Blood & Vessel
Online ISSN : 1884-2372
Print ISSN : 0386-9717
Hyperbaric oxygen treatment on cerebral thrombosis
Yasuo IMAI
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JOURNAL FREE ACCESS

1979 Volume 10 Issue 1 Pages 22-27

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Abstract

Indication of OHP treatment on cerebral thrombosis has been widely accepted. The addition of OHP treatment upon other conservative therapy resulted in better neuropsychiatrical improvement. In this paper, the difference between the mechanisms of the therapeutic effect of OHP and oxygentoxicity are mainly discussed from the biorheological point. Fluidity of the RBC membrane was determined by (1) the order parameters of electron spin resonance absorption spectra which were produced by fatty acid spin labels inserted in the membrane double layer, and (2): fluorescent polarization of anisotropic fluorescent dyes (ANS etc) inserted in membrane. The viscosity of the whole blood was measured by viscometry. The plasma MDA and VE lebels which indicate the degree of lipid peroxidation and risk factor for thrombosis were determined by spectrophotometry.
When the improvement of aphasia, agnosia and aplaxia were achieved after 10 times OHP treatment (2-2.5 ATA×1hr OHP treatment was applied with consecutive days), the whole blood viscosity, Ht, MCV, order parameter of ESR spectra and fluorescent polarization of RBC membrane were significantly decreased. These rheological improvement suspected to be effective in the supression of edema. The plasma MDA lebels were high in the beginning of OHP, but low after 10 times OHP. This tendency was more manifest in the patients who were prescribed by VE and GSH during OHP treatment. These indicate that the physiological oxygen consumption was restored and pathological process of oxygentoxicity were supressed.
Overdosis of oxygen with OHP produced inverse rheological effect on experimental animals. Though VE and GSH exerted some protective effects, all animals died from thrombosis by oxygentoxicity.
Oxygen exerts two different effects-in one hand the vicious circle are supressed by OHP therapy but in the other accelerated by oxygentoxicity.

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© The Japanese Society on Thrombosis and Hemostasis
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