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✓ Acute intracranial hemodynamic alterations consequent to arterial air embolism were studied in the dog using the radioxenon clearance technique. In eight dogs, the mean pre-embolic (control) hemispheric flow was 28.3 ml/100 gm/min. Following the injection of varying amounts of air into the right vertebral artery, there was an augmentation in the measured cerebral blood flow in all animals. Statistical analysis revealed the flow response to be independent of the amounts of air used in these experiments. The mean post-embolic cerebral blood flow was 39.3 ml/100 gm/min, representing a statistically significant increase of 11.0 ml/100 gm/min. Although the post-embolic supernormal flow may be due to the interaction of multiple pathophysiologic factors, air-induced traumatic vasodilatation is advocated as the most important pathogenetic mechanism. Prolonged vasodilatation with loss of autoregulation results in physiological shunting of blood through the affected capillary beds. Alterations in the intracerebral vasculature due to arterial air embolism are compared with studies by other investigators who have observed the effects in extracerebral vessels.

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✓ Oxygen tension and acid-base parameters of cerebral venous blood and cisternal cerebrospinal fluid, as well of femoral arterial blood, were studied in 14 dogs following injection of varying amounts of room air into the right vertebral artery. Acute elevations in oxygen tension were demonstrated in both cerebral venous blood and CSF, whereas hypoxemia occurred concomitantly in systemic arterial blood. Post-embolic increases in carbon dioxide tension with reciprocal diminutions in pH were evident in all sampling sites. The pathophysiological bases for these air-induced alterations are discussed.