Ioroi Tomoaki, Peeters-Scholte Cacha, Post Ilka, Leusink Cheraar, Groenendaal Floris, van Bel Frank
Department of Neonatology, Wilhelmina Children's Hospital, University Medical Centre, PO Box 85090, 3508 AB Utrecht, The Netherlands.
Exp Brain Res. 2002 May;144(2):172-7. doi: 10.1007/s00221-002-1030-z. Epub 2002 Mar 19.
Perinatal asphyxia models are necessary to obtain knowledge of the pathophysiology of hypoxia-ischaemia (HI) and to test potential neuroprotective strategies. The present study was performed in newborn piglets to obtain information about simultaneous changes in cerebral oxygenation and haemodynamics and electrocortical brain activity during a 60-min period of HI and up to 2 h of reperfusion using near infrared spectrophotometry (NIRS) and the amplitude-integrated EEG (aEEG). HI was induced by occluding both carotid arteries and decreasing the fraction of inspired oxygen (FiO(2)) to 0.08-0.12 for 60 min. The mean arterial blood pressure (MABP) and heart rate increased, the oxygenated haemoglobin (O(2)Hb) decreased, and the deoxygenated haemoglobin (HHb) increased, but total haemoglobin (tHb) remained stable during the 60-min HI period. The regional oxygen saturation (rSO(2)) was significantly decreased during the whole HI period, as was the electrocortical brain activity. Upon reperfusion and reoxygenation, the MABP normalised to baseline values but the heart rate remained increased. O(2)Hb and HHb recovered to baseline values and tHb remained unchanged. As indicated by the unchanged tHb values during the HI period, it was suggested that compensatory cerebral perfusion occurred during this period, probably via the vertebrobasilar arterial system. Furthermore, in this model a clear hyperperfusion period directly upon reperfusion and reoxygenation is not present. rSO(2) showed a quick recovery to baseline values, but the aEEG-measured electrocortical brain activity remained reduced following HI. In conclusion, the rSO(2) and aEEG showed a different time profile following perinatal asphyxia. The stable tHb during HI and reperfusion in this model differs from observations in human neonates.
围产期窒息模型对于了解缺氧缺血(HI)的病理生理学以及测试潜在的神经保护策略是必要的。本研究在新生仔猪中进行,目的是利用近红外分光光度法(NIRS)和振幅整合脑电图(aEEG)获取关于HI 60分钟期间及再灌注长达2小时内脑氧合、血流动力学和脑电皮质活动同时变化的信息。通过阻断双侧颈动脉并将吸入氧分数(FiO₂)降至0.08 - 0.12持续60分钟来诱导HI。在60分钟的HI期间,平均动脉血压(MABP)和心率升高,氧合血红蛋白(O₂Hb)降低,脱氧血红蛋白(HHb)升高,但总血红蛋白(tHb)保持稳定。在整个HI期间,局部氧饱和度(rSO₂)显著降低,脑电皮质活动也降低。再灌注和复氧时,MABP恢复到基线值,但心率仍升高。O₂Hb和HHb恢复到基线值,tHb保持不变。正如HI期间tHb值未变所表明的,提示在此期间可能通过椎基底动脉系统发生了代偿性脑灌注。此外,在该模型中,再灌注和复氧后不存在明显的高灌注期。rSO₂迅速恢复到基线值,但HI后脑电皮质活动经aEEG测量仍降低。总之,围产期窒息后rSO₂和aEEG显示出不同的时间变化特征。该模型中HI和再灌注期间tHb稳定,这与人类新生儿的观察结果不同。