Influence of pentoxifylline on muscle tissue oxygen tension (pO2) of patients with intermittent claudication before and after pedal ergometer exercise

Abstract

Ten patients with Stage II chronic arterial occlusive disease (intermittent claudication) took part in a randomized, intraindividual crossover study involving acute intravenous administration of 200 mg pentoxifylline or physiological saline solution (placebo). The tissue oxygen tension (pO2) response (pO2 kinetics) following treatment with placebo revealed a nominal but statistically nonsignificant increase in arithmetic mean and median pO2 immediately after the end of exercise. Values thereafter reverted approximately to the initial values recorded at rest. Comparison of the pooled pO2 histograms during the individual periods before and after the end of exercise, however, revealed a broadening of the histogram base, reflecting both higher pO2 values and, more particularly, increased numbers of hypoxic and anoxic pO2 values. This is interpreted as an expression of nonhomogeneous capillary perfusion (maldistribution). Following administration of pentoxifylline to the same patients, there was a statistically significant increase in mean and median pO2 at ten and twenty minutes after the end of exercise. Even after thirty and sixty minutes, these values were in some cases still clearly higher than the initial preexercise values. Study of the pooled pO2 histograms discloses a right shift compared with the initial preexercise histograms. This suggests that pentoxifylline exerts a positive effect on maldistribution by making capillary perfusion more homogeneous. The results support the conclusion that, in the context of reactive hyperemia after muscular exercise, tissue oxygen supply is markedly improved by pentoxifylline in comparison with saline solution. The measurement of tissue pO2 before and at intervals after pedal ergometer exercise is a new objective technique for assessing the efficacy of blood flow-promoting therapy, permitting close simulation of the pathophysiological situation in the muscles of the lower leg in intermittent claudication.