Abstract

Objective: The aim of the present study was to examine the impact of moderate and profound hyperventilation on regional cerebral blood flow (rCBF), oxygenation and metabolism. Materials and methods: Twelve anesthetized pigs were subjected to moderate (mHV) and profound (pHV) hyperventilation (target arterial pO2: 30 and 20 mmHg, respectively) for 30 min each, after baseline normoventilation (BL) for 1 h. Local cerebral extracellular fluid (ECF) concentrations of glucose, lactate, pyruvate and glutamate as well as brain tissue oxygenation (ptiO2) were monitored using microdialysis and a Licox oxygen sensor, respectively. In nine pigs, regional cerebral blood flow (rCBF) was also continuously measured via a thermal diffusion system. Results: Both moderate and profound hyperventilation resulted in a significant decrease in rCBF (BL: 37.9±4.3 ml/100 g/min; mHV: 29.4±3.6 ml/100 g/min; pHV: 23.6±4.7 ml/100 g/min; p<0.05) and ptiO2 (BL: 22.7±4.1 mmHg; mHV: 18.9±4.9 mmHg; pHV: 13.0±2.2 mmHg; p<0.05). A ptiO2 decrease below the critical threshold of 10 mmHg was induced in three animals by moderate hyperventilation and in five animals by profound hyperventilation. Furthermore, significant increases in lactate (BL: 1.06±0.18 mmol/l; mHV: 1.36±0.20 mmol/l; pHV: 1.67±0.17 mmol/l; p<0.005), pyruvate (BL: 46.4±7.8 μmol/l; mHV: 58.0±10.3 μmol/l; pHV: 66.1±12.7 μmol/l; p<0.05), and lactate/glucose ratio were observed during hyperventilation. (Data are presented as mean±S.E.M.) Conclusions: Both moderate and profound hyperventilation may result in insufficient regional oxygen supply and anaerobic metabolism, even in the uninjured brain. Therefore, the use of hyperventilation cannot be considered as a safe procedure and should either be avoided or used with extreme caution.

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