GV. Sparacia, B. Sparacia, A.
In treating encephalic lesions with hyperbaric
oxygen our experience springs from over a decade's descriptions by
various authors who worked at appraising feasible therapies using it
in experience both clinical and experimental (3,4,5,6,7,9).
Recalling the ischemic penumbra zone's physiopathology, HBO
administration offers a restriction of post-ischemic perfusional
damage both directly through improved bio-availability of oxygen in
ischemic areas, and indirectly through regulatory action of cerebral
flow that improves perfusion in "critical" areas. Without dwelling
on the problems of metabolism and perfusion that follow cerebral
lesions, we can take for certain that:
- HBO improves oxygen diffusibility both above and
beneath tentorial level, encouraging in affected areas metabolic
and ATP action by lowering lactates and raising ATP
- Improves glucose metabolisation by lowering
production of substances, like aspartate and glutamate,
responsible for over-response of the receptors (2);
- Due to improved metabolic processes and well-timed
perfusional flow redistribution with suitably controlled
treatment, the generation of radicals in the intracranial area is
brought under greater control;
- As therapy can act only on
areas not irreversibly damaged (1), treatment must occur as early
Indeed it is the bringing of dissolved oxygen up
to glial level that is truly the new fact to be attributed to HBO
in treating brain damage. And precisely where the phenomenon of
blood redistribution from non-ischemic areas to tissues around the
lesions is to be taken into account, which is affected by the
vasoconstriction effect to which unharmed areas are notoriously
more susceptible, with evident result lowering, "stealing" and
intracranial pressure and raising tissue oxygen flow.
- Dir R.C., Faiman M.D.: "Free radical formation and
lipid peroxidation in rat and mouse cerebral cortex slices exposed
to high oxygen pressure." Brain Res. 248, 355 1982
- Gelmers HI.: "New aspects of stroke therapy." Int
Sym Calcium Antagonist. New York; feb.1988.
- Kovachich G.B., Miahara O.P., Clark G.M.:
"Depression of cortical Na/K/ATPasi activity in rats exposed to
hyperbaric oxygen." Brain Res. 206,229 1981
- Nakajama S., Meyer J.S., Amato T., Shaw T., Okabe
T., Mortel K.F.: "Cerebral vasomotor responseness during 100%
Oxygen inhalation in cerebral ischemia." Arc. Neurol. 40,27, 1983.
- Neubauer R.A.: "Regional blood flow studies of the
effect of HBO in acute stroke neurologic deficits in 30 cases."
Seventh Annual Conf. on Clinical Appl. of HBO. Anaheim CA. June
- Paulson in Neubauer R.A.: "Hyperbaric oxygen
therapy of stroke." A. Review. Landerdale by the sea. Florida USA
1983 7) Shiokawa O., Fujishima M., Yuoi T., Ibayashi S., Yagi H.:
"Hyperbaric oxygen therapy in experimentally induced acute cerbral
ischemia." Undersea biomedical research 13,3, 337 1986.