Asphyxia causes acidosis which may potentiate neural injury. We hypothesized that hypoxia & hypotension cause lower brain pH and more severe neural injury than hypoxia alone. METHODS: Anesthetized piglets (age <3d) were ventilated and had a pH microprobe inserted into the brain. Hypoxic animals (HYP, n=4) breathed 5-8% O2/7% CO2 for 30 min with mean arterial pressure (MAP) kept ≥40mm Hg. Hypoxic-hypotensive animals (HTN, n=4) breathed 5-8% O2/7% CO2 for 30 min. During the last 15 min, MAP was kept at 25-30mm Hg by phlebotomy. After a 4 hr reperfusion, the brain was perfusion fixed and the histology evaluated. Brain& serum pH & somatosensory evoked potentials (SEP) were measured serially. Operated controls (SHAM, n=4) were not subjected to injury. Data are MEAN±SEM. RESULTS: Brain pH (Fig) fell rapidly to low levels (HYP 6.08±0.17; HTN 6.36±0.15; p>0.05). Brain & serum pHs did not differ in either group (p>0.05). SEP recovery in HTN (6.3± 3.3% of baseline) was less than (p<0.0001) that in HYP(31.3±13.3%). In SHAM, brain pH & SEP recovery were unchanged(p>0.05) over time. Brain and serum pH correlated (p<0.0001) in all groups. HTN pathology had severe neuronal necrosis; HYP pathology was much less severe. CONCLUSIONS: Brain & serum pH are similar with HYP& HTN. The pH changes do not correlate with pathology & SEP recovery. The results indicate that brain pH is not associated with neuropathology.Supported by the Fleur-de-Lis Foundation.

figure 1