-HT)was obviously increased more than that beforethe drug administration.Injection of exogenous 5-HT into rabbit lateral ven-tricle induced central β-EP content to decrease markedly while minute ventila-tion(V_E)was returned to control at the same time.The results suggest thatβ-EP system in CNS is the basic and direct element in the regulatory mechanismof hypoxic ventilatory inhibition,and central 5-HT system only acts as a neuro-modulator in modulating the activity of β-EP system to indirectly affect ven-titatory response to hypoxia.
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