Mismatching of ventilation and blood flow (ventila­tion perfusion inequality [Va/Q]) within diseased lungs is the most common cause of hypoxemia. Although it is not clear from our data which of pentoxifyllines numerous attributes is responsible for the observed improvement, they are consistent with several of the reported effects on the circulation, described below.

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The action of pentoxifylline on the rheologic prop­erties of blood and its use in the treatment of periph­eral vascular disease have been reviewed by Muller. Pentoxifylline appears to improve peripheral circula­tion, and thereby peripheral gas exchange, by several mechanisms that reduce blood viscosity. This in­cludes (1) increasing red blood cell deformability, (2) inhibiting platelet aggregation, and (3) promoting fibrinolysis. In addition, this medication has been shown to increase the cardiac index and decrease vascular resistance. Our data indicate that pentoxi­fylline improves indices of gas exchange in patients with COPD and in healthy volunteers during exercise.

Funding limitations precluded use of a placebo- controlled double-blinded crossover trial on a larger group of patients. Although it might have made our statistics more rigorous, the consistency of our data suggests that it would not have altered our observa­tions. Further study, however, is needed to confirm our observations.

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There was a significant increase in the healthy groups exercise Deo (Fig 3), increasing from an average baseline of 36.3 ±3.1 to a maximum of 41.8 ±3.5 ml/min/mm Hg (p<0.001). It then returned toward baseline over the following six weeks. The healthy groups stress test duration, exercise ventila­tion, heart rate, and peak oxygen consumption were not significantly affected by pentoxifylline (Table 3).

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The patients with COPD ranged from moderately impaired (FEV, = 50 percent predicted, Deo = 17 ml/ min/mm Hg) to severely impaired (FEV\<50 percent predicted, Dco<12 ml/min/mm Hg). There were no significant differences between the treatment and control groups with respect to MEFV parameters, residual volume, heart rate, oxygen saturation, or diffusing capacity (Table 1). All of the healthy subjects had normal results of pulmonary function tests (FEV, = 99.2 ±4.7 percent of predicted, resting Deo = 28.4 ±2.8 ml/min/mm Hg, mean±SE).

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The patients with COPD underwent individualized stress test protocols because they were unable to perform the standard Bruce protocol in which belt speed and inclination are both incremented  by a specified amount every three minutes. The individualized protocols began with three minutes of walking at a pace evaluated by the subject as slow. (This speed was used as the starting level for all subsequent tests.) Treadmill speed was then incremented by 0.2 mph during each subsequent three-minute period up to a speed that the patient considered “comfortable.” The healthy group, in contrast, performed the standard Bruce protocol.

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