Zwiener U, Bauer R, Buchenau W, Hoyer D, Zieger M, Wagner H
Biol Res Pregnancy Perinatol. 1986;7(1):23-9.
To study unsolved problems of the causal chain of neonatal hypoxic brain damage in 31 hypoxic newborn non-anesthetized piglets cerebro-vascular, metabolic and EEG reactions were investigated (FiO2: 0.06-0.10, 1 h). Only in artificially ventilated newborn piglets this acute hypoxic hypoxia provoked a vital decompensation by critical depression of mean arterial blood pressure (less than or equal to 4.67 kPa [35 mmHg]) and/or a critical increase of vascular resistance (Rc) in the cerebral white matter (greater than 50%). Spontaneously breathing piglets survived always showing hyperventilation, higher pHa and an increase of cerebral O2-consumption in cerebral grey matter, partly also in white matter. This critical increase of Rc was related to a critical decrease of O2-consumption in the white matter and an insufficient decrease of Rc of the grey matter. The observed strong metabolic and hemodynamic differences between these two brain compartments can explain the evaluated special morphological vulnerability of cerebral white matter in ventilated animals.
为研究31只未麻醉的新生缺氧仔猪新生儿缺氧性脑损伤因果链中的未解问题，对其脑血管、代谢和脑电图反应进行了研究（吸入氧分数：0.06 - 0.10，1小时）。仅在人工通气的新生仔猪中，这种急性低氧性缺氧通过平均动脉血压的严重降低（小于或等于4.67 kPa [35 mmHg]）和/或脑白质血管阻力（Rc）的显著增加（大于50%）引发了生命代偿失调。自主呼吸的仔猪总能存活，表现为过度通气、较高的动脉血pH值以及脑灰质中脑氧消耗量增加，部分白质中也增加。Rc的这种显著增加与白质中氧消耗量的显著降低以及灰质Rc的降低不足有关。在这两个脑区观察到的强烈代谢和血流动力学差异可以解释所评估的通气动物脑白质特殊形态学易损性。
