Several new aspects of bubble-induced central nervous system injury

Abstract

Ischaemia is a major mechanism underlying central nervous system (c.n.s.) damage in decompression sickness. Some recent experimental observations on the effect of bubble-induced ischaemia on c.n.s. tissue sharpen and extend our understanding of the pathophysiology of decompression sickness. After bubble-induced brain ischaemia, a measurable increase in 111In-labelled leucocytes occurs in the injured hemisphere. By 4 h into the recovery period the cells are concentrated in zones of low blood flow, as measured by the [14C]iodoantipyrine technique. The presence of these cells during the critical early hours of c.n.s. ischaemia suggests that they may contribute to the evolution of neuronal damage. Oedema is often cited as the cause of clinical deterioration after c.n.s. ischaemia or trauma. Recent evidence indicates that the presence and degree of circumscribed brain oedema is not a good predictor of the amount of nerve cell recovery (by using cortical sensory evoked response) after bubble-induced brain ischaemia. This brings into question the role of circumscribed oedema of the c.n.s. in dysfunction of post-ischemic nerve cells.

Cerebral arterial gas embolism in swine. Comparison of two sites for air injection

“…Although ligation of multiple cerebral vessels would also produce global ischemia (Haaland et al, 1995;Burbridge et al, 2004), the effect of intravascular air on cerebral blood flow and the blood brain barrier as well as the inflammatory response that follows passage of air would not be adequately modeled in this way (Fries et al, 1957;Meyer et al, 1962;Johansson, 1980;Hallenbeck et al, 1984). In order to determine which vessel is the most appropriate for injection of air into the pig cerebral vasculature, we measured cerebral function after air embolisation into two different arteries.…”

Hyperbaric Oxygen Does Not Improve Cerebral Function When Started 2 or 4 Hours After Cerebral Arterial Gas Embolism in Swine*

“…We believe this to be caused by the random distribution of the air bubbles through the cerebral vasculature. Our strategy using titrated embolization was based on the work of other researchers who demonstrated reproducible injury by titrating embolization based on EEG or somatosensory evoked potentials (14,16,(22)(23)(24)(25)(26)(27)(28)(29)(30)(31)(32)(33)(34).…”