Brain cell membrane modification following hypercapnia and recovery in newborn piglets

Abstract

The effect of hypercapnia on brain cell membrane structure and function was studied in anesthetized newborn piglets. Lipid peroxidation products (conjugated dienes and fluorescent compounds), Na+,K(+)-ATPase activity and enzyme affinity to ATP (substrate), K+ and Na+ ions (activators), and strophanthidin (inhibitor) were measured in three groups of animals: controls, those exposed to 90 minutes of PaCO2 > 80 mmHg (hypercapnia) and those exposed the same way, following restoration of normal PaCO2 (recovery). Enzyme activity was unchanged by hypercapnia, but enzyme affinity was altered as indicated by an increase in ATP affinity. Affinities to Na+, K+, and strophanthidin were unchanged. Restoration of normal PaCO2 resulted in an increase in conjugated dienes. The data demonstrate that hypercapnia followed by restoration of normal PaCO2 in healthy term newborn piglets is associated with mild modification of brain cell membrane Na+,K(+)-ATPase, possibly due to lipid peroxidation.

Impaired Early Neurologic Outcome in Newborn Piglets Reoxygenated with 100% Oxygen Compared with Room Air after Pneumothorax-Induced Asphyxia

“…A significant decrease in its activity, leading to an influx of sodium and calcium into the cell, accompanied by water, resulting in cytotoxic cellular edema, was experienced in both the cortex (49) and the striatum (12) in piglets treated with 100% O 2 . Moreover, a highly significant production of reactive oxygen species was recently demonstrated intravitally, in asphyxiated newborn piglets likewise resuscitated with 100% O 2 for 10 min (57), and concentrations of both conjugated dienes and fluorescent compounds were significantly elevated in the cerebral cortex of asphyxiated piglets (52,58) with almost identical arterial PO 2 values (approximately 13.0 kPa) to those we measured in animals ventilated with 100% O 2 . Although the arterial PO 2 values in our R100 group did not significantly exceed the values measured in the SHAM group, both systemic xanthine oxidoreductase conversion (54) and the accumulation of purine metabolites (5-7, 9, 13, 19, 54) must have taken place in the R100 animals during the asphyxic period with global hypoxia-ischemia, which was not present in the SHAM animals without asphyxia.…”

Permissive hypercapnia in neonates: The case of the good, the bad, and the ugly

“…86 Increased cerebral blood volume following hypercapnia seems to be unrelated to rate of CSF production. 90 Although hypercapnia may alter the permeability of the blood-brainbarrier by opening of endothelial tight-cell junctions, 91,92 experimental normoxic hypercapnia has been associated with no 93 or minor 94 cerebral edema. Hypercapniainduced increased cerebral¯ow may be harmful in conditions like neonatal hypoxic ischemic encephalopathy.…”