| Summary: | In the last three decades, autohaemotherapy with blood treated with oxygen containing low concentrations of ozone, either alone or in combination with an elevated temperature and ultraviolet irradiation (HOU), has been used in Europe for the treatment of peripheral vascular diseases. Many apparently widely differing beneficial claims have been made for this therapeutic approach. This study has provided an objective rationale as to how HOU-treated blood administered as autohaemotherapy may work as a therapeutic agent. This study has investigated the effect of the treatment of blood in vitro with HOU on the blood platelets. The results indicate that either in healthy volunteers or in patients with PVD and/or diabetes, HOU-treated blood causes a dose-dependent, reversible inhibition of blood platelet aggregation in response to ADP and collagen, calcium ionophore A23187 and thrombin. The treatment of whole blood with HOU did not result in the destruction of platelets, as indicated by a lack of increase in release of the alpha-granule component platelet-derived growth factor into the plasma, and a increase in total platelet count. The concentrations of endothelium-derived relaxing factor (EDRF, known to be closely related to or identical with nitric oxide) and prostacyclin (PGI[2]) released from immune cells in the HOU-treated blood are increased by this treatment in vitro. EDRF and PGI[2] are both well known inhibitors of platelets aggregation and vasodilators. Evidence that the observed inhibition of platelet aggregation in treated blood is at least in part caused by EDRF production is provided by the reversal of the inhibition in the presence of oxy-haemoglobin, an EDRF inhibitor. An In vivo clinical study was performed on normal healthy volunteers using autohaemotherapy with blood exposed to UV light and ozone in medical oxygen (15 mug/mL) at a temperature of 42.5 °C. These volunteers were monitored by measurement of standard haematological parameters, a clinical chemistry profile and clinical symptoms and signs. These was no evidence of harmful effects of the treatment. In vivo HOU-autohaemotherapy enhanced the expression of the activation markers IL-2R, Ber-Mac3 and HLA-DR on peripheral blood mononuclear cells demonstrating for the first time objectively -measurable systemic changes in treated individuals. There was also significant increase in plasma prostacyclin concentrations measured as its stable metabolite 6-keto-PGF[1alpha] after HOU-autohaemotherapy. Endothelial dysfunction, with a reduction in the synthesis of vasodilators, particularly nitric oxide and perhaps also prostacyclin, plays a critical role in many vascular diseases. If autohaemotherapy with HOU-treated blood can restore endothelial function, as suggested by the evidence of an increase in prostacyclin levels in treated individuals, then this therapy could represent a major advance in the treatment of a number of vascular diseases.
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