Tammpere A Ia, Kaasik A A, Tal'vik T A, Paiu A Iu
Zh Nevropatol Psikhiatr Im S S Korsakova. 1985;85(10):1494-8.
The acid-base balance of the blood and cerebrospinal fluid was studied in 90 babies born in asphyxia in order to use these data in assessing the damage to the nervous system. Analysis revealed the hypoxic nature of the cerebral affection which was manifested by anaerobic glycolysis of the cerebral tissue and arterial hypoxemia. The degree of acidosis detected in the cerebrospinal fluid correlated with the severity of the nervous system damage. Children with the lethal outcome presented deeompensated respiratory acidosis, in the cerebrospinal fluid whereas children with severe neurological pathology had alkalosis. It is concluded that alkolosis is induced by an intensified catabolism of the nervous system proteins which leads to the accumulation of ammoniac compounds. The same children showed pulmonary hyperventilation leading to respiratory acidocis which was not related to pulmonary pathology. The latter points to the hypoxic impairment of the respiratory centre. At the same time, a considerable increase in the activity of the glycolytic enzymes was observed; the activity of glutamate oxalacetate transaminase increased 5-fold, the activity of lactate dehydrogenase rose two-fold.
对90例出生时窒息的婴儿的血液和脑脊液酸碱平衡进行了研究，以便利用这些数据评估对神经系统的损害。分析揭示了脑部病变的缺氧性质，其表现为脑组织的无氧糖酵解和动脉血氧不足。脑脊液中检测到的酸中毒程度与神经系统损害的严重程度相关。致死结局的儿童脑脊液中呈现失代偿性呼吸性酸中毒，而患有严重神经病理学的儿童则出现碱中毒。得出的结论是，碱中毒是由神经系统蛋白质分解代谢增强导致氨化合物积累引起的。同一批儿童出现肺过度通气，导致呼吸性酸中毒，这与肺部病变无关。后者表明呼吸中枢存在缺氧损伤。同时，观察到糖酵解酶的活性显著增加；谷氨酸草酰乙酸转氨酶的活性增加了5倍，乳酸脱氢酶的活性上升了两倍。
