Bicarbonate conservation during incomplete cerebral ischemia with superimposed hypercapnia.

摘要: We superimposed extreme hypercapnia (arterial Pco2 400-450 mmHg) immediately before and during incomplete cerebral ischemia to distinguish the role of intracellular pH (pHi) bicarbonate [( HCO3-]i) in postischemic metabolic electrophysiological recovery. Incomplete global was produced seven anesthetized dogs by 30 min intracranial hypertension followed 4 h reperfusion. ATP, phosphocreatine (PCr), pHi were measured with 31P magnetic resonance spectroscopy, [HCO3-]i calculated from Henderson-Hasselbalch equation using sagittal sinus Pco2. Cerebral blood flow reduced 7 +/- 1 ml.min-1.100 g-1 (+/- SE) hypercapnia, decreased 5.72 0.09. During normocapnic reperfusion, rapidly returned near baseline values 14 min. fell 12.1 0.9 6.0 1.2 mM midpoint recovered PCr, O2 consumption also completely. Somatosensory-evoked potentials (SEP) 43 10% control amplitude. These results are marked contrast poor SEP recovery previously observed hyperglycemic which same range as hypercapnic ischemia, but much lower (1.1 0.5 mM). Therefore, depletion may be a more important factor than end-ischemic per se. speculate that higher improve glial cell buffering capacity or decrease iron availability for hydroxyl radical production.