Abstract

INTRODUCTION: Spreading depolarizations (SDs) are a class of pathologic electrical activity in the brain characterized by ionic equilibrium disruption and depression of brain activity. SDs are recorded in stroke and traumatic brain injury and are a predictor of secondary damage. We recently found that low end-tidal CO2 (ETCO2) may be associated with a detrimental course of SDs in patients, but it is unknown whether this association is causal. METHODS: In mechanically ventilated rats under normoxia (30% O2) assigned to either hypocapnia (ETCO2 25-30 mmHg) or hypercapnia (45-50 mmHg), we triggered SDs via microinjection of 1M KCl for 90 minutes in the cerebral cortex. Additionally, in rats brought to hypoxia (10% O2), we triggered singular SDs under hypocapnia, normocapnia (30-35 mmHg), and hypercapnia. We measured regional cerebral blood flow (rCBF), tissue oxygenation, pH, and SD electrophysiology. RESULTS: ETCO2 had no significant effect on SD duration, frequency, delay after stimulus induction, or terminal SD at the time of death. ETCO2 showed a weak negative effect on maximum rCBF, but no effect on duration or integral of rCBF response. In contrast, mean arterial pressure (MAP) showed a strong negative effect on SD duration and delay after stimulus induction but had no effect on frequency. MAP also showed a mild effect on maximum rCBF, as well as the duration and integral of rCBF response. CONCLUSIONS: This research showed that ETCO2 does not play a role in determining duration and frequency of spreading depolarizations as well as associated hyperemic response. However, we confirmed prior results that MAP may play a role since relative hypertension was shown to reduce duration of SDs and level of rCBF response.

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