Intracarotid air embolism in the baboon: Effects on cerebral blood flow and the electroencephalogram

Abstract

1. (1) Cerebral blood flow has been measured by means of isotope clearance curves before, during and after intracarotid air embolism in baboons ( Papio papio) anaesthetized with pentobarbitone. The EEG was recorded before, during and after embolism. 2. (2) Control clearance curves have been analysed in terms of two mono-exponential components, one rapid (half-time = 51.3 sec ± 1.0 sec) and one slow (half-time = 8 min 8 sec ± 17.5 sec). 3. (3) The injection of 2–5 ml of air into one carotid artery produced an immediate dimunition or abolition of cerebral blood flow. This affected principally the component with a rapid half-time which ceased to be measurable for at least 30 sec. The slow component was less severely affected; in a small proportion of cases it was severely reduced or abolished for 55–320 sec. Determinations at intervals from 3 min to 24 h after the embolism, yielded normal half-times for the rapid component (with variable individual changes). 4. (4) These findings are interpreted as showing that there was a generalized arrest of cerebral cortical blood flow in the affected hemisphere immediately after the embolism. This was restored to normal within 3 min for the majority of the cortex. Some difficulties in the interpretation of isotope clearance curves after local disturbances of cerebral circulation are discussed. 5. (5) The EEG usually showed bilateral depression or silence within 30 sec of the embolism, but sometimes no major changes were observed in spite of prominent changes in blood flow. EEG recovery was markedly delayed (30–120 min) compared with the prompt restoration of normal blood flow. Wmboli producing severe immediate effects on blood flow tended to be associated with more prolonged EEG changes. Phenomena of an epileptic nature were only rarely observed. 6. (6) It is concluded that following an air embolism fine bubbles disperse throughout the cerebral hemispheres and produce an immediate generalized reduction of cerebral blood flow, which is accompanied by EEG signs of generalized cerebral anoxia. In most of the cortex, flow is restored to normal within 3 min by the absorption or passage of the bubbles. In small foci, where the cerebral perfusion pressure is lowest ( i.e., at the boundary zones between the arterial territories), the bubbles obstruct local flow for sufficient time to produce ischaemic lesions.