Delayed Changes in Brain Cell Membrane Function, Cytochrome aa3 and Energy Metabolism after Transient Hypoxia-Ischemia in Newborn Piglets 1713

To test the hypothesis that reoxygenation-reperfusion following transient hypoxia-ischemia (HI) induces changes in brain cell membrane function and energy metabolism in newborn piglets (NP). 24 Anesthetized, ventilated NP(<3d) were divided into 2 groups. 11(HI)induced transient HI by breathing 8% O₂ and complete occlusion of bilateral common carotid arteries for 30 min followed by release of occluders and reoxygenation and maintained for up to 24 hrs(n=4) and 48 hrs(n=7), 13(S)given sham operation and maintained for 24 hrs(n=5) and 48 hrs(n=8). Monitoring of cerebral cytochrome aa3(Δ Cyt aa3) were continued throughout the experiment using near infrared spectroscopy (NIRS) to confirm whether the changes in cerebral energy metabolism can be continuously monitored in vivo. Brain cortex was harvested, frozen in liquid nitrogen and homogenized for determination of [Na⁺, K⁺ATPase(Enz)],[conjugated dienes(CDs)][ATP], and [phosphocreatine(PCr)] biochemically. Results: (Mean±SD)(*p<0.05, compared to S)Table

Table 1

[CDs] were not different between the two groups. Δ Cyt aa3 at the end of the experiment significantly correlated with brain [ATP] or [PCr] (r=0.43 p<.05; r=0.51, p<.01)

Reoxygenation/reperfusion following acute, transient hypoxia-ischemia induces delayed brain injuries in newborn piglets.