Lewis A B, Sadeghi M
Division of Cardiology, Children's Hospital of Los Angeles, Calif.
Biol Neonate. 1987;52(5):285-91. doi: 10.1159/000242722.
Though hypoxemia has been shown to stimulate adrenal medullary catecholamine (CA) release and raise plasma CA concentrations, the extent to which concomitant acidosis influences the magnitude of this response is unclear. Eleven chronically catheterized late gestation (0.8 term) fetal lambs in utero were investigated during a baseline control period and following the onset of umbilical cord constriction-induced hypoxemia (PO2 = 5-15 Torr). Plasma CA rose in response to hypoxemia in all animals but was potentiated by the development of acidemia. Baseline norepinephrine (NE = 487 +/- 113 pg/cm3 and increased to 1,386 +/- 127 pg/cm3 (p less than 0.001) in response to hypoxemia. Hypoxemia combined with acidemia promoted an even greater rise in NE to 6,726 +/- 1,289 pg/cm3 (p less than 0.05). Plasma epinephrine (E) = 99 +/- 36 pg/cm3 during baseline observations and increased to 512 +/- 81 pg/cm3 (p less than 0.001) in response to hypoxemia. However, an additional 9-fold increase (p less than 0.05) was noted when hypoxemia was combined with acidemia (E = 4,311 +/- 1,449 pg/cm3). Thus, acidosis significantly potentiates the magnitude of the plasma CA response to hypoxemia in the late gestation fetus.
虽然低氧血症已被证明可刺激肾上腺髓质儿茶酚胺（CA）释放并提高血浆CA浓度，但伴随的酸中毒对这种反应程度的影响尚不清楚。对11只在子宫内长期插管的妊娠晚期（0.8足月）胎羊在基线对照期和脐带结扎诱导的低氧血症（PO2 = 5 - 15 Torr）开始后进行了研究。所有动物的血浆CA均因低氧血症而升高，但酸血症的发展使其增强。基线去甲肾上腺素（NE）= 487±113 pg/cm3，对低氧血症反应时增加至1386±127 pg/cm3（p<0.001）。低氧血症合并酸血症促使NE进一步大幅升高至6726±1289 pg/cm3（p<0.05）。基线观察时血浆肾上腺素（E）= 99±36 pg/cm3，对低氧血症反应时增加至512±81 pg/cm3（p<0.001）。然而，当低氧血症合并酸血症时（E = 4311±1449 pg/cm3），发现其增加了9倍（p<0.05）。因此，酸中毒显著增强了妊娠晚期胎儿血浆CA对低氧血症的反应程度。
