Excretion of thromboxane A2 and prostacyclin metabolites during treadmill exercise in patients with intermittent claudication

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Abstract
Summary: Platelet activation, with subsequent formation of thromboxane A2 (TxA2), is thought to play a role in the development of arterial occlusion. In patients with severe atherosclerosis of the lower limbs, characterized by leg ulcers and rest pain, the basal formation of TxA2 and prostacyclin (PGI2) is increased. Corresponding data in patients with more moderate atherosclerosis of the lower limbs have not been reported. Since the capacity to physical exercise is not blunted in such patients proper evaluation of their TxA2‐PGI2 synthesis should comprise not only assessment of the basal formation, but also TxA2/PGI2 biosynthesis during conditions of elevated cardiovascular activity. To address this, we analysed these eicosanoids in patients with a history of intermittent claudication. Urinary dinormetabolites of TxB2 and PGI2 (Tx‐M and PGI‐M, respectively) were estimated by gas chromatography/negative ion‐chemical ionization mass spectrometry in samples collected prior to, during and immediately after 20 min of severe treadmill exertion. The basal excretion of Tx‐M was 105 ± 26 pg/mg creatinine. It was not changed during exercise, but increased to 176 ± 48 pg/mg creatinine (PP2 synthesis. The observed increase in PGI‐M in some of the patients is suggested to reflect tissue ischaemia induced by the lack of adequate hyperaemia during exercise.