Increase in regional cerebral blood flow following experimental arterial air embolism

Abstract

✓ 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.

Increased Cerebral Blood Flow And Cardiac Output Following Cerebral Arterial Air Embolism In Sheep

“…The increases in Doppler and thermocouple indices were of similar magnitude, but sagittal sinus 133 xenon clearance was greater. External detection of 133 xenon clearance during the 5–10 min immediately following CAGE finds increased cerebral blood flow in cats 5 and dogs 6 of similar magnitude to that seen in the present study.…”

“…There is a transient drop in cerebral blood flow during the passage of air through the cerebral circulation 5 . An increased global cerebral blood flow has been demonstrated during the subsequent 1–2 h 5,6 . There is a persistent dilation of cerebral pial arteries following the passage of bubbles 3,5 and increase in intracranial pressure 2,6 .…”

“…An increased global cerebral blood flow has been demonstrated during the subsequent 1–2 h 5,6 . There is a persistent dilation of cerebral pial arteries following the passage of bubbles 3,5 and increase in intracranial pressure 2,6 . Other studies have shown localized decreases in cerebral blood flow during the hours following the passage of gas 2,3 …”

“…Cerebral hyperaemia and a rise in intracranial pressure have been proposed as primary pathogenic mechanisms of CAGE, 6,7 as in other head injury. However, the observations of both high and low cerebral blood flows following CAGE have not been adequately reconciled and the mechanism of increased flow has not been investigated.…”

Experimental air embolism of the brain: an analysis of the technique in the rat.

“…Hence, "spill-over" of air, for example, into the contralateral hemisphere, or, even worse, into the vertebrobasilar territory, not only diminishes the focal nature of the model, but also may render the animal preparation unstable because of brainstem ischemia or widespread embolization. 9,13,14 Fourth, the size of individual air bubbles emerging from the intra-arterial catheter or needle has usually not been controlled. Large bubbles would, of course, possess neither the surface area nor the surface activity of an equivalent volume of small emboli that may be encountered clinically.…”