Abstract

Six patients with advanced arteriosclerosis obliterans in the lower extremities were subjected to an exercise test on a tread mill with and without dipyridamole treatment. Prostacyclin (PGI 2) release was measured by the concentration of its stable metabolite, 6-keto prostaglandin F 1α in plasma. All the patients suffered from ischemic pain during both tests, but no changes were seen in plasma 6-keto-PGF 1α. Dipyridamole did not affect the physical performance. Our results suggest that atherosclerotic vessels do not increase PGI 2 production in response to ischemia and that a single dose of dipyridamole does not change PGI 2 production.

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