de Rood M, Deloof T, Verbist A, Frühling J
Acta Anaesthesiol Belg. 1980;31 Suppl:29-41.
This study is based on the same group of neurosurgical patients as our previous publication. All, except one, had suffered from head injury. We made a first measurement of rCBF under N2O anesthesia, a second under N2O + 1% enflurane anesthesia, both at a PaCO2 of 40 Torr. A third measurement was performed under N2O + 1% enflurane but at a PaCO2 of 30 Torr. The method we used consists of the intracarotid injection of 133Xe and recording of the radioactivity by a gammacamera. Mean arterial pressure was maintained constant by an intravenous phenylephrine drip. For each measurement of each patient, a map was drawn, representing the distribution of the regional cerebral blood flows (rCBF), compared to the mean value of the hemisphere. We have studied rCBF in one case of normal hemisphere, and in cases of traumtic lesions in acute and chronic states, taking into account that the normal brain exhibits areas with higher flow in the frontoparietal and insular regions. In the normal brain, introduction of 1% enflurane decreases uniformally mean CBF, rCBF repartition not being changed. Hyperventilation to 30 Torr shows that regions with previously higher flow react more to hypocapnia by a slightly more decreased flow. In severe brain trauma, mean CBF is generally low, and it is difficult to visualize the lesions under N2O and N2O + 1% enflurane anesthesia. Neither mean CBF, nor rCBF repartition are significantly modified. On the other hand, in the acute phase, hypocapnia causes a more decreased flow in the previously well irrigated areas, and shows a lack of vascular reactivity in the damaged region. Passing to the chronic state, the patient clinically recovering, the rCBF repartition is normalized and the contused area becomes agains vasoactive. Severe losses of neuronal tissue are characterized by definitive low flows without reactivity by hyperventilation.