| pubmed-article:10362286 | pubmed:abstractText | The principles of gas-induced osmosis, demonstrated in the 1970s, have been applied to the very large steady-state gradients of O2 arising between arterial blood and hypoxic tissue during hyperbaric oxygen (HBO) therapy to produce a fluid 'pump' in the desired direction for resolving accompanying oedema. Thus, in soft-tissue injuries, an oxygen-induced fluid pump would break the vicious cycle between ischaemia, hypoxia and oedema at the point of oedema rather than hypoxia, as hitherto assumed. This osmotic mechanism enables the successes of HBO therapy in hypoxic disorders to be reconciled with early failures in such areas as hyperbaric radiotherapy, where substitution of O2 for N2 in inspired air was clearly not reflected at the tissue level. This argument also applies to the success of HBO in treating air embolism and decompression sickness over simple compression. The oxygen pump would seem to offer a more plausible explanation for the success of HBO therapy than theories based upon O2 delivery by the circulation, especially when considering cardiovascular reflexes to elevated PaO2 and the marginal increase in blood O2 content upon switching to HBO from normobaric oxygen breathing. | lld:pubmed |
