Chang Y S, Park W S, Lee M, Kim K S, Shin S M, Choi J H
Department of Pediatrics, Samsung Medical Center, Sungkyurkwan University College of Medicine, Seoul, Korea.
Neurol Res. 1999 Mar;21(2):216-24. doi: 10.1080/01616412.1999.11740921.
The present study was done to establish whether the secondary cerebral energy failure could be reproduced in the newborn piglet subjected to transient global hypoxia-ischemia, and whether the evolution of secondary cerebral energy failure could be monitored by measuring the changes of Cyt aa3 using NIRS. Fifteen anesthetized, ventilated newborn piglets (< 3 day) were divided into 2 groups. Eight of hypoxia-ischemia (HI) group were induced transient HI by breathing 8% oxygen and complete occlusion of bilateral common carotid arteries for 30 min followed by release of occluders and reoxygenation and maintained for up to 48 h. Seven were given sham operation and maintained for 48 h also. Monitoring of cerebral Hb, HbO, HbT and Cyt aa3 were continued throughout the experiment using near infrared spectroscopy. Na+, K(+)-ATPase activity, lipid peroxidation products (conjugated dienes), tissue high energy phosphates (ATP and phosphocreatine) levels and brain glucose and lactate levels were determined biochemically in the cerebral cortex harvested at the termination of experiment. HbT as an index of a cerebral blood volume increased at 2 h after resuscitation significantly in HI group. During hypoxia-ischemia Cyt aa3 fell to -2.0 +/- 0.5 mu l-1 (p < 0.01), returned to baseline on resuscitation, but decreased again progressively from 33 h, and finally fell to -2.2 +/- 0.9 mumol l-1 (p < 0.01) at 48 h in spite of normal physiologic values. There were no changes in control animals. Cerebral level of ATP and PCr in HI group decreased significantly compared to control and ATP concentrations were correlated with the final levels of Cyt aa3. In HI group, cerebral Na+, K(+)-ATPase activity decreased, but the cerebral level of conjugated dienes, glucose, lactate was not different compared to controls. These findings suggest that secondary cerebral energy failure was successfully reproduced in the newborn piglets after transient hypoxia-ischemia and the continuous in vivo NIRS monitoring can be used as a useful tool for the monitoring of delayed cerebral injury.
本研究旨在确定在经历短暂性全脑缺氧缺血的新生仔猪中是否能再现继发性脑能量衰竭，以及是否可以通过近红外光谱法（NIRS）测量细胞色素aa3的变化来监测继发性脑能量衰竭的演变。15只麻醉、通气的新生仔猪（<3日龄）被分为2组。缺氧缺血（HI）组中的8只通过吸入8%氧气并完全阻断双侧颈总动脉30分钟来诱导短暂性HI，随后松开阻断器并进行再氧合，并维持48小时。另外7只进行假手术并同样维持48小时。在整个实验过程中，使用近红外光谱法持续监测脑血红蛋白（Hb）、氧合血红蛋白（HbO）、总血红蛋白（HbT）和细胞色素aa3。在实验结束时，对采集的大脑皮层进行生化测定，以确定钠钾ATP酶活性、脂质过氧化产物（共轭二烯）、组织高能磷酸盐（ATP和磷酸肌酸）水平以及脑葡萄糖和乳酸水平。作为脑血容量指标的HbT在HI组复苏后2小时显著增加。在缺氧缺血期间，细胞色素aa3降至-2.0±0.5μl-1（p<0.01），复苏时恢复到基线水平，但从33小时开始再次逐渐下降，尽管生理值正常，但在48小时时最终降至-2.2±0.9μmol l-1（p<0.01）。对照组动物无变化。与对照组相比，HI组的脑ATP和磷酸肌酸水平显著降低，且ATP浓度与细胞色素aa3的最终水平相关。在HI组中，脑钠钾ATP酶活性降低，但共轭二烯、葡萄糖、乳酸的脑水平与对照组相比无差异。这些发现表明，新生仔猪在短暂性缺氧缺血后成功再现了继发性脑能量衰竭，并且连续的体内近红外光谱监测可作为监测迟发性脑损伤的有用工具。
