Lumbers E R, McCloskey D I, Potter E K, Courtice G P
J Auton Nerv Syst. 1986 May;16(1):23-34. doi: 10.1016/0165-1838(86)90049-4.
The effects of hypoxia on the potential for the vagus to slow the heart, and on resting heart rate, were compared in anesthetized, vagotomized adult and fetal sheep, and in a chronically catheterized fetus in utero. In adults, the action of the cardiac vagus was potentiated at and below an arterial pO2 in the range 13-27 mm Hg. In contrast, in the fetus and the neonate, vagal action was not potentiated as pO2 fell through this range to 10-12 mm Hg. Below 10-12 mm Hg baseline heart rate fell markedly, and the effect of the cardiac vagus on heart rate was diminished, but its effect on pulse interval was not consistently changed. It is concluded that potentiation of vagal action during hypoxia occurs in adult but not fetal sheep and the bradycardia seen in the fetus during severe hypoxia is probably due to direct myocardial depression.
在麻醉状态下、切断迷走神经的成年和胎儿绵羊以及慢性插管的宫内胎儿中,比较了缺氧对迷走神经减慢心率的作用以及对静息心率的影响。在成年绵羊中,当动脉血氧分压在13 - 27毫米汞柱范围内及以下时,心脏迷走神经的作用增强。相比之下,在胎儿和新生儿中,当血氧分压在此范围内降至10 - 12毫米汞柱时,迷走神经作用并未增强。在10 - 12毫米汞柱以下,基线心率显著下降,心脏迷走神经对心率的影响减弱,但其对脉搏间期的影响并非持续改变。得出的结论是,缺氧时迷走神经作用的增强发生在成年绵羊而非胎儿绵羊中,胎儿在严重缺氧时出现的心动过缓可能是由于直接的心肌抑制。