Twenty-seven subjects suffering from peripheral occlusive arterial disease (POAD, clinical stage II-III according to Fontaine) were enrolled in this study to evaluate the effect of oxygen-ozone therapy upon hemorheological parameters and hemoglobin-oxygen affinity in patients with POAD. All patients underwent a major ozonized autohemotransfusion consisting of the slow reinfusion of 100 ml of autologous blood, previously exposed to a O(2)-O(3) mixture in a glass box for 10 min. Whole blood viscosity, erythrocyte filterability, hematocrit, and fibrinogen levels were assessed at the basal time and 30 min after the reinfusion of ozonized blood. At the same time p50 standard (p50std) values (an indicator of hemoglobin-oxygen affinity) and plasma values of malonyl dialdehyde (MDA, an indicator of lipid peroxidation) were evaluated. At the baseline, patients had significantly higher ( p<0.05- p<0.001) whole blood viscosity, MDA, and p50std values and significantly lower blood filterability ( p<0.01) as compared with 20 matched healthy volunteers (controls). Thirty minutes after the end of a major autohemotransfusion, whole blood viscosity significantly decreased ( p<0.01). This was accompanied by a significant fall in plasma fibrinogen level ( p<0.01) with no change in hematocrit. Blood filterability, MDA plasma level, and p50std values increased significantly at the same time ( p<0.01- p<0.005). The 2,3-DPG value did not change significantly. No significant changes occurred when the same patients received a non-ozonized autohemotransfusion (control test). In conclusion, ozonized autohemotransfusion may be useful to improve both the poor rheological properties of the blood and the oxygen delivery to tissues in patients suffering from POAD.

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. Vigorous exercise acutely changes platelet and B-lymphocyte CD39 expression. J Appl Physiol 98: 1414 -1419, 2005; doi:10.1152/japplphysiol.00315.2004.-CD39/ATP diphosphohydrolase is expressed on B lymphocytes, cytotoxic T lymphocytes, monocytes, platelets, and endothelial cells, and it has a critical role in the inhibition of platelet responsiveness. To determine whether strenuous exercise could acutely change expression of CD39 in platelets and lymphocytes, eight healthy sedentary men, 34 yr old (SD 7), and eight physically active men, 34 yr old (SD 6), performed graded upright cycle ergometry to volitional exhaustion. Blood samples collected both at baseline and after exercise test were employed to measure CD39 expression in platelets and lymphocytes. The percentage of circulating platelet-platelet aggregates, the "in vitro" ADP and collagen-induced platelet aggregation, and the expression of both platelet glycoprotein IIb-IIIa (PAC-1) and Pselectin (CD62) were also considered markers of platelet activation. After strenuous exercise, all subjects demonstrated significant platelet activation as judged by the increased percentage of platelet-platelet aggregates. The in vitro ADP-induced platelet aggregation and the expression of CD62P on ADP-stimulated platelets significantly increased in sedentary but not in active subjects. After exercise, all of the subjects showed a significant reduction of CD39 expression in platelet [sedentary: from 2.2 (SD 0.8) to 1.1% (SD 0.8), P ϭ 0.008; active: from 0.6 (SD 0.2) to 0.35% (SD 0.1), P ϭ 0.009] and an increase of CD39 expression in B lymphocytes [sedentary: from 47 (SD 13) to 60% (SD 11), P ϭ 0.0039; active: from 46 (SD 11) to 59% (SD 11), P ϭ 0.0038]. Taken together, these findings confirm the critical role of this ADPase in inhibition of platelet responsiveness, also suggesting a possible role of B lymphocytes in thromboregulation mechanism. sedentary men; active men; thromboregulation IN EPIDEMIOLOGICAL studies, moderate and vigorous exercise have been associated with a decrease in the risk of cardiovascular disease (1,16,27,41). However, vigorous exercise can acutely and transiently increase the risk of myocardial infarction and cardiac death, especially in sedentary subjects and in those with coronary heart disease (15, 31, 37, 43). The mechanism by which exercise triggers an acute cardiac event is not entirely known, although coronary thrombosis plays a key role. Several reports have demonstrated that strenuous exercise induces platelet activation, thus increasing thrombotic tendency (5,22,25,33,34). Various mechanisms, including increased plasma levels of norepinephrine and epinephrine (36), altered response of platelet ␣ 2 -adrenergic receptors (39), and impaired sensitivity of platelets to nitric oxide (NO) (34), have been hypothesized to explain both the increased platelet activation and reactivity after strenuous exercise. The role of hemoconcentration induced by acute exercise also has been considered (8, 40). The epidemiology of coronary artery disease indi...